The Safety, Efficacy, and Cost Effectiveness

of Therapeutic Apheresis

July 1983

NTIS order #PB84-114842
ment, OTAHCS23, June 1983). This case study was performed as a part of OTAs assess

ment of Medical Technology and Costs of the Medicare Program.

Library of Congress Catalog Card Number 83-600554

For sale by the Superintendent of Documents,

U.S. Government Printing Office, Washington, D.C. 20402
Preface

The Safety, Efficacy, and Cost Effectiveness of

Therapeutic Apheresis is Case Study #23 in OTA’s

Health Technology Case Study Series. It was prepared in response to a request by the Senate

Finance Committee, Subcommittee on Health,

and is part of OTA’s project on Medical Technology and Costs of the Medicare Program, requested by the House Committee on Energy and

Commerce and its Subcommittee on Health and

the Environment. A listing of other case studies

in the series is included at the end of this preface.

OTA case studies are designed to fulfill two

functions. The primary purpose is to provide

OTA with specific information that can be used

in forming general conclusions regarding broader

policy issues. The first 19 cases in the Health Technology Case Study Series, for example, were conducted in conjunction with OTA’s overall project

on The Implications of Cost-Effectiveness

Analysis of Medical Technology. By examining

the 19 cases as a group and looking for common

problems or strengths in the techniques of costeffectiveness or cost-benefit analysis, OTA was

able to better analyze the potential contribution

that those techniques might make to the management of medical technology and health care costs

and quality.

The second function of the case studies is to

provide useful information on the specific technologies covered. The design and the funding levels of most of the case studies are such that they

should be read primarily in the context of the associated overall OTA projects. Nevertheless, in

many instances, the case studies do represent extensive reviews of the literature on the efficacy,

safety, and costs of the specific technologies and

as such can stand on their own as a useful contribution to the field.

Case studies are prepared in some instances because they have been specifically requested by

congressional committees and in others because

they have been selected through an extensive

review process involving OTA staff and consultations with the congressional staffs, advisory panel

to the associated overall project, the Health Program Advisory Committee, and other experts in

various fields. Selection criteria were developed

to ensure that case studies provide the following:

examples of types of technologies by function (preventive, diagnostic, therapeutic, and

rehabilitative);

examples of types of technologies by physical

nature (drugs, devices, and procedures);

examples of technologies in different stages

of development and diffusion (new, emerging, and established);

examples from different areas of medicine

(e.g., general medical practice, pediatrics,

radiology, and surgery);

examples addressing medical problems that

are important because of their high frequency or significant impacts (e.g., cost);

examples of technologies with associated high

costs either because of high volume (for lowcost technologies) or high individual costs;

examples that could provide information

material relating to the broader policy and

methodological issues being examined in the

particular overall project; and

examples with sufficient scientific literature.

Case studies either are prepared by OTA staff,

are commissioned by OTA and performed under

contract by experts (generally in academia), or are

written by OTA staff on the basis of contractors’

papers.

OTA subjects each case study to an extensive

review process. Initial drafts of cases are reviewed by OTA staff and by members of the advisory

panel to the associated project. For commissioned cases, “comments are provided to authors, along

with OTA’s suggestions for revisions. Subsequent

drafts are sent by OTA to numerous experts for

review and comment. Each case is seen by at least

30, and sometimes by 80 or more outside reviewers. These reviewers may be from relevant Government agencies, professional societies, consumer

and public interest groups, medical practice, and

academic medicine. Academicians such as economists, sociologists, decision analysts, biologists,

and so forth, as appropriate, also review the cases.

Although cases are not statements of official

OTA position, the review process is designed to

satisfy OTA of each case study’s scientific quality and objectivity. During the various stages of

the review and revision process, therefore, OTA

encourages, and to the extent possible requires,

authors to present balanced information and

recognize divergent points of view.

. . . 111
Health Technology Case Study Seriesa

Case Study Case Study

series Case study title; author(s); Series Case study title; author(s);

number OTA publication number number OTA publication numberb

1

2

3

4

5

6

7

8

9

10

11

12

Formal Anal sis, Policy Formulation, and EndStage Renal isease; b

Richard A. Rettig (OTA-BP-H-9(1))C

The Feasibility of Economic Evaluation of

Diagnostic Procedures: The Case of CT Scanning;

Judith L. Wagner (OTA-BP-H-9(2))

Screening for Colon Cancer: A Technology

Assessment;

David M. Eddy (OTA-BP-H-9(3))

Cost Effectiveness of Automated Multichamel

Chemistry Analyzers;

Milton C. Weinstein and Laurie A. Pearlman

(OTA-BP-H-9(4))

Periodontal Disease: Assessing the Effectiveness and

Costs of the Keyes Technique;

Richard M. Scheffler and Sheldon Rovin

(OTA-BP-H-9(5))

The Cost Effectiveness of Bone Marrow Transplant

Therapy and Its Policy Implications;

Stuart O. Schweitzer and C. C. Scalzi

(OTA-BP-H-9(6))

Allocating Costs and Benefits in Disease Prevention

Programs: An Application to Cervical Cancer

Screening;

Bryan R. Luce (Office of Technology Assessment)

(OTA-BP-H-9(7))

The Cost Effectiveness of Upper Gastrointestinal

Endoscopy;

Jonathan A. Showstack and Steven A. Schroeder

(OTA-BP-H-9(8))

The Artificial Heart: Cost, Risks, and Benefits;

Deborah P. Lubeck and John P. Bunker

(OTA-BP-H-9(9))

The Costs and Effectiveness of Neonatal Intensive

Care;

Peter Budetti, Peggy McManus, Nancy Barrartd,

and Lu Ann Heinen (OTA-BP-H-9(10))

Benefit and Cost Analysis of Medical Interventions:

The Case of Cimetidine and Peptic Ulcer Disease;

Harvey V. Fineberg and Laurie A. Pearlman

(OTA-BP-H-9(11))

Assessing Selected Respiratory Therapy Modalities:

Trends and Relative Costs in the Washington, D.C.

Area;

13

14

15

16

17

18

19

20

21

22

23

Richard M. Scheffler and Morgan Delaney

(OTA-BP-H-9(12))

Cardiac Radionuclide Imaging and Cost

Effectiveness;

William B. Stason and Eric Fortess

(OTA-BP-H-9(13))

Cost Benefit/Cost Effectiveness of Medical

Technologies: A Case Study of Orthopedic Joint

Implants;

Judith D. Bentkover and Philip G. Drew

(OTA-BP-H-9(14))

Elective Hysterectomy: Costs, Risks, and Benefits;

Carol Korenbrot, Ann B. Flood, Michael Higgins,

Noralou Roos, and John P. Bunker

(OTA-BP-H-9(15))

The Costs and Effectiveness of Nurse Practitioners;

Lauren LeRoy and Sharon Solkowitz

(OTA-Bp-H-9(16))

Surgery for Breast Cancer;

Karen Schachter Weingrod and Duncan Neuhauser

(OTA-BP-H-9(17))

The Efficacy and Cost Effectiveness of

Psychotherapy;

Leonard Saxe (Office of Technology Assessment)

(OTA-Bp-H-9(18))d

Ass*sment of Four Common X-Ray Procedures;

Judith L. Wagner (OTA-BP-H-9(19))e

Mandatory Passive Restraint Systems in

Automobiles: Issues and Evidence;

Kenneth E. Warner (OTA-BP-H-15(20))f

Selected Telecommunications Devices for HearingImpaired Persons;

Virginia W. Stern and Martha Ross Redden

(OTA-BP-H-16(21))g

The Effectiveness and Costs of Alcoholism

Treatment;

Leonard Saxe, Denise Dougherty, Katharine Esty,

and Michelle Fine (OTA-CS-H-22)

The Safety, Efficacy, and Cost Effectiveness of

Therapeutic Apheresis;

John C. Langenbrunner (Office of Technology

Assessment)

aAvaflable for de by the !juperintendent of Documents, U.S. Government dBac~ound papr #3 to Tk hp]ications of Cost--tiveness ~alYs~ of

Printing Office, Washington, D. C., 20402, and by the National Technical Medical Tixhnology.

Information Service, 5285 Port Royal Road, Springfield, Va., 22161. Call eBac~ound pawr #S to The Implications of Cost-Effectiveness ~alYs~ of

OTA’S Publishing Office (224-8996) for availability and ordering infor- Meokal Technology.

mation. fBac~ound paPr #l to OTA’S May 1982 report Technology and ~ndib~gin~ publication numbers appear in p~enth=. capped People.

c~e tit u c= in the series were 17 ~ate]y issued CiISS in &c&ound Background Paper #2 to Technology and Hand”capped People.

Paper #2: Case Studies of Med”caI Technologies, prepared in conjunction

with OTA’S August 19&l report The Implications of Cost-Eff&tivenew Anak

vsis of Medical Technology.

iv
OTA Staff for Case Study #23

H. David Banta, Assistant Director, OTA

Health and Life Sciences Division

Clyde J. Behney, Health Program Manager

John C. Langenbrunner, Study Director

Anne Kesselman Bums, Project Director

Cynthia King, Analyst

Pamela Simerly, Research Assistant

Kerry Britten Kemp, Division Editor

Virginia Cwalina, Administrative Assistant

Jennifer Nelson, Secretary

Mary Walls, Secretary

OTA Publishing Staff

John C. Holmes, Publishing Officer

John Bergling Kathie S. Boss Debra M. Datcher Joe Henson

Glenda Lawing Linda Leahy Donna Young
Advisory

Costs of

Frank Baker

Panel on Medical Technology and

the Medicare Program

Stuart Altman, Panel Chair

Dean, Florence Heller School, Brandeis University

Vice President

Washington State Hospital Association

Robert Blendon

Senior Vice President

The Robert Wood Johnson Foundation

Jerry Cromwell

President

Health Economics Research

Chestnut Hill., Mass.

Karen Davis

Johns Hopkins University

School of Hygiene and Public Health

Robert Derzon

Vice President

Lewin & Associates

Washington, D. C’.

Howard Frazier

Director

Center for the Analysis of Health Practices

Harvard school of Public Health

Clifton Gaus

Center for Health Policy Stud-es

Washington, D.C.

Jack Hadley

Urban Institute

Washington, D. C.

Kate Ireland

Chairman, Board of Governors

Frontier Nursing Service

Wendover, Ky.

Judith Lave

Graduate School of Public Health

University of Pittsburgh

Mary Marshall

filegate

Virginia House of Delegates

Walter McNerney

Northwestern University

Morton Miller

President

National Health Council

New York, N. Y.

James Mongan

Executive Director

Truman Medical Center

Kansas City, Mo.

Seymour Perry

lnstitute for Health Policy Analysis

Washington, D. C.

Robert Sigmond

Blue Goss of Greater Philadelphia

Anne Somers

Department of Evironment and

Community and Family Medicine

Rutgers University

Paul Torrens

UCLA School of Public Health

Keith Weikel

Group Vice President

AMI

McLean, Va.

vi
Contents

Chapter

Glossary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

CHAPTER 1: INTRODUCTION AND SUMMARY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Background and Scope of the Case Study... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Apheresis: Definitions, Descriptions and Developments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Scientific and Medical Aspects of Apheresis: Issues and Evidence . . . . . . . . . . . . . . . . . . . . . . . . . . .

Cost Effectiveness and Reimbursement Policy: Issues and Evidence . . . . . . . . . . . . . . . . . . . . . . . . . .

Implications for Policy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Organization of the Case Study . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

CHAPTER 2: APHERESIS: DEFINITIONS, DESCRIPTIONS, AND DEVELOPMENTS.. . . . . . . . .

Historical Development . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

The Scientific and Medical Basis for Use . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

The Treatment Process . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Organizational Settings and Staffing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Frequency, Intensity, and Duration of Blood Component Exchange . . . . . . . . . . . . . . . . . . . . . . . . .

Circulatory Access and Replacement Fluids. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Drug Therapy Used With Apheresis. , . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Equipment Technology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Centrifugal Systems . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Membrane Separation Devices . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Future Technological Directions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

FDA Device Regulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

CHAPTER 3: SCIENTIFIC AND MEDICAL ASPECTS OF APHERESIS: ISSUES AND EVIDENCE

Methodological Issues . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Treatment Design . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Research Design . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Patient Selection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Outcome Measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Safety: A Review of the Evidence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Efficacy and Effectiveness: A Review of the Evidence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Protein-Related Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Antibody-Related Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Immune-Complex Related Diseases. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Cell-Related Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Conclusions and Directions for Research . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

CHAPTER4: COST EFFECTIVENESS AND REIMBURSEMENT POLICY: ISSUES AND EVIDENCE

Cost Effectiveness . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Estimating Costs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Cost Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Third-Party Reimbursement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Federal Policies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Private Sector Policies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

CHAPTER 5: IMPLICATIONS FOR POLICY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Appendixes

A. Health Program Advisory Committee and Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

B. Apheresis for Hemolytic-Uremic Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

C. Apheresis for Inhibitors to Factor VIII . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

D. Apheresis in Guillain-Barre Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Page

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68

72
E. The Cause and Pathological Development of Autoimmune Diseases . . . . . . . . . . . . . . . . . . . . . . . . 76

F. American Red Cross Blood Services Bibliography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 159

Tables

Table No. Page

l. Reported Use of Therapeutic Apheresis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14

2. Automated Blood Cell Separation Systems . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20

3. Selected Diseases Treated With Apheresis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31

4. TherapeuticApheresis for Miscellaneous Immunological Diseases and Diseases of Unknown Cause 39

5. Present Apheresis Research Activity. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41

6. Ten General Principles of Analysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46

7. Estimating Costs of Apheresis Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48

B-1. Apheresis Experience Among Patients Diagnosed With Hemolytic-Uremic Syndrome . . . . . . . . 65

B-2. Variability in Effectiveness of Plasma Exchange Therapy for Hemolytic-Uremic

Syndrome as Expressed in Selected Outcome Measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 66

C-1. Apheresis Experience Among Patients Diagnosed With Inhibitor to Factor VIII... . . . . . . . . . . 68

C-2. Effectiveness of Apheresis for Factor VIII Inhibitors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69
Glossary

Air-emboli: A bubble of air obstructing a blood vessel.

Anaphylaxis: An unusual or exaggerated allergic

reaction.

Antibodies: The chemicals in the human body’s defense system that identify foreign substances, lock

onto them, and trigger the body’s immune attack

on foreign substances. The body makes more than

a million antibodies, each different and each capable

of recognizing and attacking only one substance—

one type virus, one type of bacteria, and so on.

Anticoagulant: Substances inhibiting normal blood

clotting.

Antigen: A large molecule, usually a protein or carbohydrate, which when introduced in the body stimulates the production of an antibody that will react

specifically with the antigen.

Atrophy: A wasting away; a diminution of the size

of a cell, tissue, organ, or part.

Autoimmune: Directed against the body’s own tissue.

In autoimmune diseases, pathological antibodies are

produced that attack the body’s own normal tissue,

such as kidney cells in glomerulonephritis or the

nerve/muscle junction in myasthenia gravis.

Cost-benefit analysis (CBA): An analytical technique

that compares the costs of a project or technological application to the resultant benefits, with both

costs and benefits expressed by the same measure.

This measure is nearly always monetary.

Cost-effectiveness analysis (CEA): An analytical technique that compares the costs of a project or of alternative projects to the resultant benefits, with costs

and benefits/effectiveness expressed by different

measures. Costs are usually expressed in dollars, but

terms such as “lives saved, ” “disability avoided, ”

“quality-adjusted life years saved,” or any other relevant objectives. Also, when benefits/effectiveness

are difficult to express in a common metric, they

may be presented as an “array. ”

CEA/CBA: A composite term referring to a family of

analytical techniques that are employed to compare

costs and benefits of programs or technologies. The

terms as used in this case study means “cost-effectiveness analysis/cost-benefit analysis.”

Cytapheresis: A type of therapeutic apheresis involving the selective removal of specific blood cells (red

cells, white cells, and/or platelets).

Cytotoxic: A specific toxic action on cells of special

organs.

Discounting: A procedure used in economic analysis

to reduce to present value those costs and effects that

occur in future years. Discounting is based on two

premises: 1) individuals prefer to receive benefits

today rather than in the future, and 2) resources invested today in alternative programs could earn a

return over time.

Drug: Any chemical or biological substance that may

be applied to, ingested by, or injected into humans,

in order to prevent, treat, or diagnose disease or

other medical conditions.

Effectiveness: Same as efficacy (see below) except that

it refers to average or actual conditions of use.

Efficacy: The probability of benefit to individuals in

a defined population from a medical technology applied for a given medical problem under ideal conditions of use.

Erythrocytapheresis: A type of cytapheresis involving

the removal of red cells.

Extracorporeal: Outside the body, as in extracorporeal

tubing for membrane apheresis equipment.

Glomerulonephritis: A variety of nephritis characterized by inflammation of the capillary loops in the

glomeruli of the kidney.

Granulocytes: Any cell containing granules, especially a leukocyte containing certain types of granules

in its cytoplasm.

Hemolysis: Separation of the hemoglobin from the red

cells and its appearance in the plasma.

Hybridoma: A hybrid cell resulting from the fusion

of two cells: a lymphocyte producing an antibody

and a myeloma (or tumor cell), which grows well

in culture and allows hybridoma to be established

permanently. The antibodies from a given hybridoma are identical (“monoclinal”).

Hyperviscosity: Excessive thickness of blood.

Hypocalcemia: Reduction of the blood calcium below

normal.

Immune complexes: Antigen-antibody complexes that

can be deposited in tissue. In immune-complex related diseases, such as rheumatoid arthritis, this

deposition occurs and produces severe inflammation

and tissue damage.

Immunoglobutin: A protein of animal origin endowed

with known antibody activity. Immunoglobulins

function as specific antibodies and are responsible

for the humoral aspects of immunity. They are

found in the serum and in other body fluids and

tissues. There are five basic classes of immunoglobulins—IgA, IgD, IgE, IgG, and IgM.

Immunosuppressive: The artificial prevention or

diminution of the immune response.

Incidence: In epidemiology, the number of cases of disease, infection, or some other event having its onset

during a prescribed period of time, in relation to the

unit of population in which it occurs. Incidence is

a measure of morbidity or other events as they happen over a period of time.

ix
Inpatient care: Care that includes an overnight stay

in a medical facility.

Leukocytes: The white cells of blood.

Leukapheresis: A type of cytapheresis involving the

reduction of excess white cells, as in leukemia.

Locke’s solution: A solution of sodium chloride,

calcium chloride, potassium chloride, sodium bicarbonate, and dextrose.

Lymphapheresis: A type of cytapheresis involving the

removal of lymphocytes (certain white cells) without

depletion of plasma components, making any

plasma replacement, therefore, unnecessary.

Lymphocytes: A type of leukocyte, chiefly a product

of lymphoid tissue, which participates in humoral

and cell-mediated immunity.

Lymphokines: The biologically active soluble factor

produced by white blood cells.

Lyrnphoplasmapheresis: A type of cytapheresis involving a combination of lymphopheresis and plasmapheresis: the removal of both lymphocytes and

plasma, usually during a single procedure, and requiring the use of replacement fluids.

Medicaid: A Federal program that is administered and

operated individually by each participating State

government that provides medical benefits to certain low-income persons in need of health and medical care.

Medical technology: The drugs, devices, and medical

and surgical procedures used in medical care.

Medicare: A nationwide, federally administered health

insurance program authorized in 1965 to cover the

cost of hospitalization, medical care, and some related services for eligible persons over age 65, persons receiving Social Security Disability Insurance

payments for 2 years, and persons with end-stage

renal disease. Medicare consists of two separate but

coordinated programs—hospital insurance (Part A)

and supplementary medical insurance (Part B).

Health insurance protection is available to insured

persons without regard to income.

Monoclinal antibodies: Antibodies derived from a

single source or clone of cells which recognize only

one kind of antigen.

Myeloma: A malignant disease in which tumor cells

of the antibody-producing system synthesize excessive amounts of specific proteins.

Outpatient care: Care that does not include an overnight stay in the facility in which care is provided.

Paraproteinemias: Presence in the blood of a paraprotein (immunoglobulin produced by a clone of neoplastic plasma cells proliferating abnormally), such

as a cryoglobulin or a macroglobulin, in amounts

not normally observed.

Pathogen: A specific causative agent of disease.

Plasma: The fluid portion of blood in which particulate

components are suspended.

Plasma exchange: An often used therapeutic application of apheresis, in which a large volume (up to

5 liters) of plasma is removed and replaced by an

equivalent volume of fluids such as fresh frozen

human plasma, plasma substitute, or combination

of albumin, calcium, and normal saline, depending

on the need of the individual patient. Some researchers make a distinction between plasma exchange and

plasma infusion. In the former case, plasma is

removed and replaced by a colloid solution, commonly albumin, fresh frozen plasma, or simple

donor plasma. Although the plasma replacement in

early cases was initiated only for purposes of expansion of the blood vessel “intravascular” volume, later

investigators suggested that the administration of

fresh frozen plasma had an independent therapeutic

effect. This led some investigators to administer it

without apheresis; this is described in the literature

as plasma infusion.

Plasma perfusion: A multiple separation technique in

therapeutic apheresis whereby the patient’s plasma

is first isolated from the cellular elements and subsequently passed through a filtration medium (either

absorptive columns or membranes) to remove unwanted plasma components. The filtered plasma is

then returned to the patient along with the cells.

Plasmapheresis: Strictly defined, a type of apheresis

that involves the removal of small amounts of plasma. The primary use of this procedure is in the collection of source plasma for subsequent processing

into serum fractions, and it has been traditionally

found in blood banks and in the plasma collection

industry.

Platelets: Oval-shaped structures found in the blood

of all mammals and chiefly known for their role in

blood coagulation.

Plateletapheresis: A type of cytapheresis involving the

reduction of abnormally high levels of platelets.

Prevalence: In epidemiology, the number of cases or

disease, infected persons, or persons with disabilities

or some other condition present at a particular time,

in relation to the size of the population. Prevalence

is a measure of morbidity at a point in time.

Proteins: The functional and structural components

of cells.

Purpura: A group of disorders characterized by

purplish or brownish-red discoloration, easily visible through the epidermis, caused by hemorrhage

into the tissues.

Randomized clinical trial (RCT): An experimental

design involving the random assignment of human

subjects either to an experimental group (in which

subjects receive the treatment being studied) or to

a control group (in which subjects do not receive

the treatment being studied). Also referred to as

“randomized controlled clinical trial” or “controlled

clinical trial.”

Registry: The collection of health or medically related

data typically abstracted from a specific document

(e.g., medical record or death certificate) using criX
teria that are applied retrospectively. In practical

terms, registries generally cover discrete political or

geographic areas.

Reliability: A measure of the consistency of a method

in producing results. A reliable test gives the same

results when applied more than once under the same

conditions. Also called “precision. ”

Remission: Abatement or diminution of the symptoms

of a disease.

Risk: A measure of the probability of an adverse or

untoward outcome and the severity of the resultant

harm to health of individuals in a defined population and associated with use of a medical technology applied for a given medical problem under

specified conditions of use.

Safety: A judgment of the acceptability of risk (see

above) in a specified situation.

Technology: The application of organized knowledge

to practical ends.

Technology assessment: A comprehensive form of policy research that examines the technical, economic,

and social consequences of technological applications. It is especially concerned with unintended, indirect, or delayed social impacts. In health policy,

the term has also come to mean any form of policy

analysis concerned with medical technology, especially the evaluation of efficacy and safety. The

comprehensive form of technology assessment is

then termed “comprehensive technology assessment .“

Validity: A measure of the extent to which an observed

situation reflects the “true” situation. Internal validity is a measure of the extent to which study results

reflect the true relationship of a “risk factor” (e.g.,

treatment or technology) to the outcome of interest

in study subjects. External validity is a measure of

the extent to which study results can be generalized

to the population that is represented by individuals

in the study, assuming that the characteristics of that

population are accurately specified.

Vasculitis: Inflammation of a blood vessel.

xi
1.

Introduction and Summary
1.

Introduction and Summary

BACKGROUND AND SCOPE OF THE CASE STUDY

For several centuries, one of the chief therapeutic methods besides the administration of herbs

was to attempt to remove noxious substances

from the body—either by a general purging, often

with drastic laxatives, or still more dramatically, by bloodletting. It has been said that several

important persons, Louis XIII of France and

George Washington, for instance, were probably

killed by such therapy (43,137).

In the past decade, the medical community has

increasingly used therapeutic apheresis, * a technology * * initially mindful of the ancient practice

of bloodletting. In therapeutic apheresis, a patient’s plasma and/or blood cellular parts are

separated and then removed from the blood and

replaced by substitute plasma or a related physiological solution. It is believed that abnormal or

harmful substances or cells are thereby removed,

leading to a cure or arrest of the disease. Results

reported in the scientific literature have been

dramatic, and apheresis is being used to treat an

increasing number of medical conditions. Skepticism over the validity of such claims and also

the high costs of apheresis, however, have

touched off recent controversies over this procedure’s use.

Therapeutic apheresis is not a new procedure

but the extent of its use has grown, and may continue to grow, substantially and rapidly. From

1977 through 1980, procedure volume increased

● There is some debate over the proper terms for the procedures

described in this case study. The term “plasmapheresis” has been

used in the medical literature since 1914. Some argue that the more

technically correct and appropriate noun to describe the separation

and removal of blood components is “apheresis” (see, e.g., 67). In

any case, the reader should be aware that the terms “plasmapheresis”

and “apheresis” are used rather interchangeably in the literature as

well as in common usage (73).

● *The Office of Technology Assessment (OTA) defines technolow as the practical application of organized knowledge. The term

meul’cal technology, as used in this case study, is a drug, device,

or medical or surgical procedure used in medical care. (The term

may also apply to the organizational and supportive systems within

which medical care is delivered, but those systems are not the focus

of this case study. ) (95).

more than 500 percent, from around 5,000 to over

40,000 procedures per year (108). These estimates

were developed retrospectively, because there has

been no formal reporting system. In the late

1970’s, the rate of growth far outpaced the estimates. The now defunct National Center for

Health Care Technology, for example, originally estimated use in 1979 at “hundreds of procedures, ” only to learn later that the actual procedure volume that year hovered around 16,000

(34). This phenomenal rate of growth between

1977 and 1980 led in turn to general estimates of

a half million procedures per year by 1985. Very

recently, however, these estimates have been revised downward because of increased concern by

health care professionals and third-party payers

alike over the technology’s safety, effectiveness,

and costs (35).

At present, apheresis is primarily accepted as

an acute therapy in a small group of relatively

obscure diseases, and the number of patients undergoing treatment totals approximately 20,000

(70). Like another new technology of recent years,

the computer, therapeutic apheresis might in some

respects be characterized as a “solution looking

for problems.” This is evidenced by the fact that

apheresis is being evaluated as a chronic treatment

modality for several major diseases, including

rheumatoid arthritis, multiple sclerosis, and certain forms of cancer. These disorders represent

a potential patient population of hundreds of

thousands of cases in this country. Because patient benefits for these disorders have often been

only partial, temporary, or equivocal, the emergence of efficacy and, especially, cost concerns

is not surprising.

The costs of apheresis have, in fact, become a

particularly volatile issue. Therapeutic apheresis

may be found to have great potential for reducing illness and death. The potential number of

medical conditions and size of the patient population that could be covered, in combination with

the costs of apheresis treatment ($400 to $1,200

3
4 ● Health Technology Case Study 23: The Safety, Efficacy, and Cost Effectiveness of Therapeutic Apheresis

per treatment, with a significant number of treatments needed per patient), however, point to a

possibly vast expenditure of funds on apheresis—

in the billions of dollars. This cost issue has been

further highlighted because some Americans already question the resource expenditures of over

$1 billion per year for each of three established

therapies: coronary bypass surgery, kidney dialysis and transplants, and treatment of newborns

in neonatal intensive care units (2).

Major market opportunities for equipment,

supplies, and services have been forecast for

apheresis technology in the next decade. As a

result, therapeutic apheresis has been the subject

of investor interest and increased industry participation. Vigorous research, development, and

marketing activities have been undertaken by

companies in the United States, Europe, and

Japan. Major American participants include

Haemonetics Corp., International Business Machines (IBM), Baxter Travenol, Cobe LaboratoSUMMARY

Apheresis: Definitions,

and Developments*

Descriptions,

Apheresis is a procedure in which blood is separated into its basic components (red cells, white

cells, platelets, and plasma), and one or more of

these is selectively removed from the blood. It is

applied therapeutically for the purpose of curing,

alleviating, or treating a disease or its symptoms.

The procedure can take several forms, though it

is usually accomplished by removing venous

whole blood from the body, separating the blood

into cellular and noncellular (plasma) parts or

“fractions,” and returning the cellular fraction to

the patient. Just as in kidney dialysis, blood flows

from a patient to a machine where it is treated

and then returned to the patient by way of an extracorporeal (i.e., outside the body) blood tubing set.

The idea of apheresis first originated in 1914,

but it was not until World War II that human

● A number of the scientific and medical terms used in this case

study are defined in the Glossary,

ries, Parker-Hannifin, Cordis-Dow, and Millipore

Corp. These companies have developed several

new therapeutic techniques in response to perceptions of a need to reduce present costs. These

techniques are discussed in later chapters, although a description or analysis of the industry

or market that has developed around the technology of therapeutic apheresis is beyond the scope

of this study.

This case study was prepared as part of OTA’s

project on “Medical Technology and Costs of the

Medicare Program.” The entire project is being

conducted in response to requests by the House

Committee on Energy and Commerce and its Subcommittee on Health, and the Subcommittee on

Health of the Senate Committee on Finance. This

particular portion of the project responds to a

specific request by the Senate Finance Committee’s Subcommittee on Health for scientifically

based information on the effectiveness of therapeutic apheresis.

apheresis was considered and used as a means of

meeting the increased demand for plasma. Over

the last 20 years, the collection and processing of

donor plasma has evolved into a major industry

as the demand for plasma fractions, such as albumin, has increased. The first successful therapeutic use of apheresis was reported in the late

1950’s, and during the next few years, reports appeared on the application of apheresis to several

diseases. Recent advances during the past decade

in basic research, in equipment, and in the technique of apheresis have provided a rationale for

carrying out apheresis on a much larger scale and

in a wider variety of diseases. To date, apheresis

has been used in the treatment of over 75 diseases,

and an additional 41 diseases have been identified

as possible candidates for this therapy.

The rationale for performing apheresis is to remove one or more components of blood that conceivably contain and carry pathogenic substances

linked to a patient’s disease process. Various

diseases have been increasingly associated with

these “abnormal” blood components in the circulation, and these components are believed to
Ch. 1—lhtroduction and Summary ● 5

initiate or aggravate the disease condition. Apheresis typically has been used in diseases involving

excessive levels of three main types of substances

found in blood components: plasma protein, antibodies, and immune complexes. Physicians reason that if they can properly identify and remove

these problem substances, the disease process may

be controlled and the patient’s clinical condition

should improve. Unfortunately, the effects of

apheresis are not well understood. The volume

and frequency of blood component exchanges

have not been well established, and for the most

part, benefits remain anecdotal and difficult to

reproduce. Effects of therapeutic apheresis are not

generally believed to be curative, but are usually

of a temporary nature. Often the procedure is

used in conjunction with other treatments,

especially drug therapy.

Apheresis treatment is provided almost exclusively through large medical school hospitals

and community/Red Cross blood banks. A few

commercial, freestanding, independent centers

have been established during the past 2 or 3 years,

although it appears that this trend may be moderating.

Approximately 5 percent of therapeutic apheresis procedures are performed manually by removing whole blood, spinning it down in a stationary centrifuge, and returning the cellular components to the patient. For most apheresis procedures, however, automated centrifuge equipment is used. Some new major developments in

hardware, including adsorption columns and

semipermeable membranes that function as

molecular sieves, are now either undergoing clinical tests or about to be marketed for general use.

These advances in equipment may, in the course

of the next decade, be improved or even overshadowed by advances in basic biomedical research or by emerging developments such as biotechnology.

understanding of reasons for its efficacy. * As a

result, much of the existing literature on the effectiveness of apheresis is not of very good methodological quality. The great majority of the reported studies are case reports without any conclusive control groups, blinding, randomization,

or other techniques used in controlled clinical

trials. Even if standardized protocols could be

developed, scientific research on the effectiveness

of apheresis might be difficult or undesirable to

conduct. Ethical and practical problems have

hindered the implementation of randomized clinical trials and other controlled research. Furthermore, the assessment of individual treatments is

difficult because apheresis procedures are often

provided in combination with drug therapy or

other treatment regimens.

Measures of outcome have been a recurring critical issue, as well, because such measures have

varied enormously, both across and within disease

indications. Outcome measures have sometimes

focused on improvement in clinical signs and

symptoms, other times focused on biologic and

chemical parameters, and in other instances been

lacking, not specified, or ill-defined. The reliability and validity** of outcome measures are also

problematic because of the nature of several illnesses treated by apheresis which are characterized by abrupt and pronounced changes that may

or may not be attributable to therapeutic effects.

Finally, the interpretation of many studies of

apheresis that are available is hindered because

only particular types of patients, i.e., the “worst

cases, ” tend to receive apheresis treatments (as a

last resort after other conventional therapies fail).

Because of these various limitations of the available research evidence, indications about the safety, efficacy, and effectiveness of apheresis are necessarily limited. Nevertheless, some tentative conclusions and directions for treatment can be discerned.

Scientific and Medical Aspects

of Apheresis: Issues and Evidence

By almost any standard, treatment by apheresis

is still in relatively early stages of development—

there are no ideal protocols based on a complete

‘Efficacy is the health benefit as measured under controlled conditions such as those in a randomized clinical trial. Efkctiveness is

the health benefit as measured under average conditions of use.

* *ReJiabiMy is a measure of consistency of a method in producing results. A reliable test gives the same results when applied more

than once under the same conditions. VaM@ is a measure of the

extent to which a situation that is observed in a study is reflective

of the true situation.

98-822 (1 - 83 - 2 : QL 3
6 ● Health Tehnology Case Study 23: The Safety, Efficacy, and Cost Efectiveness of Therapeutic Apheresis

Apheresis appears to be a relatively safe procedure, though it is not without at least short-term

risks. The long-term risks of removing useful

blood components have been termed “worrisome”

and are unclear at best. Apheresis device equipment can also be termed effective in the sense that

the technology accomplishes the intended removal

of plasma and cells. However, there is very little

definitive evidence documenting the widespread

success of the technology in actually improving

health. The use of apheresis has been generally

acknowledged as an effective treatment application for acute therapy in a small group of relatively obscure diseases. These include acquired myasthenia gravis, primary macroglobulinemia (Waldenstrom’s) and hyperglobulinemias, including

multiple myeloma. There is certainly suggestive

evidence, too, that therapeutic apheresis is successful in arresting the disease process for some

patients with other specific disease conditions.

Convincing proof of clinical efficacy, however,

is still lacking in the wider variety of diseases in

which this treatment is being used.

Large prospective randomized trials, many of

them funded by the National Institutes of Health,

have been organized for several disease applications in which apheresis therapy has been used,

in order to more precisely define what advantages,

if any, these treatments may have. Further research will be needed to both compare present

treatment approaches with new and emerging

blood filtration methods and to test related scientific advances (e.g., the use of monoclinal antibodies).

Cost Effectiveness and Reimbursement

Policy: Issues and Evidence

In addition to the issues of health status or other

health outcome related effects (i.e., safety, efficacy, and effectiveness) of apheresis, efficiency

issues must also be addressed. Two important

methods used to assess the costs and benefits of

therapeutic apheresis, and develop comparisons

among effects, costs, and benefits are cost-benefit

analysis (CBA) and cost-effectiveness analysis

(CEA). CBA is used to develop comparisons of

the benefits of treatments against the resources

they consume, with both benefits and costs expressed in dollars. It is difficult to conduct a CBA

for apheresis, because even though the therapy

has reportedly lessened suffering and helped prolong lives, reliable estimates of these benefits have

yet to be determined and quantified. CEAs are

used to evaluate the relative cost of alternative

treatments per unit of effectiveness (typically

specified in nonmonetary terms). CEAs for apheresis have not yet been conducted because sufficient data on outcomes for apheresis and alternative treatments are lacking.

Nevertheless, the task of evaluating treatments

can include the context of costs, for which there

have been several general estimates. National expenditure estimates on apheresis therapy, which

is currently performed on only selected patients,

range from $3.2 million to $240 million. If, however, apheresis therapy is extended in the future

to the wider array of diseases to which it has been

only experimentally applied thus far, total treatment costs could range from $650 million to over

$7 billion per year.

Third-party payment will bean important influence on future adoption, use, and economic effects of therapeutic apheresis, through the funding

and reimbursement policies of both private and

government insurance programs. Reimbursement

policies, like other aspects of therapeutic apheresis, have been the subject of some debate because

of the competing factors of cost and therapeutic

promise. The development of most of these policies has been recent. On September 15, 1981, the

Health Care Financing Administration issued its

first national instructions for apheresis, announcing coverage under the Medicare Program for only

a small group of relatively rare disease indications.* Medicaid coverage regulations vary from

State to State because of changes in Federal funding policies, which provide States with some latitude in deciding how Federal funds are spent.

Other governmental programs, such as the Department of Defense’s CHAMPUS, as well as pri-

● On Apr. 20, 1983, Public Law 98-21 provided for extensive

changes in Medicare reimbursement policies for hospital-based care.

Under the statute, whose provisions will be phased in over 3 years,

hospitals will receive a flat fee per patient, set prospectively, on the

basis of patient diagnosis in one or more of 467 diagnosis-related

groups (DRGs). It is unclear at this point how the DRG-based payment system will affect the adoption and use of apheresis. What

is certain, however, is that information on the effectiveness of this

treatment will be even more important as physicians and patients

face increasingly scarce resources.
Ch. l—Introduction and Summary ● 7

vate medical insurers, also vary on which disease

indications should be covered, probably stemming

from a less than consistent scrutiny of the evidence

on safety and efficacy. A widening of Medicare

and private insurer coverage of therapeutic apheresis for specific life-threatening complications

(e.g., rheumatoid vasculitis) is probable in the

near future. But direct cost estimates and the

potential cost of possibly premature diffusion

alone make it unlikely and unwise that third-party

payers will support any broad extension of benefits for apheresis treatment until more valid data

is generated. Until evidence is available, therapeutic apheresis will largely be viewed as an experimental technique, not to be considered as a

part of routine care. In light of such a situation,

present research and clinical trials being carried

out assume even greater importance.

Implications for Policy

Several recurring issues in need of further study

or resolution arise during an examination of

apheresis technology. One issue, which arises because the technology is still in the development

stage, is what the appropriate patient criteria for

use are, what the appropriate timing of intervention in the course of a disease is, and whether the

procedure to be followed in performing therapeutic apheresis is adequately standardized. Such

questions are basic in the development of a technology, and research to address these questions

is needed, as it forms a necessary foundation for

the conduct of well-controlled testing and clinical

trials. Interim apheresis registries could track conditions of use and forma knowledge base for development of well-controlled studies.

A second issue, which arises where conditions

of use have been sufficiently standardized, is the

lack of and need for well-designed clinical trials

of apheresis. There has been a recent infusion of

government and foundation funding to offset the

high costs of such trials. Should costs continue

to be a problem, one alternative might be to have

third-party payers, including Medicare, selectively

reimburse for therapeutic apheresis in return for

clinical data. If implemented properly, this alternative could substantially increase the quality of

information available for public and private reimbursement coverage decisions. Evidence of the

technology’s cost effectiveness could result in

yielding substantial budgetary savings. Even if the

results of such trials were disappointing, they

could lead the way to unexpected advances in research.

A third issue is the possibly transitional nature

of apheresis technology. Advances in apheresis

equipment, advances in related areas of basic

biomedical research, and emerging parallel developments such as biotechnology, indicate that

policies affecting therapeutic apheresis must be

considered in the larger context of present scientific and technological flux. Considerable attention will be needed to establish the most rational

and productive balance between development and

support of apheresis technology and that of basic

and applied research toward other technologies

of similar or more favorable promise.

ORGANIZATION OF THE CASE STUDY

This case study is organized into five chapters. Chapter 3 reviews research on the scientific and

Chapter 2 provides definitions and descriptions medical aspects of therapeutic apheresis. Included

of the various types of apheresis technology, along is a description of methodological issues involved

with perspectives on the history and etiology of in therapeutic apheresis evaluation. The evidence

apheresis use. It also describes the current treat- on the safety, efficacy, and effectiveness of the

ment process and future trends, especially as they procedure for the wide range of specific diseases

involve changes in apheresis equipment devices. and conditions is examined. The results of three
8 ● Health Technology Case Study 23: The Safety, Efficacy, and Cost Efectiveness of Therapeutic Apheresis

methodological reviews of therapeutic apheresis

for treatment of hemolytic uremic syndrome, acquired Factor-VIII inhibitor, and Guillain-Barre

syndrome, prepared for this case study, are also

discussed. (The full reviews are presented as apps.

B, C, and D.)

Chapter 4 focuses on reimbursement and costeffectiveness issues. Data and estimates on the

costs and benefits of providing therapeutic apheresis and policy issues of the current system are

considered in relation to safety and efficacy data

regarding treatment. In chapter 5, implications for

policy are provided in light of several recurring

issues that emerge from an assessment of this technology.

There are six appendixes to this case study. Appendix A acknowledges the valuable assistance

of the Health Program Advisory Committee and

several other individuals for their review and advice in putting together this report. Appendixes

B, C, and D contain the previously mentioned

methodological reviews, while appendix E briefly discusses the cause and pathological development of autoimmune diseases. A full bibliography

of the scientific literature on therapeutic apheresis,

compiled by the American Red Cross and organized by disease categories, is included in appendix F. (The bibliography specific to this case study

can be found in the References section following

the appendixes. )
2 ■

Apheresis: Definitions,

Descriptions, and Developments
2

Apheresis: Definitions;

Descriptions, and Developments

Apheresis is a procedure in which blood is separated into its basic components (red cells, white

cells, platelets, and plasma), and one or more of

these is selectively removed from the blood. It is

applied therapeutically for the purpose of curing,

alleviating, or treating a disease and/or its symptoms. The procedure is usually accomplished by

removing venous whole blood from the body,

separating the blood into cellular and noncellular

(plasma) parts or “fractions,” and returning the

cellular fraction to the patient (59,86). Just as with

kidney dialysis, blood flows from a patient to a

machine where it is treated and then returned to

the patient by way of an extracorporeal (i.e., outside the body) blood tubing set (39). *

In simplest terms, apheresis involves separating

“bad blood” from good. Blood comprises four

basic components: red cells, white cells, platelets,

and plasma. A typical adult male has 3 trillion

red cells in the blood. The red cells deliver oxygen throughout the body and carry carbon dioxide back to the lungs, where it is exhaled. For

every 800 red cells, the blood contains about 1

white cell. The several types of white cells (leukocytes) play key roles in the immunological defense

system (lymphocytes), fight infections (granulocytes), and respond to foreign materials. Platelets,

of which there are about 1 for every 20 blood cells,

are spherical or oval bodies that help the blood

to clot. Lastly, plasma, which contains large quantities of proteins, ions, and organic and inorganic

molecules, makes up about 55 percent of blood

volume, and is the straw-colored, fluid portion

of circulating blood. The rationale for performing apheresis is to remove one or more of these

components of blood that conceivably contain

specific pathogenic substances linked to a patient’s

disease process (2).

● In kidney dialysis, however, the dialysis device does not separate

the blood’s cellular and plasma components of blood, but rather

removes only unwanted metabolizes and waste products from the

blood (39).

A variety of diseases have been associated with

abnormal proteins or blood components in the circulation, which are believed to initiate or aggravate the disease condition. Apheresis typically has been used in diseases involving three main

types of abnormal levels of blood components:

plasma protein, antibodies, and immune complexes.

Protein-related diseases involve either excessive

levels of proteins in plasma (e.g., the macroglobulins in Waldenstrom’s syndrome) or excessive levels of other substances which are “carried”

in the blood by the plasma proteins (e.g., thyroid

hormone in thyrotoxicosis). The antibody-related

diseases are often termed “autoimmune” diseases.

Normally, antibodies are produced by the immune system to attack foreign substances (“antigens”) such as bacteria. However, in autoimmune diseases, pathological antibodies are produced which attack the body’s own normal tissue,

such as kidney cells in glomerulonephritis or the

nerve/muscle junction in myasthenia gravis. Immune complexes are antigen-antibody complexes

that can be deposited in tissue. In immune-complex related diseases, such as rheumatoid arthritis,

this deposition occurs and produces severe inflammation and tissue damage (117).

The therapeutic goal of apheresis is to decrease

the levels (through removal) of these abnormal

components in the circulating blood. Physicians

reason that if they can properly identify and remove these problem substances, the disease process may be controlled and the patient’s clinical

condition should improve.

Unfortunately, the effects of apheresis are not

well understood. For the most part, its benefits

remain anecdotal and difficult to reproduce. Its

effects are not generally believed to be curative;

rather, they are usually of a temporary nature.

Often the procedure is used in conjunction with

other treatments, especially drug therapy, making it difficult to assess the effectiveness of

11
12 ● Health Technology Case Study 23: The Safety, Efficacy, and Cost Efectiveness of Therapeutic Apheresis

apheresis therapy. The scientific and medical applications of apheresis and corresponding levels

of efficacy and effectiveness gained from such

treatment are discussed at length in chapter 3.

Apheresis can take several forms: plasmapheresis, plasma exchange, plasma perfusion, cytapheresis, lymphapheresis, and lymphoplasmapheresis. Strictly defined, pkrqdxmsis involves

the removal of small amounts of plasma. The primary use of this procedure is in the collection of

source plasma for subsequent processing into

serum fractions, as has been traditionally found

in blood banks and in the plasma collection industry.

The plasma separation process, however, has

been increasingly used over the last decade for

therapeutic uses. The therapeutic application most

often includes two general techniques. In plasma

exchange, a large volume (up to 5 liters) of plasma

is removed and replaced by an equivalent volume

of fluids such as fresh frozen human plasma, a

plasma substitute, or combinations of albumin,

calcium, and normal saline, depending on the

need of the individual patient. * Plasma perfusion

refers to a multiphase separation technique in

which the patient’s plasma is first isolated from

the cellular elements and subsequently passed

through a filtration medium (either adsorptive columns or membranes) to remove unwanted plasma

components. The filtered plasma is then returned

*It is important to note that some researchers also make a distinction between plasma exchange and plasma infusion. In the former

case, plasma is removed and replaced by a colloid solution, commonly albumin, fresh frozen plasma, or simple donor plasma. Although the plasma replacement in early cases was initiated only for

purposes of expansion of the blood vessel “intravascular” volume,

later authors suggested that the administration of fresh frozen plasma

had an independent therapeutic effect. This led some investigators

to administer it without apheresis; this is described in the literature

as plasma infusion.

HISTORICAL DEVELOPMENT

to the patient along with the cells (39,108). Only

recently has equipment for this technique been approved for general therapeutic use by the Food

and Drug Administration (FDA) (see “Equipment

Technology” section later in this chapter for a

more complete discussion of plasma perfusion).

Another form of therapeutic apheresis is cytapheresis, the selective removal of specific blood

cells (red cells, white cells, and/or platelets).

Cytapheresis is usually subdivided according to

plateletapheresis (the reduction of abnormally

high levels of platelets), leukapheresis (the reduction of excess white cells, as in leukemia), and

erythrocytapheresis (the removal of red cells)

(105). Cytapheresis can also include lymphapheresis, the removal of lymphocytes (certain

white cells) without depletion of plasma components, making any plasma replacement, therefore, unnecessary. Lymphoplasmapheresis is a

combination of lymphapheresis and plasmapheresis: the removal of both lymphocytes and

plasma, usually during a single procedure, and

requiring the use of replacement fluids.

There are different types of hardware used for

performing apheresis. One is a centrifugal type

machine that spins the blood in a chamber and

uses centrifugal force to separate the heavier parts

of the blood from the lighter ones. The filter type

uses a flat sheet or hollow fiber porous membrane

to separate the larger blood components from the

smaller. This type is only capable of removing

plasma from the cellular portion of the blood:

plasma and plasma proteins easily pass through

the pores in the membrane but the red cells, white

cells, platelets, and large protein molecules are too

large to pass. Thus, the filter-type device can only

perform plasmapheresis. Although the centrifugal

type of device is more versatile, the filter type has

fewer moving parts and is easier to operate (39).

The idea of apheresis (from the Greek, aphair- of this work, they investigated the effect “of the

esis, meaning “taking away”) first originated in repeated removal of considerable quantities of

1914 with a group headed by John J. Abel at Johns blood, replacing the plasma by Locke’s solution,”

Hopkins Medical School (l), which attempted to and infused the mixture back into the dogs. They

develop an artificial kidney in dogs. In the course showed that dogs were able to tolerate the ex-
Ch. 2—Apheresis: Definitions, Descriptions, and Developments ● 13

change of substantial volumes of plasma and

coined the term “plasmapheresis” to describe the

procedure. They suggested that “if this method

can be employed without harmful consequences

it is probable that it could be applied in a bolder

manner in a greater variety of morbid states than

the time honored but often debatable” medical

practice of bloodletting (67).

For 30 years, plasmapheresis was used mainly

in experimental animals, to study the metabolism

of plasma proteins (67). The possibility of human

plasmapheresis was first considered during World

War II as a means of meeting the increased demand for plasma. A trial conducted in 1944 demonstrated the feasibility of weekly plasma donations. Over the last 20 years, the collection and

processing of donor plasma has evolved into a

major industry as the demand for plasma fractions, such as albumin, has increased (108).

The first successful therapeutic use of plasmapheresis was reported in the late 1950’s in the

management of macroglobulinemia (thickened

blood due to the accumulation of proteins) and

multiple myeloma, a malignant tumor of the bone

marrow. During the next few years, reports appeared on the application of plasmapheresis to

several other diseases, including rheumatoid arthritis in which a circulating “plasma factor” was

implicated. In these treatments, a small volume

of plasma was removed and replaced only with

isotonic saline solution. The procedure was slow

and limited by the tendency to deplete all plasma

proteins (both beneficial and harmful) if conducted too often (108).

Over the past 10 years, however, several types

of cell separators have been developed which can

efficiently separate large quantities of red cells,

white cells, platelets, and plasma either continuously or on an intermittent basis. In the late

1960’s, International Business Machines (IBM)

Corp. developed the first cell separator in a collaborative effort with the National Cancer Institute. A second type of device was subsequently developed commercially by Haemonetics,

Corp., of Massachusetts (80,108).

During the early 1970’s cell separators were

mainly used by blood banks to harvest white cells

and platelets, and to collect plasma and plasma

fractions intended for transfusions or research.

But as apheresis evolved more toward a therapeutic application in the mid 1970’s, the equipment-embodied cell-separator technology was

easily and rapidly modified for therapeutic use.

The medical literature has reflected this burgeoning interest in therapeutic apheresis. In 1981,

there were approximately four times as many articles on the subject appearing in lndex Medicus

as there were in the 1970’s (85). To date, apheresis

has been used in the treatment of over 75 diseases,

and an additional 41 diseases have been identified

as possible candidates for this therapy (22,117).

Table 1 presents a listing of diseases in which the

use of therapeutic apheresis has been reported in

the medical literature.

The growing interest in therapeutic apheresis

is further exemplified by the emergence of professional societies, scientific meetings, and journals devoted entirely to this subject. The membership in the American Society for Apheresis has

increased dramatically, for example, and the journals, Plasma Therapy and Transfusion Technology and Journal of Clinical Apheresis have initiated publication only within the last 5 years

(43,49,145).
14 ● Health Technology Case Study 23: The Safety, Efficacy, and Cost Effectiveness of Therapeutic Apheresis

Table I.—Reported Use of Therapeutic Apheresis

Acute necrotizing hemorrhagic encephalomyelitis

Acute disseminated encephalomyelitis

Acute post-streptococcal glomerulonephritis

Acute rheumatic fever

Addison’s disease

Adenocarcinoma of the colon

Adenocarcinoma of the breast

Allergic granulomatosis and angiitis

Amyloidosis

Amyotrophic lateral sclerosis (ALS)

Ankylosing spondylitis

Aplastic anemia

Atopic dermatitis

Atrophic gastritis type A

Autoimmune infertility & gonadal insufficiency

Autoimmune hemolytic anemia (AIHA)

Autoimmune hypogammaglobulinemia

Autoimmune neutropenia

Behcet’s syndrome

Bone marrow transplant

Bronchial asthma

Bronchogenic carcinoma

Bullous pemphigoid

Cardiac allograft rejection

Chronic membranoproliferative hypocomplementemic

glomerulonephritis

Chronic active hepatitis

Circulating anticoagulant (Anti-Factor Vlll)

Cold agglutinins

Colon carcinoma

Crohn’s disease

Cryogenic fibrosing alveolitis

Cryoglobulinemia

Cutaneous vasculitis

Dermatitis herpetiformis

Dermatomyositis

Discoid lupus erythematosus

Disseminated intravascular coagulation (DIC)

Dressier’s syndrome

Eaton-Lambert syndrome

Endomyocardial fibrosis

Erythema multiform

Fabry’s disease

Felty’s syndrome

Gastric carcinoma

Gaucher’s disease

Giant cell arteritis

Glomerulonephritis in subacute bacterial endocarditis

Goodpasture’s syndrome

Graft versus host disease

Graves’ disease

Graves’ ophthalmopathy

Guillain-Barre syndrome

Acute

Chronic

Relapsing

Hashimoto’s thyroiditis

Hemolytic uremic syndrome

Henoch-Schonlein purpura

Hepatic coma

Herpes gestations

Hodgkins disease

Hypercholesterolemia

Hyperglobulinemic purpura

Hypersensitivity pneumonitis

Hypersensitivity angiitis

Hypertension

Hypertriglyceridemia

Hyperviscosity syndrome

Idiopathic membranous glomerulopathy

Idiopathic thrombocytopenic purpura (ITP)

Idiopathic hypoparathyroidism

Insulin resistant diabetes mellitus due to

anti-receptor antibody

Juvenile onset diabetes mellitus

Lipoid nephrosis

Lymphomas

Malignant melonoma

Mixed connective tissue disease

Multiple sclerosis

Multiple myeloma

Myasthenia gravis

Necrotizing cutaneous angitis

Neuroblastoma

Other neoplasms

Pemphigus vulgaris

Pernicious anemia

Poisoning or overdose (paraquat, mushroom, digitalis)

Polyarteritis nodosa

Polymyositis

Post-transfusion purpura

Primary cardiomyopathy

Primary biliary cirrhosis

Proliferative/membranoproliferative glomerulonephritis

Psoriasis

Pure red cell aplasia

Rapidly progressive glomerulonephritis

Raynaud’s disease

Refsum’s syndrome

Reiter’s disease

Renal allograft rejection

Reye’s syndrome

Rhesus iso-immunization

Rheumatoid arthritis

Sarcoidosis

Scleroderma

Sjogren’s syndrome

Subacute bacterial endocarditis

Systemic lupus erythematosus (SLE)

Takayasu’s arteritis

Thrombotic thrombocytopenic purpura (lTP)

Thyroid storm

Ulcerative colitis

Viral hepatitis

Waldenstrom’s macroglobulinemia

Wegener’s granulomatosis

White cell isoantibodies

SOURCE: Off Ice of Technology Aseeesment, 19S3.
Ch. 2—Apheresis: Definitions, Decriptions, and Developments ● 15

THE SCIENTIFIC AND MEDICAL BASIS FOR USE’

For therapeutic use, apheresis technology came

along at an opportune time—when there is a

growing support for the theories that a large

number of chronic conditions occur because the

antibodies of the immune system, instead of attacking foreign substances as they are supposed

to, attack the body’s own tissues. This results in

a build-up of so-called immune complexes, which

are carried in the blood (34).

Indeed, many diseases that appear to respond

to apheresis seem to have common elements: they

reflect failures in the immune system, the body’s

defense network of sorts, which is designed to protect the individual against viruses, foreign cells,

and some poisons. The cells of the immune system

circulate in the blood and lymph systems and also

reside in specialized tissues such as the thymus,

spleen, and lymph nodes. There are two principle modes of immunity: humoral immunity and

cell-mediated immunity. Humoral immunity is

realized through antibodies, which are proteins

produced by lymphocytes and which circulate in

the blood system. They represent the major defense against bacterial infections. Cellular immunity is realized through lymphokines (also

lymphocyte products) which are responsible for

a variety of phenomena including influencing migration of inflammatory cells, allergic responses,

dilation of the blood vessels, rejection of tissue

grafts, and other foreign matter.

The foreign agents eliciting immune responses

are called ant&ens, which may be circulating proteins or other types of molecules, or also substances on the surfaces of bacteria or foreign

tissue. When individuals are exposed to an antigen, their lymphocytes respond by making antibodies specifically directed against the antigen.

The antibodies have binding sites which attach

to the antigen, and together they form aggregates

called immune complexes. These complexes cirIUnless otherwise noted, this section is condensed from Frost &

Sullivan, Inc., Zn-Vivo Hernock+oxification and Hemoprocessing

Markets in the U. S., New York, June 1981.

culate in the bloodstream and are subsequently

processed and removed from the body by cells

located in the liver, spleen, and other organs. It

is in this manner that foreign agents are eliminated.

The formation of immune complexes triggers

many other reactions. One of these is activation

of the complement system, a set of proteins found

in the blood. Complement products can kill cells

with antigens on them, such as bacteria. They also

attract inflammatory cells to the area where the

antigen-antibody reactions are taking place, and

these cells assist in clearing the antigens.

Antigens also stimulate specific lymphocytes,

Tlymphocytes, to proliferate and then differentiate. Some T lymphocytes differentiate into

“helper cells” which assist the lymphocytes in

making antibodies; some differentiate into “killer”

lymphocytes which can kill foreign cells having

antigen on their surface; and some cells differentiate into “suppressor cells” which regulate the immune response by inhibiting further antibody production against the specific antigen.

The exact nature and extent of the immune response depend on many factors: the type of antigen, its route of entry into the body, the genetic

makeup and state of health of the host, the types

of antibodies made, and the relative proportions

of helper, killer, and suppressor cells generated.

A fundamental property of an individual’s immune system is that it distinguishes between the

antigens on the body’s own tissues and those on

foreign agents. Unfortunately, this system occasionally breaks down, and individuals mount immune responses, most often antibody production,

directed against their own tissues. The diseases

that result from such a disorder are referred to

as “autoimmune diseases. ”

The cause and pathological development of

autoimmune diseases are thought to be due to

several mechanisms: inactivation reactions,

cytotoxic reactions, immune complex deposition,

anaphylaxis, and delayed hypersensitivity. These

mechanisms are briefly discussed in appendix E.
16 ● Health Technology Case Study 23: The Safety, Efficacy, and Cost Effectiveness of Therapeutic Apheresis

THE TREATMENT PROCESS

Until the advent of automated devices, the

process of apheresis was exhausting and timeconsuming, requiring 4 to 5 hours, for example,

to remove about 1 quart of plasma. It was a

tedious manual procedure in which the patient’s

blood was drawn one bag at a time, separated in

a centrifuge so that the target components could

be removed and the remaining blood returned to

the patient before drawing another bag. Now,

automated cell separators reduce the procedure

to a simple, straightforward exchange which can

be completed in 2 to 4 hours. The patient is connected to the cell separator, which draws the

blood, separates the components, and returns the

rest of the blood to the patient. The volume exchange for each procedure is calculated for each

patient according to size and the type of treatment

modality desired (73).

Organizational Settings and Staffing

Apheresis treatment is provided almost exclusively through large medical school hospitals and

community/Red Cross blood banks. A few commercial, freestanding, independent centers have

been established during the past 2 or 3 years;

however, it appears that this trend maybe moderating.

Most of the existing therapeutic apheresis programs originally evolved in conjunction with the

donor facilities at community and hospital blood

banks. However, some of the larger institutions

have since established independent hemapheresis

units (which undertake and perform hemodialysis

and other blood filtration procedures in addition

to apheresis) that perform leukapheresis and

plateletapheresis in addition to plasma exchange.

The hemapheresis center is normally staffed by

nurses with special (usually “on-the-job”) training in the operation of the cell separator equipment, administration of replacement fluids, circulatory access techniques, and the treatment of

apheresis complications. The operation of the unit

is directed by a physician, often a hematologist.

In most centers the actual procedure is conducted by one or two apheresis nurses. Usually

a physician (who is often the center director) is

required to be immediately available in the event

that complications should develop. In many of

the smaller facilities the supervising physician is

in direct attendance during the procedure, while

in the larger apheresis centers he or she is generally

on call within the unit (49,108).

Frequency, Intensity, and Duration of

Blood Component Exchange

The volume and frequency of blood component

exchange depend to a large degree on the disease

being treated as well as the individual patient

response. To date, temporal considerations have

been more influenced by factors such as circulatory access and scheduling than by uniform

protocols, because the metabolism, kinetics, and

pathogenicity of the abnormal blood component

constituents removed by apheresis have not been

largely established (144). Therapy regimes that

have evolved from clinical studies vary as a result.

Frequency of treatment ranges from an average

of 3 procedures in the management of myeloma

to approximately 16 treatments per year for patients with chronic myasthenia gravis (though

severely debilitating rheumatoid arthritis may require up to 30 treatments in the first year, with

that number decreasing thereafter (47). The average for all reported diseases treated by apheresis

ranges from approximately 5 to 15 treatments per

year per patient, at a volume of 3.2 liters (the

range is 2.0 to 4.5 liters per treatment) (108).

A survey of hospital and community blood

banks by Scoville Associates (108) indicated,

however, an average of only 5.6 treatments per

patient during 1980. Average volume per exchange was 2.8 liters (1.5 to 3.5 liters). The difference in treatment schedules was hypothesized

to stem from several factors. For example, the

hospital and blood bank averages included schedules for just 30 different disorders, many of which

were treated on an acute basis only. Also, a major

objective in acute treatment settings is to obtain

rapid patient response, and several centers reported that they usually terminated apheresis after

three to four procedures if improvement is not

apparent.
Ch. 2—Apheresis: Definitions, Descriptions, and Developments ● 17

Circulatory Access and

Replacement Fluids

The initial step in the apheresis procedure involves the removal of whole blood from the patient for subsequent separation. Blood vessel access is not (because of relative infrequency) as

critical in this procedure as it is, for example, in

chronic hemodialysis in end-stage renal disease

applications. The preferred access site is a simple

puncture into the vein at the elbow. Such access

is adequate for most patients even with extended

series of exchanges.

The cellular elements and replacement fluids are

normally returned to a vein in the other arm.

Other return sites include the femoral vein, forearm, or through a small vein in the hand or foot.

Sometimes repeated apheresis treatment requires

surgeons or other qualified staff to make a shunt

or fistula, a sort of permanent “tap,” between an

artery and a vein to give them ready access to the

circulatory system. Clotting and site infections can

be significant complications in the use of such

taps.

Crystalloid solutions (saline, Ringer’s solution,

Hartman’s solution) are normally used routinely

as replacement fluid in small volume apheresis

procedures. These involve removal of 1 to 2 liters

of plasma every 2 to 3 weeks as in some cases of

hyperviscosity syndrome. Crystalloid solutions

have the advantage of low cost. Larger volume

exchanges run the risk of protein depletion, and

as a rule, require the use of colloid replacement

fluids such as albumin, fresh frozen plasma (FFP),

or plasma protein fraction (PPF). Guidelines have

been established by FDA for safe levels of plasma

donation without protein replacement in the average size adult.

The typical plasma exchange schedule, however, involves the removal of between 2 to 3 liters

of plasma at a frequency of two to four times per

week, and protein replacement is routinely utilized

in these cases. In general, little is known about

the correlation between specific disease states and

the effectiveness of various replacement fluids.

Fluid volume removal is normally replaced on

an equal basis. Since continued exchange will

remove the replacement fluids as well as the patient’s own plasma, many centers are now beginning to use a technique whereby saline or dextran is administered at the beginning of the procedure, and the protein replacement portion (FFP,

PPF, or albumin) is infused toward the end of the

exchange, thus saving some depletion of the more

expensive colloid solutions. This proportion of

protein solution to total replacement fluid generally ranges between 30 to 50 percent (2,108).

Drug Therapy Used With Apheresis

Apheresis used alone has often provided only

transient results because cells making deleterious

antibodies may not be affected. In fact, a “rebound effect” can sometimes occur when apheresis

is used by itself, where posttherapy antibody levels are even higher than initial levels. Apheresis

has, as a result, often been more effective when

used in combination with immunosuppressive,

cytotoxic, and anti-inflammatory drugs. Examples

of these include cyclophosphamide, azathioprine,

and steroids (e.g., prednisone). In specific diseases

these drugs may be used individually, but they

are often administered together.

Steroids have many complex physiological effects, and the effects of those that are responsible for suppressing inflammation, immune responses, and symptoms of autoimmune diseases

are not completely understood. The basis of action of cytotoxic drugs is that they kill lymphocytes, and thus antibody production is decreased.

With corresponding drug therapy, then, the low

levels of circulating antibodies and immune complexes rapidly achieved by apheresis may be maintained, since the rebound effect and the production of antibodies by lymphocytes are inhibited

by the drugs. Other internal repair mechanisms

can then intercede, correcting or repairing damage induced by the immune complexes or antibodies. For example, in myasthenia gravis, lowering the concentrations of antibodies allows new

muscle membrane proteins to be synthesized.

Removal of circulating immune complexes may

also “desaturate” the immune complex clearing

mechanisms in lymphoid tissues and allow them

to function better.
18 ● Health Technology Case Study 23: The Safety, Efficacy, and Cost Effectiveness of Therapeutic Apheresis

For some diseases, apheresis, in combination

with the drugs, has been claimed to result in complete remission. For others, long-term benefits

have been reported. On the other hand, some

diseases thought to be autoimmune have not been

improved with apheresis. Ultimately, the sucEQUIPMENT TECHNOLOGY

Centrifugal Systems

Approximatelys percent of therapeutic apheresis procedures are performed manually by removing whole blood, spinning it down in a stationary centrifuge and returning the cellular components to the patient as is done in source plasma

collection. Manual apheresis has the advantage

of requiring relatively inexpensive equipment.

However, its use is limited to the removal of small

volumes of plasma (1.0 liter or less) due to the

inconvenience and additional time requirements

as compared to automated techniques. The rate

of plasma removal using manual procedures runs

approximately 2.5 hours per liter as compared to

1.2 hours per liter for automated cell separation

equipment. Also, the use of a “non-closed” (manual) system runs a higher risk of infection and

presents the possibility of returning the wrong red

cells to the patient.

Most apheresis procedures are earned out using

automated centrifuge equipment. There are two

basic types of automated centrifuge devices currently in use for apheresis: the intermittent flow

centrifuge (IFC) and the continuous flow centrifuge (CFC). Both systems provide a significant

advantage over manual apheresis because large

volumes of plasma maybe processed quickly with

less risk to the patient. IFC devices are manufactured and sold by Haemonetics Corp. The Haemonetics Model 30 is used for a majority of the

therapeutic plasma exchange procedures performed in the United States. This equipment was

originally designed for the collection of leukocytes

and platelets, but has been found to be effective

for large-scale plasma exchange, lymphoplasmapheresis, and lyrnphapheresis as well (57,108).

cessful treatment of autoimmune diseases will

hopefully rely on more specific therapies, because

these drugs are not without complications and can

deplete sets of cells required for other vital bodily functions (42). Chapter 3 more fully discusses

scientific and medical issues of apheresis.

Generally, in the IFC system, blood is drawn

from a blood vessel in the arm and pumped

through tubing into a disposable bowl placed in

the well of the centrifuge. Several lines are also

connected to the bowl leading to collection bags.

Anticoagulant is introduced into the lines to be

mixed with the donor/patient blood. As centrifugation begins, plasma is the first fraction of

blood to be separated and collected into a container. Platelets and white cells are separated later

in the process and are then diverted to other containers. When the process is completed, the pump

action reverses and the red cells remaining in the

bowls are reinfused into the patient via a blood

vessel in the other arm. When the bowl is empty

the whole procedure is repeated according to the

effect desired (42).

The first CFC device, developed in the late

1960’s by IBM in conjunction with the National

Cancer Institute, involved a rotating seal which

enabled the continuous infusion of whole blood

and removal of separated components from a

rotating centrifuge bowl. This basic CFC design

was commercialized by IBM as the Model 2990

and by American Instrument Co. (now a division

of Travenol Labs) as the Aminco Centrifuge. A

few of these devices are still in use throughout the

United States, but most have been replaced by the

Haemonetics 30 or the second generation IBM

Model 2997, which employs a ring-shaped separation channel in place of the previous centrifuge

bowl (108}.

Fenwal Laboratories (Division of Travenol

Labs) has developed a series of CFC instruments

(CS-3000 and Centrifuge II) in which the blood

and separated components pass to and from the
Ch. 2—Apheresis: Definitions, Descriptions, and Developments ● 19

separation chamber through continuous tubing,

without the requirement of a rotating seal. A

counter rotating mechanism is employed which

enables the tubing to be continuously unwound

without twisting or coiling (108).

The disposable equipment associated with

apheresis varies according to the technique used.

In the mechanical plasma separation application,

disposable consist of tubing to connect the patient to the equipment and vice versa. A disposable bowl is fitted into the centrifuge and the

separation takes place, then various bags are connected to the bowl to collect plasma and/or cellular components. Since the cellular components

extracted during therapeutic apheresis are not intended for reuse in other patients, the disposable

are simpler and less costly than those used in most

blood banking operations (42).

Some new major developments in hardware are

now undergoing clinical tests. These include adsorption columns and semipermeable membranes

that function as molecular sieves.

Membrane Separation Devices

Membrane separation devices have evolved as

parallel flow (or flat sheet) or hollow fiber configurations similar to those found in basic types

of hemodialyzers. Membrane blood separators

can only filter plasma from cellular components

(as opposed to centrifugal systems that can also

be used for specific cell separation (cytapheretic)

applications as well as for plasma exchange).

Membrane systems, however, are expected to

allow simpler, more rapid and more precise treatment. They are currently being reviewed by FDA

(see the “FDA Device Regulation” section of this

chapter) for use in this country.

The disposable associated with membrane

apheresis represent the heart of the plasma separation process. The plasma separation membrane

replaces the centrifuge in this process. Tubing is

used to form the extracorporeal circuit, very much

as in dialysis (42).

Membrane disposable are expected to be initially priced higher than those required for centrifugal machines, but it should be noted that in

Europe, especially in West Germany, many clinicians use Asahi-brand hollow fiber membranes

in preference to centrifugal systems despite the

higher costs. Membrane systems, in fact, are

dominant in the European and Japanese markets,

accounting for 70 to 80 percent of the procedures

performed. If membrane systems become accepted

in U.S. markets, manufacturing costs could decrease substantially to reflect economies of scale,

although prices are not expected to approach

those for similar membranes used for dialysis ($15

to $25 per patient). Apheresis membranes will be

initially more expensive because they are more

delicate and their quality constraints will be more

demanding in terms of pore size and wall thickness

consistency (117).

Future Technological Directions

Current apheresis therapy most often entails

plasma replacement, which is not only expensive

but also removes normal as well as adverse plasma

constituents. Therefore, future systems will likely emphasize more selective removal of undesirable components and return of the patient’s own

plasma, probably by one of the following techniques. (In most instances, however, the specific

unwanted target components underlying the usefulness of plasma exchange have not yet been precisely identified. )

Cryoprecipitation.— Certain macromolecules in

the plasma will precipitate (come out of suspension) when exposed to cold temperatures. When

applied in conjunction with apheresis, the patient’s

plasma is circulated through a cold environment,

where cryoprecipitation occurs. These precipitant

are removed by filtration, and then the remaining plasma and cells are returned to the patient.

Other macromolecules in addition to unwanted

immune complexes are removed by this procedure. However, most normal plasma proteins,

especially albumin, are retained. Parker-Hannifin

Co.’s Cryomax system (see table 2) is likely to be

the first selective entry.

Mechanical Double Filtration. —Another approach to avoiding the replacement of plasma in

therapeutic apheresis is double filtration for

‘This section is drawn from L. F., Rothschild, Unterberg, Towbin,

‘Therapeutic Apheresis,” New York, 1981.
20 ● Health Technology Case Study 23: The Safety, Efficacy, and Cost Effectiveness of Therapeutic Apheresis

Table 2.—Automated Blood Cell Separation Systems

Approximate Approximate

machine disposables Components

Manufacturer Models Introduced cost separated Membrane type

Continous-flow centrifuge

Fenwal CS-3000

(Travenol/Baxter) Centrifuge II

IBM Biomedical 2997

1979

1981

1977

$32,000

$19,700

$31,000

$65-$80

$65-$80

$65-$60

Cells, plasma

Cells, plasma

Cells, plasma

None

None

None

None

None

None

Sheet

Hollow fiber

Hollow fiber

Hollow fiber

Hollow fiber

Hollow fiber

Hollow fiber

Intermittent-flow centrifuge

Haemonetics 30

V-50

PEX

1973

1980

1980

$21,600

$28,800

$25,600

$65-$80

$30-$49

$49 avg.

Cells, plasma

Cells, plasma

Cells, plasma

Continuous-flow membrane

Cobe Laboratories Centry

TPE

Parker-Hannifin Cryomax

March 1982

1983

(expected)

Late 1981

in Europe

NA

$30,000

$30,000

$80-$90

$390

Plasma only

Plasma only

Fenwal PS-400 $20,000 $75-$200 Plasma only

(Travenol/Baxter)

Organon-Teknika Curesis

(Netherlands)

Asahi (Japan) Plasmaflo@

NA NA Plasma only

(expected)

NA

NA $175-$400 Plasma only

Fresenius Plasmaflux@

(West Germany)

Toray (Japan) Plasmax

NA NA

NA

Plasma only

NA NA Plasma only

aDigpo8ableg cost eatirnatee are exclusive of other deposable items such as needles, seilne bags, transfer pecks, and PM’M9 aOIUtlOnS which may dso be u$ed In

conjunction with apheresls treatments.

NA - Not available.

SOURCES: L. F. Rothschild, Untertxg, Towb{n, 1981; Friedman, American Red Cross, 19S2; Colllns, Cobe Labs, 19S2; Cluryla, Du Pent, 19S2.

albumin recovery. This type of system is essentially similar to the Cryomax approach, but the

plasma fraction is not chilled to produce precipitation. After the plasma is separated from the cellular fractions by a membrane, it is passed

through another membrane with smaller pores

that allow only smaller proteins, especially albumin, to pass while retaining the larger macromolecules including immunoglobulins. The albumin fraction is then combined with the cellular

fraction and returned to the patient. Albumin recovery systems are under investigation by several

groups around the world.

Hemoperfusion.— This approach involves the

passage of whole blood through an adsorption

column (e.g., activated charcoal) to remove the

unwanted substance(s) somewhat more selectively. This technique has been used primarily for

detoxification in acute chemical or drug poisonings, and is being investigated for use in renal and

liver failure. It offers desired speed in emergency

cases, but for broader usage is not as promising

as plasma perfusion (described below) due to unwanted cellular adherence to the columns and potential release of particles from columns.

Adsorptive Plasma Perfusion. -This technique

should permit considerably greater selectivity in

plasma component removal. It involves separation of plasma from cells, passage of the plasma

through an adsorptive column (which specifically removes the unwanted substance), and return

of the plasma and cells to the patient. Beneficial

results in recurrent breast cancer treated with

plasma exchange with on-line adsorptive column

treatment have been recently claimed. Future development of adsorptive plasma perfusion may

well involve columns containing monoclinal antibodies produced to specifically bind and, thus,

selectively remove undesirable constituents.

Artificial Antibodies. —As previously discussed, antibodies are synthesized by lymphoid

tissue to bind to and inactivate antigens (generally

foreign substances). Antibodies are made to bind

very selectively to specific antigens like a key in

a lock. Unwanted plasma antibodies could be re-
Ch. 2–Apheresis: Definitions, Descriptions, and Developments ● 21

moved by allowing them to bind to: 1) their natural antigenic “lock,” which is held within a column (“antigenic columns”); or 2) an artificially

produced antibody to the patient’s normal and unwanted antibody, which is held within a column

through which the plasma passes (“antibody column”), i.e., the unwanted antibody serves as an

antigen to another manufactured antibody.

Artificial antibodies are currently produced for

use in diagnostic tests using the immune response

of goats or other animals especially for radioimmunoassays, a technique that allows an accurate

measurement of biological and pharmacological

substances in the bloodstream and other fluids of

the body. Recent advances in gene splicing technology have given rise to monoclinal antibody

or hybridoma (hybrid cell) techniques which

allow the production of more specific antibodies

at less cost than conventional procedures.

Based on current technology, economic factors

may delay the development of monoclinal antibody columns for on-line plasma processing, except in certain diseases with only a few definable

types of unwanted factors. Other diseases may

require a constellation of distinct antigens or antibodies held within a column. Another potential

problem for immunological adsorption columns

concerns the quantity of unwanted substance to

be removed. If, for example, large quantities of

immune complexes must be removed, large quantities of antibodies would be needed in the columns. It is currently uncertain whether monoclonal production would be inexpensive enough

to allow columns with large quantities of manufactured antibodies to be economically feasible.

FDA Device Regulation

FDA regulations currently governing centrifugal cell separators on the market only concern

blood banking applications. The centrifugal

apheresis devices have been classified into Class

III (premarket approval or PMA) for use with

donors in the preparation of blood products,3

although data indicate many clinicians are using

them for therapy. Machines introduced prior to

3

21 CFR 864.9245.

the Medical Device Amendments in 1976 have

“grandfathered” approval, while centrifugal

machines introduced after 1976 have gained FDA

premarket approval by being considered by FDA

to be substantially equivalent to pre-1976 devices.

The membrane-based devices being developed,

and mostly being tested in clinical trials, were not

permitted to simply file a premarket notification

with FDA. * They are considered essentially new

devices for which investigational device exemptions (IDEs) are required. IDEs are granted with

sufficient demonstration of safety, after which the

clinical protocols can then proceed. Results of the

clinical trials are used in filing for premarket approval. No attempts to reclassify separators as

Class II devices, which would only require the

manufacturers to meet certain product performance standards specifications, are being pursued

at present. It has been speculated that the industry, on its own initiative in the future, could

develop such standards for FDA approval (117).

In October 1981, the Gastroenterology-Urology

Device Section of FDA’s General Medical Devices

Panel reviewed the Cobe Centry TPE System for

total plasma exchange and recommended approval of the device for therapeutic applications.

On March 16, 1982, FDA granted the premarket

approval.

A second and third membrane apheresis PMA

(Parker-Hannifin’s Cryomax model and Asahi’s

Plasmaflo model) were reviewed and recommended for approval by FDA’s General Medical

Devices Panel in late 1982. These models are expected to receive FDA’s premarket approval and

to be generally marketed in early 1983 (21). In

addition, there are currently in excess of 20 IDEs

for conducting clinical investigations with apheresis membrane devices which are manufactured

by five different manufacturers (39).

● Sec. 510(k) of the 1976 Medical Device Amendments requires

any distributor of a medical device intended to be marketed for the

first time to file a notice with FDA at least 90 days in advance to

permit the agen~ to decide whether the device is determined to be

“substantially equivalent” to devices already on the market before

the passage of the 1976 amendments or, if not found to be substantially equivalent, whether the device needs premarket approval to

assure safety and efficacy.

98-822 0 - 83 - 3 : QL 3
3

Scientific and Medical Aspects of

Apheresis: Issues and Evidence
3 ●

Scientific and Medical Aspects of

Apheresis: Issues and Evidence

Various types of apheresis procedures have

been performed on a clinical basis for many years,

but the number of patients and types of diseases

treated have risen significantly in the last 5 years.

This increase is partially due to increased understanding of the disease and partially due to engineering advances in equipment technologies. By

almost any standard, treatment by apheresis is still

in relatively early stages of development—there

are no ideal protocols based on a thorough understanding of reasons for its efficacy. Nevertheless, there is an increasing flow of clinical data,

sometimes describing dramatic patient improvement, supporting the view that apheresis is a

rapidly emerging technology with significant

promise (117). Such evidence of treatment effectiveness’ is even today, however, often based on

unsystematically collected data. Because of the

*Ef&tiveness is the health benefit as measured under average conditions of use. Efficacy is the health benefit as measured under controlled conditions such as those in a randomized clinical trial (104).

METHODOLOGICAL ISSUES

An assessment of any medical technology depends, in part, on the development of a strategy

for identifying technologies to be evaluated, and

on the development of clear-cut standards for the

quality of the evidence that should be considered

(104,147). Proper research methods, as a result,

become essential to the evaluation of a technology. Careful and systematic investigations are the

essential ingredients in establishing that observed

effects are due to the medical intervention. Poorly

and haphazardly conducted research studies are

plagued with problems of validity and generalizability, and these same issues continue to hinder

attempts to perform assessments based on such

research (85).

paucity of high-quality research, conclusions

about the safety, efficacy, and effectiveness of

apheresis are necessarily limited, although some

tentative conclusions and directions for treatment

can be discerned.

The present chapter analyzes the methodological problems in conducting apheresis research and

examines available evidence of the safety, efficacy, and effectiveness of apheresis. Following

a discussion of methodological issues, several

major reviews of apheresis research will be summarized and evaluated. This chapter will further

include the findings of a primary literature review

and assessment of apheresis in the treatment of

three diseases—namely, hemolytic uremic syndrome, acquired Factor-VIII inhibitor, and Guillain-Barré syndrome— where preliminary reports

and evidence have been “promising” in utilizing

apheresis as a therapeutic approach (57). (A full

discussion of these findings can be found in apps.

B, C, and D.) Present and future research directions for apheresis will be considered last.

To be valid, and to permit generalizations to

be drawn, there must be clarity about what is being tested, what is being compared, which subject populations are involved in the research, and

what is being measured. Operationally, these four

factors refer to treatment design, research design,

patient selection, and outcomes (102,104).

Treatment Design

Treatment design involves the extent to which

clarity about the “active ingredients” of the procedure being tested can be achieved. Questions

to be answered include whether the procedure involves a single treatment, a combination of treat25
26 ● Health Technology Case Studies 23: The Safety, Efficacy, and Cost Effectiveness of Therapeutic Apheresis

ments, or a combination of treatment and nontreatment factors. Often, because apheresis procedures involve a complex interplay of many factors (i.e., are “multivariant”), resulting research

is confounded by inability to separate effects

(85,117). The extent to which researchers can

measure the impact of any one component of the

procedure is limited when all patients receive or

have access to multiple components concurrently. Clarity of design is essential to being able to

attribute outcomes to particular treatments or

packages of treatments.

Because it is an experimental therapy, the use

of apheresis has not been standardized. Protocols

in various studies have varied considerably. Variables include type of replacement fluid, patient

selection criteria, other medications, extended

respirator and intensive care therapy, and intensity of plasma exchange (i.e., frequency and

volume exchanged in each treatment). Many different protocols have been used for apheresis,

even in the treatment of a single disease, so that

variation in procedures undoubtedly has led to

variation in results (117). These variations make

it difficult if not impossible to achieve some level

of comparison between studies.

For example, apheresis is often used as an “adjuvant” or auxiliary therapy to immunosuppressive since drug therapy is required to inhibit the

rebound reaction (see ch. 2). Although apheresis

is used as an adjuvant therapy to anti-inflammatory, immunosuppressive, or cytotoxic drugs, this

fact should not be viewed as a threat to its validity: any improvement in the course of disease

would not be attributable to the pharmacological

agents alone, but rather to the combined (or synergistic) effects of apheresis and drug therapy.

There could be a validity problem, however, with

the application of the treatment when the concomitant drug therapy varies across studies. When

there is differential improvement by type of drug

used, the integrity of the definition of treatment

is called into question. Even though treatments

are presented in the literature in a similar fashion,

they may, in fact, operate quite differently. It may

be the case that the combined (or synergistic) effects of apheresis and drug therapy may vary according to the strength of the drug and the frequency with which it is administered (85).

Even if standardized protocols could be developed, however, it maybe difficult or undesirable

to administer them. This is particularly problematic if, for research purposes, assignment to

one group or another is required. Use of sham

treatment in control groups, for example, could

very well cause this group of patients to suffer

some of the side effects of apheresis, raising the

ethical question of subjecting them to a potentially

harmful technique. (See the next section, “Safety: A Review of the Evidence, ” for a discussion

of the safety and risk issues of apheresis.) Another

obvious ethical concern is whether treatment can

be denied patients in near-fatal, disease states in

which apheresis has served as the treatment of last

resort. A third issue is the difficulty of setting up

a controlled trial for some rare autoimmune diseases such as Goodpasture’s syndrome, which

strikes only 2 out of 100,000 people in the United

States every year (22,34). Even with autoimmune

diseases of more common occurrence, such as systemic lupus erythematosus, presentation of disease

symptoms can occur with such broad variety that

setting up controlled trials for these conditions can

become equally difficult (49).

A last treatment design problem has to do with

possible placebo effects of the therapy itself. For

example, among the several explanations discussed in the literature for improvement of patients undergoing apheresis was the possible

psychotherapeutic effects of such therapy. Few

studies have involved double blind protocols (with

sham apheresis) which are necessary to eliminate

the possibility of “placebo improvements” (85,

117,138).

Research Design

A valid research design, perhaps most importantly, requires systematic comparison. At minimum, these comparisons involve the same group

of patients measured before and after treatment;

optimally, they involve two or more randomly

assigned groups tested before and after treatment

(147). The latter design is usually called a true experiment (25,122) or, in health care research, a

randomized clinical trial (RCT). The advantage

of this design, in comparison to nonrandom selection design, is that differences in outcomes can
Ch. 3—Scientific and Medical Aspects of Apheresis: Issues and Evidence ● 27

be attributed more confidently to the treatment,

rather than preexisting differences in the sample

populations tested (102,104).

Evaluating existing research on apheresis therapy poses difficulties in any attempt to draw valid

conclusions. Other than references to prior treatment regimens, comparative data on treatment

groups are typically not available. The great majority of the reported studies are case reports

without any concurrent control groups, blinding,

randomization, or other techniques used in controlled clinical trials.

Because of operational and ethical difficulties

discussed with treatment design issues (see last section), even well-controlled trials of apheresis have

often suffered from small sample sizes. A small

sample size for RCTS, for example, can undermine

what would otherwise be considered a strong

methodological study (85).

Related to the issue of appropriate research design is that multivariate analyses (useful for examining differences by such factors as age, sex,

disease state, and levels of disability) are largely

unavailable. Studies which statistically control

outcome data have not been conducted because

such analyses require large patient populations

and present difficulties both in data collection and

analysis. Their absence from the literature, along

with the lack of controlled research, hinders informed development of treatment strategies tailored to subpopulation needs (102,104).

Apheresis researchers, however, seek to generate systematic experimental designs with comparison group information and multiple, longitudinal outcome measures. This is reflected by the

increasing number of well-controlled studies both

recently reported and presently being carried-out

(see “Conclusions and Directions for Future Research” section of this chapter).

Patient Selection

Patient selection refers to decisions concerning

eligibility for treatment, selection for participation in research, and availability for follow-up

research. If the general population of apheresed

patients is not represented in the research samples

because of particular characteristics (e.g., poorer

prognosis, differing remittive drug regimens), the

generalizability of the research findings is limited

and selection bias is bound to occur (102,104).

Perhaps the most severe sampling problem in

apheresis studies stems from the use of the therapy

as a last resort, i.e., for the “worst cases.” Typically, apheresis therapy has been initiated when patients diagnosed with a specific disease do not respond to other conventional therapies, including

drug therapies and other forms of dialysis such

as hemodialysis or peritoneal dialysis. The application of apheresis in the most severe cases of

rheumatoid arthritis with multiple complications,

for example, has been reported to correspond to

what Warner (141) has labeled the “desperation

reaction, ” where patients and their physicians are

highly motivated to try any promising therapy

because continued painful symptoms or death is

the likely outcome without the therapy and there

is no effective alternative treatment available.

High motivation can likely play an important role

in the patient’s response to a number of subjectively determined outcome criteria, producing

overly optimistic results (85). At the same time,

if only the “worst cases” are selected for apheresis,

its potential effectiveness may be underestimated

because of its initiation at too late a stage in the

disease process.

There is further the problem of statistical regression. According to Wortman and Saxe (147) “statistical regression arises when patients are chosen

because of their extreme value on a laboratory

test or other measure relevant to treatments.” Investigators have found that subjects with high pretreatment measures tend to have lower scores after

the treatment-when, in fact, no change has taken

place. This is the statistical regression effect and

it can deceive clinicians into believing that apheresis has been effective when it really has not (85).

Outcome Measures

A recurring critical issue in any attempt to

analyze the effectiveness of a medical technology

is the selection of appropriate endpoints for

evaluating the success or failure of the intervention. The way in which outcomes of apheresis

therapies are measured significantly affects interpretation of apheresis therapy research.
28 ● Health Technology Case Study 23: The Safety, Efficacy, and Cost Effectiveness of Therapeutic Apheresis

Measures of assessment of outcome have varied

enormously, both across and within disease indication categories. Appropriate outcome measures have at times focused on clinical improvement (i.e., improvement in signs and symptoms)

often with reports of dramatic change. Clinical

improvement measures, as defined in some apheresis studies, however, have been relatively “soft”

or subjective endpoints where researchers fail to

establish standards for any of the criteria, but

rather look for general improvement across series

of measures (85). In other instances, outcome

measures are lacking, not specified, or ill-defined

in the written reports.

Even when clinical outcome measures are well

defined, it is important that the appropriate

measure is used. When an outcome measure such

as mortality is used to evaluate the effectiveness

of apheresis therapy for hemolytic-uremic syndrome (characterized by a decay of general kidney

function), for example, the benefits of apheresis

may be substantially understated. Plasma exchange may, for instance, bring about a temporary improvement in the patient’s clinical

status, but other intervening factors may ultimately cause the patient’s death. Most clinicians, however, would probably agree that the ultimate objective of apheresis therapy is to increase the

likelihood of survival, which suggests that survival (or mortality) is an important outcome

measure of the efficacy of apheresis and should

not be disregarded. The need for chronic dialysis,

on the other hand, could be a more appropriate

outcome measure for determining the ultimate

success of plasma exchange in the treatment of

hemolytic-uremic syndrome, since renal failure is

a major element of the syndrome (146).

Interpretation of clinical improvement for many

diseases treated by apheresis is further confounded

by the variability produced by a basic “remittingexacerbating” nature of the illness. Specifically,

rheumatoid arthritis, systemic lupus erythematoSUS, myasthenia gravis, and Guillain-Barré syndrome patients frequently experience abrupt and

pronounced improvements or worsening of the

illness, and such spontaneous change can easily

be mistaken for therapeutic effect. This leads to

greater variability in results in clinical studies and

to difficulty in interpreting the results (115,117).

Outcome measures have also focused on hematologic and biochemical parameters, such as nerve

conduction tests, and immunological changes.

These measures have not necessarily demonstrated any correlation to clinical responses,

though. Sometimes they have preceded or coincided with clinical changes, while for other disease

indications, they have shown no association to

a clinical response. In short, such outcome

measures may be necessary but insufficient indicators of the efficacy of apheresis (146). Simon

(127), for example, recently reported the case of

a woman with pemphigus vulgaris (a sometimes

fatal skin disease), where apheresis allowed the

disappearance of both skin and tissue-fixed antibodies, but in which the patient continued to

have manifestations of the disease and subsequently died.

Perhaps hematologic and biochemical parameters could be combined in some way as comeasures with clinical improvement outcomes.

The problem of combining multiple evaluation

criteria and assessing the significance of the results

is a difficult one. For example, researchers may

choose to assign different weights to each outcome

measure which would lead to disagreement and

perhaps a lack of consensus on the effectiveness

of apheresis therapy for certain disease indications

(146).

Finally, outcome measures probably suffer from

the lack of systematic documentation of adverse

effects. As a new technology is developed, used,

and reported, researchers and practitioners may

also champion the technology for a variety of personal and professional reasons (104). Apheresis

therapy reporting may have been biased by the

tendency to report the more successful uses of the

new therapy (115).
Ch. 3—Scientific and Medical Aspects of Apheresis: Issues and Evidence ● 29

SAFETY: A REVIEW OF THE EVIDENCE

The paucity of well-controlled trials creates difficulties for an unreserved assessment that apheresis is a safe procedure. Doubts about short- and

long-term safety have neither been confirmed nor

dispelled. Plasmapheresis, in its use for plasma

collection in blood banking, has been demonstrated as a relatively safe procedure. Apheresis

in its other forms does appear to carry some

degree of risk, however, and results in a number

of complications, especially when applied repeatedly for therapeutic applications (42).

Observational studies have generally asserted

the procedure to be relatively safe and well

tolerated by most patients, especially when performed by experienced personnel. Close and continual monitoring of the patient (at least during

initial treatments that establish individual tolerance levels), however, is usually recommended

to ensure that any complications be treated immediately should they occur. Unlike hemodialysis,

where patients receive their blood back almost unchanged, there is much more room for error and

miscalculation, because of the newness of the replacement mixture (80).

Borberg (13) reported that in 205 plasma exchange procedures, 4 serious reactions (anaphylaxis, collapse) and 23 moderate reactions

(chills, stiffness, low blood calcium, fever) occurred. He further stated that the incidence of side

effects was significantly reduced as the apheresis

staff gained experience with the procedure.

Wenz and Barland (144) conducted a lo-year

historical survey on plasma exchange and reported it to be a relatively safe procedure when

performed by experienced personnel. Among the

risks reported were massive extracorporeal blood

clotting and viral hepatitis. However, there have

been no clinical problems with hemorrhagic tendencies despite decreases (30 percent) in platelet

counts following plasma exchange. Coagulation

parameters returned to normal levels within 4 to

24 hours following the exchange.

In another study of the safety issue, Sutton, et

al. (130), reported that of 887 plasma exchange

procedures performed over a 3-year period, minor

complications (chills, hypotension) occurred in

less than 7 percent of the exchanges. Citrate (an

anticoagulant) toxicity (paresthesia and nausea)

occurred in 5 to 15 percent of the exchanges. Sutton, et al. (130), did not see an increased risk of

infection in these patients despite low levels of the

third component of complement and immunoglobulins following the exchanges and the concurrent use of immunosuppressive drugs. In addition only two episodes of minor bleeding were

reported, a further argument that patients receiving this type of therapy may not be predisposed

to bleeding (145).

Generally, the major risks associated with

apheresis may be grouped according to:

●

●

●

Problems of technique. —Manual apheresis

may run a risk of infection and also presents

the possibility of returning the wrong cells

to the patient. Automated centrifuge machines may create problems with hemolysis,

platelet loss, or air-emboli entering the patient’s bloodstream.

Complications associated with fluid transfer. —Improper control of fluid balance may

result in hypertension or cardiac arrhythmias

in patients undergoing plasma exchange. The

infusion of large volumes of intravenous

fluids at room temperature may lead to hypothermia or chill reactions.

Side effects with replacement fluids. —Each

of the major types of protein replacement

carries particular risks. The use of fresh

frozen plasma may introduce hepatitis. Immunological reactions, including chills, skin

eruptions, wheezing, and stiffness may occur in patients who are allergic to certain antigens in transfused plasma. The use of plasma protein fraction or albumin may cause

hypotensive reactions or may result in platelet loss (108).

Long-term effects of fluid replacement are

also worrisome. Removing lymphocytes and

large volumes of plasma repeatedly could decrease immunocompetence levels, increasing

the probability of patients’ susceptibility to

pneumonia and the like. A related concern

is the risk of removing the cells that carry

long-term immunological memory-B-cell
30 . Health Technology Case Study 23: The Safety, Efficacy, and Cost Effectiveness of Therapeutic Apheresis

●

●

lymphocytes. Apheresis could make patients

susceptible to some childhood disease they

had been immune to formerly. Such diseases

are often more serious for adults than children (57,80).

Anticoagulant reactions. —The use of large

amounts of citrate may result in hypocalcemia (low blood calcium) which requires the

addition of calcium to the replacement fluids.

The use of heparin as an anticoagulant can

result in significant platelet loss (thrombocytopenia) if the procedure is extended

over long periods (108).

Immunosuppressive drug reactions. - - —As

already discussed in chapter 2, the apheresis

procedure is often accompanied by an immunosuppressive drug treatment regimen.

These drugs are not without complications,

either. Since they are relatively nonspecific,

the immune system in general is suppressed,

and consequently patients on these drugs are

prone to infection. These potent drugs can

also damage vital organs, sometimes resulting in life-threatening inflammation and fibrosis of lungs, heart, intestines, or kidneys

(42).

While all the above situations can result in

serious complications, particularly for severely ill

patients, many of these problems appear to occur rarely and often can be overcome by prompt

diagnosis and attention. There have been six

known fatalities among the thousands of apheresis

procedures reported performed during the last 10

years (108).

EFFICACY AND EFFECTIVENESS: A REVIEW OF THE EVIDENCE

Ideally, for any procedure, criteria should exist

for the selection of patients; the intensity, frequency, and duration of the procedure; the choice of

replacement fluids; the immunological parameters

to be followed; and the clinical evaluation of the

effects of the procedure. However, after a decade

of use no firm guidelines for apheresis have been

established (144).

Despite the lack of well-controlled and generalizable research on the efficacy and effectiveness

of apheresis, there is a vast literature that describes

and analyzes treatment effects. Because it is highly

anecdotal, discussion of the evidence has sometimes been confined to speculation and generalities. Still, the amount of research has dramatically increased and its quality has improved in recent years.

This section presents and analyzes the evidence

from several reviews of available literature. The

discussion includes the scientific and medical

assessments conducted by the National Center for

Health Care Technology (NCHCT or Center) for

Medicare coverage and reimbursement policy, *

● The National Center for Health Care Technology (now succeeded

by the Office of Health Technology Assessment) in the Department

of Health and Human Services has been authorized by law since

and a number of assessments undertaken by medical associations and specialty societies. This section further presents evidence from original assessments completed for this case study on three

disease indications for which apheresis therapy

has been used experimentally, with somewhat

favorable and hopeful results.

Medical applications and effects of apheresis are

usually classified according to medical discipline,

such as neurology and hematology, or according

to the type of abnormal blood component removal (i.e., protein, antibody, immune complex,

or cell). This section will utilize the latter approach. Table 3 classifies various diseases by both

categories. For protein, antibody, and immunecomplex component removal, the apheresis modality generally employed is plasma exchange,

with lymphapheresis and lymphoplasmapheresis

used to a lesser extent.

1978 to advise on issues related to the evaluation of health care technologies for reimbursement purposes by the Health Care Financing

Administration and other third-party payers. For a complete discussion concerning this process the reader is referred, for example, to

references 103, 104,
Ch. 3—Scientific and Medical Aspects of Apheresis: Issues and Evidence ● 31

Table 3.—Selected Diseases Treated With Apheresis

Medical Plasma exchange

discipline Protein related Antibody related Immune complex related Cytapheresis

Hematology Waldenstrom’s

macroglobulinemia

Rheumatology

Neurology

Oncology Multiple myeloma

Nephrology —

Other Toxins

Poisons

Hypercholesterolemia

Thyroxtoxicosis

Primary biliary cirrhosis

Hypertriglyceridemia

Idiopathic

thrombocytopenic

purpura (ITP)

Factor Vlll antibody

Rh disease

—

Guillain-Barré syndrome (GBS)

Myasthenia gravis (MG)

Multiple sclerosis (MS)a

Polymyositis

Transplant rejection

Goodpasture’s syndrome

(GS)

Thrombotic Sickle cell

thrombocytopenic Polycythemia

purpura (lTP)b

Rheumatoid arthritis

(RA)a Rheumatoid

Systemic lupus arthritis

erythematosus (SLE)

Scleroderma

Other

Multiple

sclerosis

Other cancers Some Ieukemias

Progressive nephritis

Glomerulonephritis

apreferr~ aDheresls theraD~ not yet decirjed: clinical stuclles have employed plssmapheresis, Plasma exchange, Iymphapheresis, andior Iymphopl=mapheresis.

DDi~cu3sd in th[s chapter Under”C’Antibody Related Diseases.”

SOURCE: Adapted from L. F. Rothschild, Unterberg, Towbln, 1981.

Protein-Related Diseases

As discussed in chapter 2, protein-related diseases involve either excessive levels of proteins in

plasma or excessive levels of other substances

which are “carried” in the blood by the plasma

proteins.

Hyperviscosity Syndrome

The earliest therapeutic use of plasmapheresis

was in the management of hyperviscosity syndrome associated with paraproteinemias. This

group of diseases is characterized by the production of enormous amounts of protein molecules

known as immunoglobulins, which are endowed

with known antibody activity. Waldenstrom's

macroglobulinemia results in the overproduction

of one type of immunoglobulin-IgM-and an increase in plasma viscosity or thickening leading

to ocular, neurological, and cardiovascular problems. Multiple myeloma, a malignant tumor of

the bone marrow, involves excessive production

of other types of immunoglobulins—IgG, IgA,

IgE, or IgD—and may result in various symptoms

including hyperviscosity syndrome, excessive

bleeding, and renal failure. Cryoglobulinemia is

characterized by the presence of abnormal immunoglobulins which “precipitate” or form antibody-antigen complexes in temperatures below

37 C. Symptoms include necrologic abnormalities, purpura, and “skin ulcers” (108).

Clinical studies as early as 1960 have generally confirmed the effectiveness of massive plasma

exchanges in treating the hyperviscosity syndrome. A major reason for these findings is that

patients’ symptoms have classically correlated

with levels of viscosity and direct removal of

substances. Observers have rarely been led astray,

with symptoms normally following the lowering

of the viscosity levels in these disease states

(58,108,127).

In Waldenstrom’s syndrome, there seems to be

little dispute that apheresis is an effective palliative

measure in the removal of excess protein. In severe

cases, it probably represents the only effective
32 ● Health Technology Case Study 23: The Safety, Efficacy, and Cost Effectiveness of Therapeutic Apheresis

treatment modality (42,117). With multiple myeloma, apheresis has been demonstrated to be effective in the acute treatment of crises associated

with this condition. Improvement is temporary,

but it can permit chemotherapeutic attempts to

bring the disease under control. In terminal patients who fail to respond to chemotherapy,

apheresis is finding use as a palliative measure to

manage hyperviscosity symptoms. The disease is

ultimately fatal, but apheresis has improved and

prolonged the quality of life for some patients

(117). Several groups have reported definite

responses from apheresis for treating the symptoms of cryoglobulinemia, but there are no known

results of controlled studies for this indication

(58,108).

In February 1981, NCHCT in response to a

Medicare coverage issue request, recommended

that, as a safe and effective therapy, apheresis be

covered in the “treatment of primary macroglobulinemia (Waldenstrom) and hyperglobulinemias, including multiple myeloma. These indications would include hyperviscosity states and

cryoglobulinemias associated with these conditions” (54). The American College of Physicians,

through its Clinical Efficacy Assessment Project

(for more information see, for example, 104), also

seems ready to concur. In a draft statement (4)

prepared for NCHCT, they call apheresis an “efficacious and standard therapy in the treatment

of hyperviscosity syndromes such as those secondary to Waldenstrom’s macroglobulinemia and

multiple myeloma. ”

Hypercholesterolemia

Likewise, apheresis has been used to remove

other direct substances in the plasma such as

cholesterol. Familial hypercholesteroleznia is a

common, usually inherited disease characterized

by increases in plasma cholesterol leading to

nodules of cholesterol forming on the skin or

within the nervous system and to premature closing of the arteries. The use of apheresis has been

undertaken at several hemapheresis centers with

varying results. There has also been some anecdotal evidence of cholesterol levels being lowered

and resulting clinical improvements in patients

suffering from disorders related to primary biliary

cirrhosis, characterized by enlargement of the liver

and retention of bile (108).

Protein Bound Factors

Certain classes of hormones, toxins and poisons

have also been found to be bound to plasma proteins, and this has provided the rationale for the

use of apheresis in treating the life-threatening

symptoms that often result from the presence of

excessive concentrations of these substances.

Again, the removal of these substances has often

correlated with clinical success, but controlled

studies have not been earned out. In most of these

conditions, however, apheresis is utilized only as

a short-term, emergency measure (108,127).

Thyrotoxicosis is a condition that results from

excessive production of hormone by the thyroid

gland. Removal of the substance by apheresis has

been reported to alleviate crisis symptoms (a crisis

stage is referred to as a thyroid storm).

Hepatic coma is thought to be due to the accumulation of protein bound toxins in the bloodstream as a result of acute liver failure arising from

a number of causes such as acute viral hepatitis,

cancer, or reaction to anesthesia. Plasma exchange, and more recently plasma perfusion, have

been observed to be effective in reducing toxins

until the liver has had a chance to regenerate itself.

Plasma exchange regimes, though, remain highly

variable for treatment of hepatic coma (108).

Refsum's disease is a chronic, hereditary disease

characterized by ocular disorder, loss of sensory

and motor function, and dry scaly skin. Equivocal

responses in individual cases have been reported

(80).

Lastly, apheresis has been used in the treatment

of poisonings. The procedure has been thought

to be particularly applicable to those toxins that

are not removed by dialysis, such as mushroompoisoning. Protocols have varied widely, according to setting and according to type and amount

of poison (108,144).

Antibody-Related Diseases

As discussed in chapter 2, these diseases are

often termed “autoimmune” diseases, in which
Ch. 3—Scientific and Medical Aspects of Apheresis: Issues and Evidence ● 33

pathological antibodies are produced and, in turn,

attack the body’s own normal tissues. Researchers

began to look to apheresis for treatment of this

class of diseases because of the success in removing substances associated with hyperviscosity. It

was hypothesized that by removing the antibodies

which were thought to mediate the disease process, clinical results would correlate in a fashion

similar to those found when immunoglobulins

were removed for hyperviscosity symptoms (127).

The two examples in this category with the most

data are myasthenia gravis and Goodpasture’s

syndrome, both discussed in this section.

Neurological Disorders

Apheresis has been applied in the treatment of

several diseases of the nervous system. Apheresis

research has been pushed on by the discovery that

many of the necrologic diseases have immune

components and perhaps may have an antibody

associated with them that may be removed (127).

Myasthenia gravis (MG) is characterized by severe

muscular weakness (without atrophy) and progressive fatigue. The symptoms are generally

thought to result from an autoimmune attack on

acetylcholine receptors in muscles. Because apheresis removes the anti-acetylcholine receptor antibodies from plasma, it has been evaluated with

approximately 125 patients at five major clinical

centers over the past 4 years. Results have shown

significant short-term improvements in selected

MG patients in clinical studies. The therapy is

generally becoming considered appropriate in

severe cases as well as for patients who exhibit

progressive myasthenia symptoms despite treatment with corticosteroids. It has also been favorably reviewed as being beneficial in the long term

and among the most promising applications of

plasma exchange in autoimmune disease (42,108,

177,144). Additional presumptive evidence of effectiveness is the Health Care Financing Administration’s (HCFA) reimbursement of apheresis for

acquired MG since September 1981. While

NCHCT never issued a formal assessment recommending coverage of this indication, it did specify

in November 1980 that it had “no objection” to

HCFA’S preparation of a national coverage instruction for apheresis in treating acquired MG

(56).

Multiple sclerosis (MS) is a chronic neurological

disease characterized by patches of hardened

tissue in the brain or the spinal cord producing

partial or complete paralysis, jerking muscle

tremor, and a variety of other symptoms and

signs. The cause of MS is unknown, but there is

some evidence to indicate that the presence of increased amounts of immunoglobulins and antibodies in the nervous system may contribute to

the disease. It has been suggested and reported

that two types of apheresis procedures—plasma

exchange and lymphapheresis—may be effective

in controlling MS through removal of toxic blood

factors (108,117).

Preliminary studies involving very small numbers of patients have reported significant improvement in the majority of “progressive MS” patients

treated with plasma exchange. Several factors,

however, make any conclusions from these studies

tentative: 1) a plasma factor “specific” for the

disease, such as an antibody, has yet to be identified; 2) the disease has a relapsing and remitting nature which makes conclusions from small

samples extremely tenuous; and 3) immunosuppressive therapy, reported to be useful in MS by

itself, accompanied plasma exchange in the studies

(so that the effect of plasma exchange alone could

not be determined) (117). An assessment of MS

was conducted by NCHCT in response to a Medicare coverage issue, and reviewed both published

and ongoing research. The Center concurred with

the findings of the National Institute of Neurological and Communicative Diseases and Stroke

(NIH) and the National Multiple Sclerosis Society that there is currently inadequate justification

for the routine use of any form of apheresis in the

management of MS. Although apheresis is still

considered experimental, however, the Center

noted several controlled clinical trials about to

begin or underway that should help clarify the

appropriate role for apheresis in the treatment of

MS (91).

Guillain-Barré syndrome (GBS) is a viral inflammatory disorder of the brain, characterized

by a great increase in the protein in the cerebrospinal fluid and in accompanying loss of sensory

and motor function. The condition may be acute

or chronic, and is sometimes fatal. Several cases

of GBS have been associated with swine flu vaccinations (108,117).
34 ● Health Technology Case Study 23: The Safety, Efficacy, and Cost Effectiveness of Therapeutic Apheresis

A primary review, including a methodological

assessment, of the apheresis literature in the treatment of GBS was prepared as part of this study.

Case reports and small-scale, mostly uncontrolled

trials provide suggestive evidence that apheresis

may be effective for some patients with GBS. Because of the low mortality and good prognosis

for most patients with GBS, however, the safety

of the procedure and indications for its use need

to be delineated prior to nonexperimental use of

plasma exchange in GBS.

The conditions for use of plasma exchange in

acute GBS have been sufficiently standardized to

enable a controlled clinical trial of the procedure.

The potential cost saving and potential for shortened disability make well-designed controlled

studies of this therapy important. Controlled

studies currently in progress should be adequate

to provide data which address the essential clinical

questions. Until the results of these studies are

available, though, the use of plasma exchange in

GBS can only be considered an experimental procedure (115). The full review and assessment of

apheresis for the treatment of GBS is presented

in appendix D.

Another neurological disorder for which apheresis has been reported (108) as a treatment approach is amyotropic lateral sclerosis (ALS), a

progressive disease marked by muscular weakness

and atrophy. Norris, et al. (89), noted some improvement in three of ten ALS patients who underwent plasma exchange sessions. This has not

been confirmed by other studies, however, and

no rationale yet exists as to why it should be effective (43).

Lastly, two neuromuscular disorders, polymyositis and dermatomyositis, have been reported

(108) as responsive clinically to apheresis therapy.

Both disorders, characterized by progressive muscular inflammation and weakness, have been

linked to antimuscle antibodies. The evidence in

both disorders, however, is anecdotal. The American College of Physicians (4) has called apheresis

an “investigational therapy” in the treatment of

patients with polymyositis, but has also stated

that it “maybe indicated . . . . in patients in the

severe, imminently fatal polymyositis . . . . who

are resistant to all other therapies. ”

Renal Diseases

Goodpasture's syndrome (GS) is characterized

by a combination of glomerulonephritis (kidney

disease) and pulmonary hemorrhage. The incidence of GS is approximately 4,000 to 5,000 cases

annually in the United States. GS is believed to

be caused by an antibody directed against glomerular (kidney) and alveolar (lung) basement

membranes and is characterized by a rapidly failing course terminating in asphyxia from lung

hemorrhage or in death from renal failure. Historically, the treatment of GS has involved immunosuppressive/anti-inflammatory drugs with

only modest success. The mortality rate for this

disorder has typically run about 75 percent

(22,108).

It is possible that apheresis removes enough circulating antibodies to alter the course of the

disease, but reports are mixed. Again, there have

been no controlled trials, but case studies and

literature reviews claim that apheresis has been

effective for those patients with mild to moderate

renal dysfunction, but who are suffering acute

pulmonary complications or who are experiencing rapidly progressive kidney deterioration

(4,108,117,144). It has been speculated that early

diagnosis and apheresis therapy could prevent irreversible renal failure (42).

The American Medical Association has also

supported apheresis in use of treatment of GS

though it has not specified under what conditions

(s). The American College of Physicians, however, has called apheresis an “investigational”

therapy for GS, stating that studies to date have

failed to demonstrate improved survival among

patients with this disease receiving apheresis (4).

A more thorough review and assessment of the

use of apheresis for GS was completed in early

1983 by the Office of Health Technology Assessment (OHTA) in response to a Medicare coverage

policy issue. The OHTA assessment reported the

beneficial effects of plasma exchange for some

groups of GS patients. However, probably because of the absence of prospective RCTs, OHTA

recommended plasma exchange only be considered standard therapy for “life threatening forms”

of GS (94).
Ch. 3—Scientific and Medical Aspects of Apheresis: Issues and Evidence ● 35

In a related area of renal disorders, rejection

of the donor kidney remains the major problem

in renal transplantation. Acting on the hypothesis

that rejection is due in part to a circulating antibody directed against the vascular endothelium,

several groups have used intensive plasma exchange to treat renal allograft rejection. Scoville

Associates (108) has reported that apheresis is apparently effective in controlling approximately 50

percent of acute rejection episodes, and that the

graft survival period has been lengthened when

apheresis is used in a combination therapy regimen with steroids versus use of steroid therapy

alone. The role of apheresis in the management

of acute renal transplant rejection (particularly in

those cases which do not respond to steroid therapy) has been called promising, though, more

well-controlled studies need to be undertaken at

this point (30).

Blood Disorders

Another disorder for which use of apheresis has

generated some initial response and promise has

been in treatment of patients with antibodies to

Factor VII. Apheresis has been investigated as a

potential therapy for patients with antibodies or

inhibitors to Factor VIII during the past 10 years.

Factor VIII is a substance in the blood involved

in hemostasis (i.e., the normal process of blood

clotting for control of bleeding). Patients with the

most common type of hemophilia lack Factor VIII

and are at risk of developing Factor VIII antibodies when given supplemental, exogenous Factor VIII to help control bleeding episodes. It has

been estimated that as many as 20 percent of such

patients may develop this condition. Factor VIII

inhibitors can also arise spontaneously in other

patients. This so-called idiopathic or acquired inhibitor to Factor VIII can occur in women in their

first year after giving birth, persons with rheumatoid arthritis, the elderly, and persons suffering a variety of other disorders (57,146).

As part of this case study, a primary literature

review, analysis, and evaluation were undertaken

for treatment of this disorder with apheresis. Nine

studies were reviewed and both immediate and

long-term findings were tallied. For 16 of the 18

patients at risk due to severe bleeding from surgery, the immediate clinical results were uniformly

successful. In all cases hemostasis was achieved,

and the patient fully recovered from the acute

episode. Nine patients were reported to have poor

long-term results, but several patients were reported to have achieved a permanent reduction

in Factor VIII inhibitor antibodies without the

need for additional therapy. Importantly, though,

the overall quality of the research evidence was

found to be poor: the studies were all pretrial

clinical reports (generally of one patient), there

was no agreed upon treatment, the goals of the

studies differed, and, with so few patients, the

issue of sample bias should not be discounted

(146). The complete assessment of apheresis in the

treatment of antibodies to Factor VIII is presented

in appendix C.

Antibodies to Factor VIII are encountered in a

number of hematological (and nonhematological)

disorders. Likewise, a host of hematological disorders are thought to be related to a gone-awry

immune mechanism, and as a result, several blood

disorders have been treated with apheresis, including thrombotic thrombocytopenic purpura,

hemolytic-uremic syndrome, idiopathic thrombocytopenic purpura, autoimmune hemolytic

anemia, and rhesus hemolytic disease.

Thrombotic thrombocytopenic purpura (TTP)

is an interesting example of a disorder for which

apheresis appears to be of benefit as a lifesaving

measure although the rationale for its use is still

very speculative. It is a condition involving the

development of diffuse, small blood clots and a

deficiency of platelets. Its cause is unknown but

may be related to a disordered immune mechanism acting directly on the platelets or on the

blood vessels, or on both concurrently. Apheresis

has been reported to have benefits in several cases,

possibly by removing circulating immune complexes or an antiplatelet antibody. * Results of

apheresis for TTP have been encouraging with up

to 80 percent response rates reported in some

studies. The American College of Physicians’

assessment (4) is typical of several reviews and

of the research community (7,42,108,117,125,127,

144) in stating that “apheresis in conjunction with

*Because of TTP’s possible relation to immune complexes, this

disorder is sometimes grouped under the immune-complex related

disease category, and could logically be included in the next section’s discussion (“Immune-Complex Related Diseases”) as well.
36 ● Health Technology Case Study 23: Tth Safety, Efficacy, and Cost Electiveness of Therapeutic Apheresis

exchange transfusions, corticosteroids and platelet

inhibitors, appears to be efficacious and standard

in the treatment of thrombotic thrombocytopenic

purpura.” The American College of Physicians

noted further that, “Despite the fact that trials indicating efficacy were uncontrolled, the reductions

in mortality in patients with TTP compared to

those not receiving apheresis were so significant

that apheresis appears to be beneficial.” Simon

(128) has also claimed that selective use of apheresis can also decrease morbidity, hospital stays,

long-term chronic dialysis, and maintain a productive lifestyle for patients longer. NCHCT (92)

conducted an assessment of TTP for Medicare

coverage policy, and noted the reported beneficial

effects, but cautioned that the quality of research

was plagued by the complete absence of controlled

clinical trials to confirm these findings. (Some

have argued that such trials are impossible given

the sudden and life-threatening intensity of the

disorder’s onset.) NCHCT, because of the lifethreatening nature of TTP, stated that the use of

apheresis (specifically, plasmapheresis and plasma

exchange) “seems justified when other conventional therapies have failed.”

Hemolytic-uremic syndrome (HUS) is characterized by a decay of kidney function, destruction of red cells, and a dramatically reduced level

of circulating platelets. It shares a number of

features with TTP. In fact, HUS has been considered by some clinicians to be a variant of TTP,

this being supported by overlapping clinical and

pathologic characteristics and the possibility of

similar precipitating events. There is no objective

method at present to distinguish HUS from TTP,

although in the case of the former, the kidney is

typically the main and often only target organ,

children are primarily affected, and the prognosis

is generally much better (71,146).

A primary literature review and assessment was

conducted by Wortman and Murt (85) for this

case study on the use of apheresis in the treatment

of HUS. Data from the eight communications that

have appeared in the literature during the past 3

years are presented on a total of 11 patients, but

each case is described individually. Only one of

the communications suggests that plasma exchange has limited effectiveness on the disease

process (11). However, the authors in this article

add that the clinical benefit may have been compromised because apheresis was performed during a recurrent phase of the illness (which is

recognized as being associated with poor prognosis). The remaining seven studies are almost

uniformly favorable in suggesting that apheresis

contributes to clinical improvement although

there is no explanation provided about which

measures are used to gauge this improvement.

Several authors add the caveat that apheresis be

initiated during the early stages of the disease in

order to realize its full benefit (132). Parries, et

al. (106), caution that apheresis alone is associated

with complications (e.g., hepatitis) and that these

risks should be weighed against the potential benefits of apheresis.

As might be expected with a total reporting of

11 patients, the research base is too small and incomplete to endorse apheresis as a treatment for

HUS. Furthermore, the studies contain no comparison groups, while treatment designs and outcome measures varied widely, further limiting the

ability to make any conclusion or recommendation. A full discussion of this assessment is found

in appendix B.

Rhesus hemolytic disease (Rh disease) of the

newborn is characterized by fetal anemia, jaundice, enlargement of the liver and spleen and general edema. Approximately 65 percent of untreated cases result in stillbirth or infant mortality. The disease is caused by Rh antibodies produced in maternal blood which may cross the placenta and destroy fetal red blood cells. Antibodies, directed against an Rh positive fetus, develop

in an Rh negative mother following a previous

pregnancy in which the fetus was Rh positive or

following transfusion of Rh positive blood (108).

Murt (85) has reported that between 1968 and

1981, 13 studies were published on the effects of

apheresis in the management of severe Rh disease.

The quality of the research studies is quite poor:

all 13 studies are observational, and all but one

are reports of individual case studies. The number

of patients in these studies ranges from 1 to 96

and the median is 3. Only 3 of the 13 studies have

given plasma exchange an unfavorable review,

and 2 of these studies are the initial published

reports of the use of apheresis in treating pregnant women with Rh disease (14,112).
Ch. 3—Scientific and Medical Aspects of Apheresis: Issues and Evidence ● 37

There are a host of other autoimmune hematological disorders treated by apheresis. Such

disorders include autoimmune hemolytic anemia

and idiopathic thrombocytopenic purpura. They

are caused by antibodies which characteristically attack and lead to the destruction of valuable

blood components. These diseases have been

treated with some success with apheresis, but the

reports are anecdotal (42).

lmmune-Complex Related Diseases

In immune-complex related diseases, antigenantibody complexes can be deposited in tissue and

produce severe inflammation and tissue damage.

Just as researchers and clinicians reasoned that

protein plasma substance removal could be extended to antibody removal, circulating immune

complexes began to be experimentally removed

through apheresis methods.

Renal Disorders

This further extension to immune complexes

was particularly notable in England and Australia

where there was an initial interest by nephrologists

in the application of apheresis for rapidly progressive glomerulonephritis (GN) (127). Characterized by a rapid deterioration of renal function,

GN appears to arise from two mechanisms. The

first mechanism stems from the deposition of immune complexes which are formed in the circulation and subsequently lodge in the glomeruli

(small structures in the kidney which contain capillary blood vessels surrounded by a thin membrane which acts as a filter for the separation of

urine). The second mechanism, the much rarer,

arises when an antibody is generated against the

kidney, which sets in process a chain of inflammatory events leading to GN. Plasma exchange

for rapidly progressive GN has been evaluated as

a therapy mode with rather uncertain results

(90,108). Several case studies have been published

reporting the clinical success of patients treated

with concurrent plasma exchange and immunosuppressive drug therapy. However, there is some

speculation that similar results may be obtainable

with immunosuppressive drug therapy alone (108,

128). Apheresis in rapidly progressive GN has also

been associated with a high degree of infection

caused by a variety of unusual pathogens (42).

NCHCT was requested by HCFA in May 1981

to conduct an assessment of the safety and clinical

effectiveness of “membranous and proliferative

glomerulonephritides” for Medicare coverage and

reimbursement policy (38). Due to budgetary and

staff cutbacks, that assessment was not issued until early 1983 by NCHCT’s successor organization,

the Office of Health Technology Assessment (28).

The OHTA assessment concluded that for rarer

types of GN (antibody related), it appeared that

plasma exchange “favorably affected” GN, and

“should be recommended as standard therapy” for

these conditions. However, for those more common cases of GN associated with immune complex mechanisms, OHTA concluded that the role

of apheresis is “much less clear-cut and should be

investigated further” (94).

Connective Tissue Disorders

The advocated clinical successes in GN led to

investigative and experimental usage of apheresis

in a whole host of connective tissue diseases which

were thought to be possibly related to immune

complex deposition in tissues and often correlated

with levels of circulating immune complexes (127).

Systemic lupus erythematosus (SLE) is a chronic

and often fatal disease characterized by pathological changes in the vascular system, manifested

in skin rashes, fever, arthritis, and heart, lung,

and kidney damage (108). Preliminary reviews indicate that apheresis has produced “striking short

term clinical improvement” in some patients with

high levels of circulating immune complexes

before treatment. However, other patients with

SLE, but not high levels of circulating immune

complexes before treatment, have also responded

to therapy. Study results have also been confounded by poorly controlled immunosuppressive

and anti-inflammatory drug therapy accompanying apheresis (117, 128). As with apheresis in the

treatment of rapidly progressive GN, HCFA requested NCHCT in May 1981 to assess the safety and clinical effectiveness of apheresis therapy

for SLE as a candidate technology for Medicare

coverage and reimbursement. That assessment,

now under the aegis of OHTA, has not yet been

completed (28). The American College of Physicians (4) and the American Society of Hematology

(7) have both judged apheresis for SLE as “in98-822 0 - 83 - 4 : QL 3
38 ● Health Technology Case Study 23: The Safetyr Efficacy, and Cost Effectiveness of Therapeutic Apheresis

vestigational” only, noting that no adequately

controlled scientific studies have established its

efficacy. Both groups, however, cautiously allow

for the possibility of use in critically ill SLE patients who fail to respond to conventional drug

therapy.

Rheumatoid arthritis (RA) is a chronic disease

of the joints marked by inflammation and atrophy

of the bones. In late stages, deformity and immobility develop. While it is unclear at present

which plasma factors are involved in RA (immunoglobulins, immune complexes, lymphokines,

etc.), several medical centers have reported beneficial effects of plasma exchange or related procedures: lymphapheresis and lymphoplasmapheresis. Several apheresis protocols have been

reported. Clinical responses have been claimed in

the remission of symptoms that lasts several

months (117). Rothwell, et al. (118), however,

reported no statistically different clinical response

in a controlled study that had one group receive

plasma exchange and drug therapy while a second

group received drug therapy only.

Because RA affects approximatelys million to

7 million individuals in the United States, with

no known cure, the question of apheresis treatment benefits has become a somewhat volatile

issue. Over the past 2 years, the Council on Scientific Affairs of the American Medical Association,

the American Rheumatism Association, the

American College of Physicians (who consulted

with the American Society of Hematology and the

American Society of Oncology, as well), and

NCHCT have all formally considered the evidence. All have concurred that apheresis for treatment of RA is an experimental therapy but have

suggested its possible use in serious, lifethreatening complications of RA, such as vasculitis, cryoglobulinemia, or hyperviscosity syndrome (59,86). In a separate assessment, NCHCT

explicitly recommended apheresis in the management of life-threatening rheumatoid vasculitis* as

a treatment of last resort and possibly lifesaving

intervention when more conventional therapies

have failed. The Center stated that such “pro-

“Rheumatoid vasculitis is marked by a destruction and necrosis

of sections of the body, particularly toes and fingers and areas served

by small vessels that are inflamed.

cedures are usually reserved for those patients

who have failed to respond to more conventional

therapies and it is usually combined with them”

(93).

There is also some current debate about the

proper mix of apheresis therapy and drug therapy

for RA and about the relative effects of plasma

exchange and lymphocyte removal. Studies are

still needed to define the role of each therapy in

the management of severe RA. Wallace, et al.

(139), have recently reported the results of a

double-blind, controlled study of lymphoplasmapheresis versus sham apheresis in RA for 14

patients. The results proved mixed. Whereas some

measures of disease severity improved significantly in the treated group as compared with the control group, others did not. All reported benefits

of therapy were temporary (12).

Cutaneous vasculitis, an additional connective

tissue disorder treated with therapeutic apheresis,

is characterized by inflammation of the small

blood vessels of the skin. Temporary clinical responses have been reported in the literature. There

are no known controlled studies (108).

Skin Disorders

Several dermatologic diseases which are

thought to involve immune mechanisms have indicated a response to therapeutic apheresis.

Pemphigus vulgaris is a rare disorder characterized by bubblelike lesions on the surface of the

skin. Remissions have been reported with apheresis, but there are no published clinical trials

(2,108,144). Single cases of clinical responses to

herpes gestationis, a subepidermal blistering condition of pregnancy, and psoriasis, a chronic,

genetically determined dermatitis, have also been

reported (108).

Cancers

Therapeutic apheresis in the treatment of multiple myeloma was discussed earlier in this chapter.

Several reports have also described recent attempts to treat various forms of other cancers with

plasma exchange. Animal studies have suggested

that the growth of the tumors is related to deficiencies in the immune process (144). The rationale for apheresis is that the removal of immune
Ch. 3—Scientific and Medical Aspects of Apheresis: Issues and Evidence ● 39

complexes or blocking factors might improve immune responsiveness to tumors. Preliminary results have been mixed and further evaluation will

be required. A refinement of plasma exchange,

involving modification of plasma (by circulating

it through protein-A columns) has recently been

reported to produce benefits in several forms of

cancer, including breast cancer (117).

At the beginning of this century, hopes for developing vaccines for treatment and specific

diagnostic tests for cancer were based on remarkable advances in immunology and their successful

application to many infectious diseases. Early efforts to relate immunology and cancer failed because of a lack of understanding of the complexity of the immune response. In recent decades,

however, investigations have discovered a probable role of the immune system in both the development and spread of tumor cells (108). At

present, apheresis for cancer is experimental, but

it could broaden the fundamental understanding

between malignancy and the immune response

(144).

Miscellaneous Disorders

Table 4 presents a list of diseases either believed

to be of immunological origin or of unknown

cause for which plasma exchange has been experimentally employed as a therapy and positive

clinical responses reported. Typically, in each

disease category, plasma exchange procedures

have involved only a small sample group anywhere from 1 to 30 patients and there have been

no control or comparison groups against which

to measure treatment results. Evidence, then, is

Table 4.—Therapeutic Apheresis for Miscellaneous

immunological Diseases and Diseases of

Unknown Cause

Miscellaneous immunological diseases

Graves’ disease

Crohn’s disease

Severe asthma

Insulin-resistant diabetes

Scleroderma

Diseases of unknown cause

Hypertension (idiopathic only)

Raynaud’s phenomenon

Idiopathic pulmonary hemosiderosis

SOURCE: Adapted from Scoville Associates, 1981.

anecdotal and awaits additional research before

reliable conclusions can be drawn regarding the

potential role of apheresis for these disorders

(42,80,108,144).

Cell-ReIated Diseases

The use of apheresis (specifically cytapheresis)

therapy has been anecdotally reported to be quite

beneficial in the treatment of diseases involving

excess or abnormal blood cellular components.

While not common, certain clinical situations may

benefit from the removal and lowering of a

platelet count or white blood cell count in a patient. Very high white counts, such as in granulocytic leukemia, can cause immediate and

severe crises with cerebral hemorrhaging, and possibly death. Emergency removal of white cells can

be lifesaving while chemotherapy is initiated,

although chronic treatment has generally failed

to alter the outcome of the diseases. Sickle cell

disease (SCD) is characterized by red blood cells

(RBCs) containing abnormal hemoglobin. The

“sickling” of RBCs in capillaries impairs blood

flow and can produce severe complications. Exchange transfusion (removal of RBCs followed by

replacement with normal RBCs) has been reported

to produce beneficial results in SCD crises. Also,

long-term use of platelet removal and white cell

removal in the treatment of autoimmune diseases,

including multiple sclerosis and rheumatoid arthritis, have also been reported, and research in

those areas continues.

Although not for therapeutic purposes, cytapheresis applied to healthy donors also has important clinical applications in the preparation of

component concentrates. Many diseases involve

decreased levels of white cells or platelets. Cancer

chemotherapy, as well, often depresses bone marrow production of white cells and platelets so that

transfusions of the deficient components are clinically beneficial. Recent refinements in blood separator devices make it practical to collect large

numbers of platelets or white cells from a single

donor rather than pooling separate components

from multiple donors. This is of considerable benefit in minimizing the risk of donor/recipient antigenic incompatibility and hepatitis transmission

(117).
40 ● Health Technology Case Study 23: The Safety, Efficacy, and Cost Electiveness of Therapeutic Apheresis

CONCLUSIONS AND DIRECTIONS FOR RESEARCH

Clearly, a variety of diseases-often rare-have

been treated by apheresis in circumstances where

conventional therapy has not been beneficial.

There is a great deal of enthusiasm among researchers and clinicians who wish to explore all

the possibilities for therapeutic apheresis. Medical

journals are replete with anecdotal reports of

physicians’ trying apheresis as a last resort in a

wide range of diseases. These cases, however, do

not provide a strong systematic base for recommending the widespread use of apheresis as a

mature and effective technology.

Apheresis appears to be a relatively safe procedure, though it is not without at least short-term

risks. The long-term risks of removing useful

blood components have been termed “worrisome”

and are unclear at best (80). Apheresis device

equipment can also be termed effective in the sense

that the technology accomplishes the intended removal of plasma and cells.

However, there have been very few well-controlled studies documenting the efficacy of the

technology in actually improving health (53).

More specifically, there have been few situations

in which isolated pathogenic proteins, antibodies,

immune complexes, and blood cells were removed

and unequivocal clinical results observed. The use

of apheresis has been generally acknowledged as

an effective treatment application for acute

therapy in a small group of relatively obscure

diseases. These include acquired myasthenia

gravis, primary macroglobulinemia (Waldenstrom’s), and hyperglobulinemias, including multiple myeloma. There is certainly suggestive evidence, too, that therapeutic apheresis is successful

in arresting the disease process for some patients

under some disease conditions. Convincing proof

of clinical efficacy, however, is still lacking in the

wider variety of diseases in which this treatment

is being used.

Any interpretation of clinical results has been

further hampered by the lack of standardized application of this therapy. Criteria for patient selection and treatment schedules for many disease applications still need to be developed. The relative

roles of exchange, drugs, and supportive care need

to be further defined and clarified.

The problem of standardized application of

apheresis is not surprising in considering that the

scientific rationale for use of the technology to

treat a specific disease category is sometimes very

weak. Because the disease-causing mechanisms remain largely unknown, speculation has necessarily determined the intensity of the apheresis schedule, the volume exchanged, and whether there

should be concomitant removal of cellular components with or without the addition of immunosuppressive drugs. Each of these aspects of

apheresis has been the subject of much discussion

and disagreement (12).

Though some researchers say it is “too early”

to do controlled trials because doctors have not

yet determined the theoretically best treatments

to be tested, research in apheresis seems to be in

transition. In an effort to document the value of

therapeutic apheresis, large prospective randomized trials have been organized for several disease

applications in which apheresis therapy has not

been shown to be either clearly effective or ineffective (2,12). Although some of this research is

being done without direct government support,

a substantial portion of experimental and clinical

trial work is being undertaken with the help of

the National Institutes of Health (NIH). Because

of the high costs of these studies, it is not surprising—or unreasonable—that public moneys

support such a significant number of them. Table

5 presents a listing of major ongoing research

studies.

In order to precisely define what advantages,

if any, apheresis would have, controlled trials

need to address the safety and efficacy issues

discussed in this chapter of present apheresis

technologies. Long-term studies will also be

needed to detect any additional unforeseen or

unspecified questions of safety, as well as effectiveness. Importantly, future research must also

compare the present treatment modalities with

new and emerging approaches such as plasma filtration through specific affinity columns (with the

return of the patient’s own plasma) or related

scientific advances such as the use of monoclinal

antibodies (see “Future Technological Directions”

section in ch. 2 for a discussion of these treatment

approaches). Many researchers and observers in
Ch. 3—Scientific and Medical Aspects of Apheresis: Issues and Evidence ● 41

both the public and private sectors speculate that diseases (53). If the present applications of thertherapeutic apheresis as now applied will be re- apeutic apheresis are indeed in such a period of

placed over the next 10 years by either advances flux, great care must be taken to target research

in equipment-embodied apheresis technology or and clinical efforts into the most promising and

basic scientific research into the causes of various beneficial technology-related developments.

Table 5.—Present Apheresis Research Activity

Location Principal investigator Disease indication

Major NIH Stud/as

SUNY—Stony Brook . . . . . . . . . . . . . . . . . . . . . .

Washington University. . . . . . . . . . . . . . . . . . . . .

Cincinnati General Hospital . . . . . . . . . . . . . . . .

Johns Hopkins University . . . . . . . . . . . . . . . . . .

NIADDK, NIH . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Walter Reed Army Medical Center . . . . . . . . . .

University of Cincinnati . . . . . . . . . . . . . . . . . . . .

Massachusetts General . . . . . . . . . . . . . . . . . . . .

NIADDK, NIH . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Rush-Presbyterian St. Lukes. . . . . . . . . . . . . . . .

Cincinnati General Hospital . . . . . . . . . . . . . . . .

Rush-Presbyterian St. Lukes. . . . . . . . . . . . . . . .

George Washington University. . . . . . . . . . . . . .

University of lowa. . . . . . . . . . . . . . . . . . . . . . . . .

University of Pennsylvania . . . . . . . . . . . . . . . . .

NIADDK, NIH . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Scripps Clinic and Research Foundation . . . . .

Columbia University . . . . . . . . . . . . . . . . . . . . . . .

Mayo Foundation . . . . . . . . . . . . . . . . . . . . . . . . .

SUNY at Brooklyn. . . . . . . . . . . . . . . . . . . . . . . . .

Columbia University. . . . . . . . . . . . . . . . . . . . . . .

Boston Children’s Hospital. . . . . . . . . . . . . . . . .

University of Utah Medical Center. . . . . . . . . . .

Peter Bent Brigham Hospital . . . . . . . . . . . . . . .

Johns Hopkins Hospital . . . . . . . . . . . . . . . . . . .

Miami Veterans Medical Center. . . . . . . . . . . . .

University of Rochester. . . . . . . . . . . . . . . . . . . .

Cincinnati General Hospital . . . . . . . . . . . . . . . .

Columbia University . . . . . . . . . . . . . . . . . . . . . . .

Johns Hopkins University . . . . . . . . . . . . . . . . . .

NCI, NIH . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

NCI, NIH . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

University of Texas. . . . . . . . . . . . . . . . . . . . . . . .

University of New Mexico, Albuquerque . . . . .

Columbia University. . . . . . . . . . . . . . . . . . . . . . .

Columbia University . . . . . . . . . . . . . . . . . . . . . . .

Columbia University . . . . . . . . . . . . . . . . . . . . . . .

Tufts University. . . . . . . . . . . . . . . . . . . . . . . . . . .

Johns Hopkins University . . . . . . . . . . . . . . . . . .

Other major studies

Rogosin Kidney Center . . . . . . . . . . . . . . . . . . . .

Evanston Hospital (Ill.). . . . . . . . . . . . . . . . . . . . .

Southwestern Medical School . . . . . . . . . . . . . .

El Dorado Hospital . . . . . . . . . . . . . . . . . . . . . . . .

Froedtert Memorial Lutheran Hospital . . . . . . .

Kingston General Hospital, Ontario . . . . . . . . 

Toronto Western Hospital . . . . . . . . . . . . . . . . . .

Froedtert Memorial Lutheran Hospital . . . . . . .

Victoria Hospital, Ontario . . . . . . . . . . . . . . . . . .

Hammersmith Hospital, London . . . . . . . . . . . .

Canadian Red Cross (sponsor). . . . . . . . . . . . . .

Gorevic, Peter

Shonfeld, G.

Stein, Evan

Kwiterovich, Peter

Balow, J. E.

Johnson, John

Pollak, Victor

Coggins, Cecil

Klippel, J. H.

Lewis, Edmund

Kashvap, Moti

Lewis, Edmund

Lachin, John

Hunsicker, Lawrence

Schumacher, H.

Wilder, R. L.

Vaughan, John

Jacobs, Jerry

Bunch, Thomas W.

Diamond, Herbert S.

Chess, Leonard

Weiner, Howard

Petajan, Jack

Weiner, Howard

McKhann, Guy

Lian, Eric

Marder, Victor

Glueck, Charles

Edelson, Richard

Moser, Hugo

Stevenson, H. C.

Schiffer, C. A.

Tindall, Richard

Simon, Toby

Grossman, Marc

Jaffe, Israeli

Resor, Stanley

Agnello, Vincent

Moser, Hugo

Saal, Stuart

Dau, Peter

Tindall, Richard

Giordano, Gerald

Khatri, Bhupendra

Giles, Alan

Cardella, Carl

Kaufman, H. Myron

Clark, William

Lockwood, Martin

Rock, Gail

Cryoglobulinemia

Familial hypercholesterolemia

Familial hypercholesterolemia

Hypercholesterolemia, xanthomatosus,

atherosclerosis

Goodpasture’s syndrome

Goodpasture’s syndrome and rapidly progressive

glomerulonephritis

Glomerulonephritis

Glomerulonephritis

Systemic lupus erythematosus

Systemic lupus erythematosus

Systemic lupus erythematosus

Lupus nephritis

Lupus nephritis

Lupus nephritis

Rheumatoid arthritis

Rheumatoid arthritis

Rheumatoid arthritis

Rheumatoid arthritis

Rheumatoid arthritis

Rheumatoid arthritis

Rheumatic disease

Multiple sclerosis

Multiple sclerosis

Multiple sclerosis

Guillain-Barré syndrome

Thrombotic thrombocytopenic purpura

Idiopathic thrombocytopenic purpura

Lipoprotein metabolism

Pemphigus

Refsum’s disease

Cancer

Leukemia

Neuromuscular disorder

Neonatal adaptation

Porphyria cutanea tarda

Connective tissue disorder

Dermatomyositis, polymyositis, and

Immune complex disease

Hunter’s syndrome

Myasthenia gravis

polyneuropathy

Myasthenia gravis, multiple sclerosis

Myasthenia gravis

Multiple sclerosis

Multiple sclerosis

Rheumatoid arthritis

Renal transplant rejection

Renal transplant rejection

Lupus nephritis

Rapidly progressing glomerulonephritis

TTP, ITP, Rhesus Iso-immunization

SOURCE: National Institutes of Health, 1982
4

Cost Effectiveness and

Reimbursement Policy:

Issues and Evidence
,

4.

Cost Effectiveness and Reimbursement

Policy: Issues and Evidence

In addition to the issues of health status or other

health outcome related effects (i.e., safety, efficacy, and effectiveness) of apheresis, efficiency

issues must also be addressed. The cost of providing apheresis therapy is a matter of almost

universal concern in the available literature. As

spiraling health care costs continue to plague

medical care delivery in this country and elsewhere, it is important to examine whether there

is improvement in the quality of life and which

therapies offer the greatest value for the resources

invested.

Because of the broad and pervasive influence

of third-party payment mechanisms on health care

delivery, any discussion of economic effects of

therapeutic apheresis must also be closely tied to

an examination of funding and reimbursement

policies of both private and government insurance

programs. Reimbursement policies have profound

effects on the adoption and use of medical technologies, as well as the innovation process itself

of medical procedures such as therapeutic apheresis. Informed coverage decisions require information concerning medical technologies, that is

at least as detailed as that needed for the

regulatory decisions of the Food and Drug Administration (FDA) regarding device equipment.

Whereas regulatory decisions tend to be of a “go”,

“no go” nature, reimbursement decisions are, or

at least could be, more related to appropriate use

of technologies, a much finer distinction (104).

Appropriate use decisions would support the provision of effective apheresis therapy and efficient

COST EFFECTIVENESS

Two important methods used to assess the costs

and benefits of therapeutic apheresis, and developing comparisons among effects, costs, and benefits

are cost-benefit analysis (CBA) and cost-effectivecare. That is, only proven treatment alternatives

would be considered for widespread clinical application and the lower cost treatment alternative

would not only be available but used (102,104).

Until recently, apheresis was routinely reimbursed for by some third parties when prescribed

by a physician. However, concerned about costs

and estimates of expansion of use over the next

5 years, third-party payers are now attempting

to tailor their policies according to the principle

of appropriate use—i.e., to pay for apheresis

where and when it is a proven and efficient therapeutic method (80,117). Medical insurers are,

however, far from a consensus on how, when,

and if they should cover apheresis (34,49).

The research and policy issues regarding the

costs and benefits of apheresis therapy, including

a discussion of third-party reimbursement, form

the substance of this chapter. It is a discussion that

initially examines the methods that can be used

in assessing the economic effects of therapeutic

apheresis. Currently, the most visible and potentially most useful of methods is cost-effectiveness

analysis (CEA). As CEA is not simply an economic technique, but rather a blend of economic and

clinical information, it will serve to conceptually

integrate cost concerns with the assessment of

safety and efficacy issues in chapter 3. An absence

of reliable estimates of the efficacy and safety of

apheresis treatment and of its costs and savings

prohibits conclusive results, but gaps in present

knowledge can be identified and directions for

future research can be addressed.

ness analysis (CEA). CEA implies a comparative

analysis of the costs and health effects of alternative treatments. In a CEA, a common outcome

is specified (e.g., functional status) and the costs

45
46 . Health Technology Case Study 23: The Safety, Efficacy, and Cost Effectiveness of Therapeutic Apheresis

of providing alternative treatments are compared.

Treatment costs are typically specified in monetary terms. CBA, on the other hand, requires that

both cost and benefits be assigned monetary values. A CBA examines the ratio of resources used

(cost) to resources saved (benefits) when particular

treatments or even different treatment regimens

or programs are employed (102, 104).

While CEA/CBA can be thought of as an aid

to synthesis of both health effects and economic

effects, the value of a CEA/CBA lies more in the

process of performing the analysis than in any

numerical results. There are a number of reasons

for this, among the most important of which are

CEA/CBA’s inabilities to adequately address

ethical issues and the uncertainty of specifying

comprehensively the costs and benefits of alternative treatments. This is clearly the case with

therapeutic apheresis because there are no reliable

estimates of savings due to treatment benefits that

are available or known. In addition, factors other

than those qualified in a CEA/CBA (e.g., social,

ethical, or value influences) should be considered

in making a decision (12,98,102,104).

OTA, in its assessment of the methods of CEA/

CBA (98) developed 10 principles to guide the conduct, use or evaluation of CEA/CBA studies (see

table 6). The Principles most relevant to the assessment of therapeutic apheresis are that alternative

means (technologies) to accomplish the stated objectives should be identified and subjected to analyses; all foreseeable benefits/effects should be defined and, if possible, measured, as should all expected costs; present value discounting should be

performed; sensitivity analyses should be conducted to show a range of possible outcome valTable 6.—Ten General Principles of Analysis

(for CEA/CBA Methodology)

1. Define probiem

2. State objectives

3. identify alternatives

4. Analyze benefits/effects

5. Analyze costs

6. Differentiate perspective of analysis

7. Perform discounting

8. Analyze uncertainties

9. Address ethical issues

10. Interpret results

SOURCE: Office of Technology Assessment, 1980.

ues; and ethical issues (that have surfaced in

significant ways in therapeutic apheresis) should

be addressed. The rigorous specification of data

sources for quantitative analyses was another important criterion for CBAS.

Potential costs and benefits can be assessed with

varying degrees of comprehensiveness. Further,

means for estimating them vary (102,104). Thus,

in a CBA, the cost of a treatment procedure includes not only the direct costs of salaries of treatment providers and support staff, disposable, replacement fluids, drug therapies, administrative

and overhead costs, but also indirect costs such

as lost productivity due to patient’s time missed

in work. Additionally, it should be noted that uncritical use of market prices can lead to large gaps

between cost estimates and true costs. Illustrative

of this problem is the use of hospital charge data

to reflect the costs of hospital care. A common

practice, this form of “pricing” ignores the known

idiosyncrasies of hospital accounting in which

hospitals charge well above true marginal costs

for certain services and use the profits to subsidize

other services for which charges do not cover marginal costs. For example, hospital pharmacy

charges can vary from 10 to 1,000 percent of the

true cost of drugs depending on the frequency of

their use, their level of cost, purpose, etc. (104).

In the case of apheresis therapy, replacement

fluids such as albumin, saline solutions, and fresh

frozen plasma are particularly vulnerable to such

pricing practices. For example, a recent survey by

Levy (74) of Los Angeles hospitals showed almost

all paid $28 to $29 for one unit of albumin. In

turn, these hospitals charged the patient any

where from a low price of $90 to a high of $175

per unit.

In conducting a CBA or CEA one must decide

which benefits to measure and how to measure

them, if measurement is at all possible. For example, it has been argued that substantial savings

from reduced expenditures on drugs, surgery, and

hospitalization accrue from therapeutic apheresis

treatments, although this will vary depending on

the differing lengths and intensity of the disease

remission.

Unemployment and lost productivity could be

reduced in the long-term as well. Limiting analyses
Ch. 4—Cost Effectiveness and Reimbursement Policy: Issues and Evidence ● 47

to work-related measures, however, may have the

effect of underestimating the potential benefits of

apheresis therapy to a significant number of individuals not currently in the work force—e.g.,

the chronically ill, the retired elderly, students,

full-time homemakers, etc. A further point is that

the efficiency of apheresis may decline—as evidenced by frequent usage as a treatment of last

resort—with severity of impairment. In addition,

savings on such items as reduced expenditures for

quack remedies need to be calculated. It is reported that rheumatoid arthritis patients, for example, spend over $1 billion a year on purported

remedies ranging from the “night shade diet, ”

which prohibits tomatoes, eggplant, and potatoes,

to devices such as vibrators and drugs such as

DMSO (dimethyl sulfoxide). Some arthritic sufferers even sit in uranium mines in their search

for relief (34). Other benefits, such as the sense

of well-being that apheresis reportedly generates

in many patients (108), may be more difficult to

quantify.

Despite problems, when it is done well, the use

of CEA/CBA does aid the complete listing of expected costs and benefits as well as the explicit

consideration of assumptions underlying them.

Assuming such specification is possible, such analyses provide a better scientific basis to aid in making decisions. Given the current debate over the

relative costs and benefits of apheresis, and the

increasing debate over reimbursement policy, such

information does indeed appear to be essential.

Estimating Costs

While no reliable estimates of savings due to

treatment benefits are available or generally

known (12), the present task of evaluating

treatments can include the context of costs, for

which there have been several general estimates.

There has additionally been a more specific study

concerning the costs of reimbursing for apheresis

of rheumatoid arthritis patients under the Medicare program.

By almost any standard, the costs of providing

this therapy are a concern. It is the issue of costs

that has aroused the greatest controversy surrounding the technology and is the most obvious

explanation for the increasing scrutiny of apheresis by a variety of health care professionals. The

concerns over costs have focused not only on the

price of a single treatment session, but also the

dramatically rising use of apheresis for therapeutic

purposes in recent years.

Calculations

There are two dimensions (124) to expenditure

determination-price and quantity. Many technologies become expensive because of high cost

even when applied to a small number of patients

(e.g., end stage renal disease), while others

generate large expenditures because the procedure

is so extensively used even though the cost per

patient is relatively low (e.g., routine in-hospital

lab tests). Apheresis represents an interesting combination of a technology which is, on the one

hand, extremely expensive per patient, but is

simultaneously of potential benefit to great numbers of patients.

Simple cost projections for therapeutic apheresis

can be said to depend on three variables: the price

of each unit of service (cost per treatment), the

quantity of services that would be used (treatments per patient), and the size of the population

potentially benefiting from treatment (patient

populations). By multiplying these variables

together, an estimate of total expenditures can

then be determined.

Cost per Treatment

Estimates of the costs of individual apheresis

treatments are very much available, but vary

widely according to individual author and analysis from $400 to $1,200. (A midpoint estimate,

then, is $800 per treatment. ) An investment of

$19,000 to $32,000 for a blood cell separator is

the initial cost here, and disposable sets produced

by manufacturers will vary between $40 and $90

per treatment. (Membrane disposable prices may

be substantially higher—as much as $400-at

first.) Space (overhead expense), trained staff, and

a physician-director are also essential ($27 to

$300). Replacement fluids (at an average volume

of 2.8 liters), such as albumin or fresh frozen

plasma, make up the remainder of the costs, running $125 to $600 per treatment (the exception is

cytapheresis, which usually does not require re-
48 ● Health Technology Case Study 23: The Safety, Efficacy, and Cost Effectiveness of Therapeutic Apheresis

placement proteins because volume loss is small)

(2,8,12,22,34,42,108,117,75,125) .

Treatments per Patient

Most studies estimate the number of treatments

per patient as averaging about 10 per year, though

a few estimate that number to be as low ass and

as high as 15 to 20 per year. As already discussed,

apheresis protocols for various diseases will differ dramatically in number and frequency of treatments. Some applications will entail single treatments for emergencies, while it is likely that

chronic diseases such as rheumatoid arthritis will

generally require 15 to 20 treatments, although

more than 30 will be used in some cases (2,34,73,

108,42,117).

Patient Populations

The potential patient population for apheresis

can be appreciated in a number of different ways.

If the potential patient population is defined as

those persons with any of more than 75 diseases

currently treated with apheresis, the potential

population is significant. There are an estimated

5 million to 7 million people with rheumatoid arthritis, 400,000 to 500,000 persons with multiple

sclerosis, 400,000 to 500,000 persons with systemic lupus erythematosus, 100,000 myasthenia

gravis patients, and at least 50,000 to 60,000

others with one of the other diseases. However,

many patients in each disease category are presently being treated satisfactorily with drug

therapy, and thus they may not now be considered candidates for apheresis (though in some

diseases, such as multiple sclerosis and Goodpasture’s syndrome, effective alternative therapy

is very limited, so that virtually the entire patient

population could eventually become candidates

for apheresis). If apheresis is used only on patients

who have failed to respond to traditional forms

of therapy, the potential total patient population

is reduced to about 5 percent. of its original size,

and estimates place this population at from

325,000 to 427,000 (22,34,73,80,117,125). These

must be considered conservative estimates because

they limit the potential candidate population to

those patients who have reached a severely debilitating or life-threatening state in these disease

states. If apheresis therapy replaces other therapy

modes in routine maintenance programs for various disorders, the patient population would be

much higher (117).

Results

Having determined estimates for each of these

several variables, and multiplying these variables

together, total cost estimates for apheresis therapy

per year can be projected to range from $650 million to $7.69 billion, with a midpoint estimate of

$3.01 billion (see table 7). Importantly, these pmjections are simple cost calculations that carry

with them a number of methodological caveats.

Caveats

For one, there are no cost calculations of accompanying hospitalization, ancillary services or

essential adjuvant therapies, such as immunosuppressive drugs, which would increase cost estimates. Secondly, there is no determination here

of “adoption share, ” a yearly measure of market

penetration, defined as the proportion of eligible

candidates for which treatment was indicated and

on which it would have actually been performed.

Calculation of the adoption share requires fairly

accurate procedural use data, as well as projecting what the diffusion rate for the procedure is

Table 7.—Estimating Costs of Apheresis Therapy

High estimate Midpoint Low estimate

Costs per treatment . . . . . . . . . . . . . . $1,200 $400

Treatments per year . . . . . . . . . . . . . . 15 10 5

Patient population . . . . . . . . . . . . . . . 427,000 376,000 325,000

Total costs . . . . . . . . . . . . . . . . . . . . $7.69 billion $3.01 billion $650 million

SOURCE: Off Ice of Technology Assessment, 1983.
Ch. 4—Cost Effectiveness and Reimbursement Policy: Issues and Evidence ● 49

and will be. * Prediction of adoption share is one

of the most difficult tasks, but one of the most

important for predicting future costs. The adoption share subsequently allows for the discounting back of future costs over a determined patient

care time horizon, and the accumulation of a present value.

Currently, apheresis is performed on only selected patients. Unfortunately, no accurate data

exists on national figures, with estimates placing

the number of procedures performed at from

80,000 to 200,000 per year (22,34,73,80,117).

These estimates, if accurate, would mean that,

using OTA treatment estimates (see table 7), current national expenditures on apheresis range from

$3.2 million to $240 million. According to

Schweitzer and Foxman (124), however, if one

assumes availability of reimbursement for this

therapy, then one must also assume expansion of

availability of service, and utilization would increase over time to essentially the point where all

who could derive benefit from treatment would

do so. The importance of reimbursement policies

covering apheresis becomes apparent, then, if such

policies push the adoption share to 100 percent.

Given present reimbursement policies (see section

on “Third-Party Reimbursement”), this represents

an extreme estimate but is useful for cost purposes

here.

The economic and cost implications of a decision by a third-party payer to reimburse for

apheresis is a last but crucial caveat to cost

estimates. As Schweitzer and Foxman (124) further point out, if medical services were not linked

to one another, and criteria determining appropriateness or need for a service were unambiguous, the relationship between reimbursement

● The classical pattern of diffusion has been the ascending logistic

curve, which indicates that the proportion of adopters for a new

technology rises with time according to an S-shaped pattern. This

pattern is appropriate for technologies for which continued ascendancy is likely over the immediate horizon, and for which subsequent

high utilization can be expected. For many applications of apheresis,

however, the pattern is probably more complex. Warner (141) has

proposed a three-stage “desperation-reaction” model of medical diffusion, in which initial enthusiasm is followed in the second stage

by an adjustment, followed subsequently by informed decisions.

The informed decisions could represent mature, high use (as in accepted innovation) or zero use (for an unacceptable innovation).

Furthermore, disapproval of reimbursernent could occur at any point

in this process (19).

and expenditure would be a simple one. Under

these conditions, one would simply identify the

quantity and price of the service in question prior

to a change in the reimbursement policy, and

assume that these expenditures would be shifted

to the new payer. However, both the demand for

and the supply of medical care are price sensitive.

A decision to reimburse, by lowering the net price

to consumers and raising it to those who produce

medical care—physicians and hospitals—will,

therefore, have a tendency to increase the quantity of the service consumed. In addition, price

effects will arise involving not only the service in

question, but other services which are either substitutes for or complements to it. Failure to fully

appreciate these quantity and price effects contributed to the serious underestimate of the EndStage Renal Dialysis program in 1972 (113).

Cost Studies

Only one known study, prepared under contract to the National Center for Health Care

Technology (NCHCT) in 1981, has systematically

examined the costs of apheresis. The study only

estimated savings, if any, anticipated as a result

of the disapproval of coverage for a medical procedure. The study was carried out following

NCHCT’s recommendation to the Health Care Financing Administration (HCFA) not to reimburse

for therapeutic apheresis in the treatment of

rheumatoid arthritis. The cost projections, by

most sensibilities, were considered startling. The

study used a Wallace, et al. (140), estimate that

as many as 700,000 Americans might be candidates for apheresis at a first-year cost of $40,000

per patient and $18,000 per patient each year

thereafter. This implied a cost of up to $28 billion

in the first year. If 5 to 10 percent of the nearly

1 million Medicare-eligible patients with rheumatoid arthritis were to be given apheresis, it would

cost between $2 billion and $4 billion (124).

NCHCT noted that these were gross cost projections, and could be modified by projected savings from reduced expenditures for hospitalized

bed rest, medication, and joint surgery. Maintenance of, or return to, a productive lifestyle would

also have to be considered (as noted previously

in this section) if apheresis were shown to be effective (107) 0
50 ● Health Technology Case study 23: The Safetyr Efficacy, and Cost Effectiveness of Therapeutic Apheresis

The NCHCT study of potential costs, by comparison, casts OTA cost estimates as conservative,

both from the standpoint of potential patient population and cost per treatment estimates. The

NCHCT study, however, has been criticized for

usage of “inflated” estimates pertaining to potential patient population. More widely accepted

figures come from Max Hamburger, in concurrence with the American Society for Apheresis

(49), who estimates the potential RA patient population at less than 70,000, or about 10 percent

of NCHCT estimates.

THIRD-PARTY REIMBURSEMENT

Reimbursement policies by third parties, like

other aspects of therapeutic apheresis, has been

the subject of some debate because of the competing factors of cost and therapeutic promise that

this case study has variously discussed. The development of most of these policies has been recent, and there would appear to be the groundwork for an even more intensified period of

evaluation, debate, and formulation of these

policies in the near future. The following review

elaborates on these developments and issues.

Federal Policies

The Federal Government has been substantially

involved in the funding of apheresis through

research support (see ch. 3); benefit programs such

as Medicare, Medicaid, military, and Veterans’

Administration hospitals; and employee insurance

packages such as the Department of Defense’s

Civilian Health and Medical Program of the Uniformed Services (CHAMPUS) and the Federal

Employee Health Benefit Plans.

Medicare*

Although the cost of apheresis has focused attention on reimbursement, cost information has

not been explicitly or directly considered in

Regardless of which estimate is selected, the effect of reimbursement policy on potential direct

expenditure estimates is clear from both studies.

Furthermore, as alluded to earlier, the expenditure

implications of a reimbursement decision are intertwined with the technology’s diffusion, producing direct and indirect effects, some of which may

be wide-reaching. The magnitude of the direct cost

estimates alone suggests that the procedure’s safety and efficacy should be closely scrutinized because of the potential cost of possibly premature

diffusion.

Medicare coverage determinations. The legislatively mandated practice of paying usual and

customary fees does not easily accommodate such

analyses. Instead, Medicare coverage determinations have relied on safety and efficacy criteria

in an effort to “sketch the boundaries of accepted

good medical practice” (98).

Formal Federal policies for reimbursement of

apheresis under its Medicare program have developed almost completely over just the past few

years, probably reflecting the fact that HCFA procedures for making coverage decisions were highly

informal until early 1980. The staff of the Office

of Coverage Policy, often with assistance from

the Health Standards and Quality Bureau, would

review the issue, consult experts in the field with

whom they were acquainted, and come to a decision (104). Three or four regional office inquiries

concerning coverage positions on apheresis surfaced during that period, but no national instructions were issued.

Although a formal agreement between HCFA

and the Public Health Service had existed since

around 1966, a somewhat more formal, systematic, and credible assessment process involving

a panel of physicians within HCFA and from

NCHCT was established in early 1980. When

● On Apr. 20, 1983, Public Law 98-21 provided for extensive

changes in Medicare reimbursement policies for hospital-based care.

Under the statute, whose provisions will be phased in over 3 years,

hospitals will receive a flat fee per patient, set prospectively, on the

basis of patient diagnosis in one or more of 467 diagnosis-related

groups (DRGs). It is unclear at this point how the DRG-based payment system will affect the adoption and use of apheresis. What

is certain, however, is that information on the effectiveness of this

treatment will be even more important as physicians and patients

face increasingly scarce resources.
Ch. 4—Cost Effectiveness and Reimbursement Policy: Issues and Evidence ● 51

HCFA decided that a procedure involved a question of national importance, a request for a technology assessment was sent to NCHCT. Usually

such a request asked NCHCT to determine the

safety and efficacy of a particular technology and

to recommend whether HCFA should reimburse

(103,104). Because the number of questions about

coverage of apheresis increased substantially beginning in 1979-80 (56), HCFA, on the advice of

NCHCT, issued its first national instructions on

apheresis in August 1981. Effective September 15

of that year, HCFA announced the coverage of

therapeutic apheresis for the following indications

(52):

1.

2.

3.

plasma exchange for acquired myasthenia

gravis;

leukapheresis in the treatment of leukemia;

and

plasmapheresis in the treatment of primary

macroglobulinemia (Waldenstrom) and hyperglobulinemias, including multiple myeloma.

The HCFA policy statement went on to say that

apheresis should be denied for other indications,

but that information on claims for what seems to

be other nonexperimental uses should be provided

to HCFA’S central office (53).

Even before the August policy release-in May

of 1981—HCFA requested that NCHCT evaluate

the safety and clinical effectiveness of apheresis

for the treatment of (38):

1.

2.

3.

4.

5.

6.

Goodpasture’s syndrome;

systemic lupus erythematosus;

membranous and proliferative glomerulonephritides;

multiple sclerosis;

potentially life-threatening complications of

rheumatic diseases (rheumatoid arthritis, systemic lupus erythematosus, polymyositis/

dermatomyositis, and progressive systemic

sclerosis); and

thrombotic thrombocytopenic purpura

(TTP).

NCHCT issued formal assessments on the indications of multiple sclerosis, rheumatoid arthritis,

rheumatoid vasculitis, and TTP. Two other indications— Goodpasture’s syndrome and membranous proliferative glomerulonephritides-were

evaluated in early 1983 by the Center’s organizational successor, the Office of Health Technology

Assessment (OHTA) (28). (NCHCT and OHTA

assessments are discussed in ch. 3.) HCFA has yet

to implement instructions on any of these six categories for national coverage policies.

Although Medicare’s national coverage is relatively new, it is not unlikely that many hospital

apheresis treatments for Medicare patients with

covered and noncovered disease indications have

been performed and reimbursed without official

sanction of HCFA. Because Professional Standards Review Organizations do only a limited job

of surveillance, because descriptions in the line

item billings are very general, and because new

procedures often do not have a procedure code

number, the identity of Medicare reimbursements

for apheresis therapies may have been concealed

(104,117).

Medicare provides coverage for apheresis regardless of whether or not it is performed at a

hospital (108). It has been reported, however, that

independent, freestanding settings are less likely

to receive reimbursement at this time, fueling

speculation that HCFA hopes to control the use

of apheresis by limiting reimbursement to hospital-based therapy (73). There is no known intention by HCFA to implement such a regulation

at this time or in the near future.

Medicaid

Medicaid provides medical assistance to lowincome individuals. Treatment costs are shared

by the States and the Federal Government, Each

participating State must provide certain basic

health services, but the States have a great deal

of leeway concerning specific coverage (102).

Medi-Cal (California Medicaid), for example, will

approve payment only for apheresis conducted

in the treatment of certain diseases, including

myasthenia gravis, lupus, and Goodpasture’s syndrome. Treatment of such disorders as rheumatoid arthritis and multiple sclerosis, on the other

hand, are at present considered investigational

and are thus not covered (108). As of August

1982, Medi-Cal was in the midst of a review of

all its apheresis coverage policies, and was ex-
52 ● Health Technology Case Study 23: The Safety, Efficacy, and Cost Effectiveness of Therapeutic Apheresis

pected to formulate a new policy statement concerning its coverage policies (58).

Veterans’ Administration (VA) and Department

of Defense (DOD)

The extent of VA and DOD involvement in the

use of apheresis is reflected in a hospital and blood

bank survey by Scoville Associates (108). That

survey revealed that 30 VA and military hospitals

performed therapeutic apheresis, on 260 patients,

and a total number of 1,350 procedures. No

breakdown of usage by disease, or whether use

was for clinical or research purposes, is available.

Under DOD’s CHAMPUS program, the use of

apheresis in the treatment of any condition prior

to August 1981 was considered investigational and

not a CHAMPUS benefit. Since then, however,

the CHAMPUS program has taken the basic Medicare policy and expanded it somewhat.

CHAMPUS now extends coverage to use of the

procedure as a “last resort treatment of certain

medical conditions. ” The specified indications are

(8):

1. myasthenia gravis during a life-threatening

crisis;

2. anti-basement membrane antibody nephritis

(i.e., as a result of Goodpasture’s syndrome);

3. life-threatening immune complex vasculitis;

4. hyperviscosity of the blood associated with

multiple myeloma, Waldenstrom’s macroglobulinemia, and hypergammaglobulinemia

purpura; and

5. TTP.

Private Sector Policies

Like their Federal counterparts, private insurers

historically reimbursed on a routine basis for both

apheresis procedures and replacement fluids, but

have recently begun to examine apheresis procedures more closely and issue explicit policy

statements concerning coverage. In March of

1981, Blue Shield of California approved payment

for therapeutic plasma exchange and lymphapheresis in the treatment of severe cases of

rheumatoid arthritis if there are acute lifethreatening complications or if conventional drug

therapy has failed (80,117).

At present coverage under Blue Cross insurance

programs varies greatly from State to State. For

example, the Southern California, Texas, and

South Carolina Blue Cross organizations generally

follow the Medicare guidelines and will normally approve payment for apheresis. Illinois Blue

Cross indicated that their reimbursement schedule

depends on the disease being treated and what

other therapies have been tried, but that in

general, they will approve most requests. Massachusetts Blue Cross covers apheresis for 14 different disease indications. The Greater New York

Blue Cross, on the other hand, does not cover

apheresis therapy under any of their plans (61,

79,108).

The National Blue Cross/Blue Shield Association issued a policy statement in May 1982 as a

guideline to local Blue Cross/Blue Shield plans.

That policy recommends coverage—in hospital

settings only-of nine disease categories including

severe myasthenia gravis and leukemia (34). The

National Blue Cross-Blue Shield Association policy does not necessarily mandate acceptance and

implementation by individual plans, however,

and is subject to a possible future review at an

appropriate time (16).

Many private insurance companies, too, including Pacific Mutual and Prudential, provide coverage for apheresis regardless of whether or not

it is performed at a hospital. As with Federal

policies, uniform private third-party coverage is

pivotal to the future development of the procedure, particularly in freestanding and commercial settings. The growth of commercial centers

has been slowed in some States by the fact that

some insurance organizations do not provide benefit payments for apheresis procedures performed

outside the hospital. FDA has yet to establish

licensing procedures for apheresis centers, and

many private insurers have indicated a reluctance

to provide reimbursement for therapy under uncontrolled conditions, which could lead to possible treatment overuse and abuse. There appears

to be less overall concern, though, in the case of

private payers, about future restrictions on reimbursement for apheresis treatment (108).
Ch. 4–Cost Effectiveness and Reimbursement Policy: Issues and Evidence ● 53

CONCLUSIONS

Acknowledgment of apheresis as a safe and effective treatment application, as an acute therapy

in a small group of relatively uncommon diseases,

is reflected in present Medicare reimbursement

policy. Suggestive evidence of the safety and efficacy of apheresis in a host of other disorders has

also forced a flurry of reimbursement policy reviews and formulations among both government

and private party insurers.

Reimbursement policies to the present have revealed an increasingly cautious and explicit approach to coverage of apheresis for almost all

disease indications, and understandably so.

Apheresis is still not a proven cure for any disorder. It may need to be done repeatedly for certain disease conditions, at a cost of up to $1,200

or more each time. Total cost estimates potentially

run into the billions of dollars. Nevertheless, by

treating certain disease complications, apheresis

has reportedly lessened suffering and helped prolong lives. Reliable estimates of these benefits have

yet to be determined and quantified. As a result,

cost-benefit ratios and CEAS have not yet been

conducted.

It should be reemphasized that the formation

of cost-benefit ratios and CEAS should not be considered only economic tools. This point is not

negated by the fact that CEA/CBA is described

as an efficiency-based technique. Measurement of

the efficiency of therapeutic apheresis will depend

as much on output as on resources used to produce the output. One of the critical output or outcome measures that can be addressed by CEA/

CBA is the effect of apheresis on health status or

other health outcome related effects. Any CEA/

CBA that attempts to analyze such outcomes for

an evaluation of therapeutic apheresis will only

be as comprehensive and valid as the data on the

efficacy and safety of apheresis. Thus, health outcome related CEA/CBAs for apheresis are dependent on the existence of an adequate efficacy

and safety information base. The status of such

information for many disease indications for

which therapeutic apheresis has been used, however, is inadequate. As a result, it may be exceedingly difficult to demonstrate therapeutic

apheresis a cost-effective technology for which

third-party payment is justified.

Medical insurers are presently far from a consensus on which disease indications should be

covered, probably stemming from a less than consistent scrutiny of the evidence on safety and efficacy. A widening of Medicare and private insurer coverage of therapeutic apheresis for specific

life-threatening complications (e.g., rheumatoid

vasculitis) is probable in the near future. But direct

cost estimates and the potential cost of possibly

premature diffusion alone make it unlikely and

unwise that third-party payers will support any

broad extension of benefits for apheresis treatment

until more valid data is generated. Until evidence

is available, therapeutic apheresis will largely be

viewed as an experimental technique, not to be

considered as a part of routine care. In light of

such a situation, present research and clinical trials

being carried out assume even greater importance.

It will be several years, though, before all the

results are in.

Lastly, a significant (but still speculative) factor amidst the cost and reimbursement policy debate is the potential cost reductions of new apheresis equipment and treatment modalities. The

present trend towards plasma perfusion (more

selective removaI of undesirable plasma fractions)

offers the possibility of eliminating the need for

replacement fluids which could reduce the present

cost per treatment by 20 to 50 percent. Staffing

charges are presently based on a large proportion

of acute treatments which are usually performed

on an in-patient basis, often at the patient’s bedside. Some observers predict the future growth

in apheresis to involve increases in maintenance

therapies which could be performed on an outpatient basis, with reduced involvement of hospital staff (74,108).

On the other hand, there seems to be a trend

toward in-hospital use in areas such as Washington, D.C. In that region, after the Red Cross

started doing therapeutic apheresis in March 1978,

only one of the first 16 months’ 106 procedures

was done in a hospital. But from July 1980 to

98-822 0 - 83 - 5 : QL 3
54 ● Health Technology Case Study 23: The Safety, Efficacy, and Cost Effectiveness of Therapeutic Apheresis

April 1981, nearly five out of six were. Future tivities for freestanding, independent commercial

decisions regarding treatment settings will no clinics, reimbursement policies, and whether

doubt depend on a number of factors such as hos- apheresis is administered largely for reasons of

pital charges, regulation and standard setting ac- acute or maintenance therapy in specific disorders.
5 .

Implications for Policy
5.

Implications for Policy

In summary, the confluence of technological

advances in apheresis equipment and recent scientific research linking many chronic disease conditions to immunological dysfunction has served

to expand dramatically the number of apheresis

procedures in the pasts to 10 years. Therapeutic

apheresis has exhibited many of the classic features that have come to characterize the hopes,

concerns, and fears about medical technologies

over the last three decades.

Utilization and diffusion of therapeutic apheresis seems to have closely followed Warner’s (141)

“desperation-reaction” model. Initial rapid diffusion has occurred in the absence of safety and efficacy evidence. The rapid diffusion is due in part

to a lack of a suitable alternative technology, in

part to claims—some of them dramatic—of the

technology’s beneficial effects, and in part to

desperation on the part of patients and of providers responsible for treatment. In chronic and

life-threatening situations, apheresis has found its

broadest and most frequent application.

Most recently, however, the lack of well-validated clinical evidence has influenced provider

behavior. Ambiguous results have given rise to

physician caution, while lack of evidence and high

costs have provoked increased regulation by medical insurers, possibly slowing diffusion. Best

estimates are that utilization and diffusion have

plateaued, at least for the present. The future of

therapeutic apheresis seems predictable in that increases or declines in use will be predicated on

newly available evidence (35,95).

Several recurring issues in need of further study

and resolution have run through the examination

of therapeutic apheresis. One issue, given the current state of this technology and many unanswered questions about patient criteria for use,

is what constitutes the appropriate timing of intervention in the course of a disease and whether

the procedure to be followed in performing therapeutic apheresis is adequately standardized. Such

questions are basic in the development of the technology, and research to address them is necessary,

as it forms a foundation for the conduct of wellcontrolled testing and clinical trials. The Apheresis

Panel of the American Medical Association’s

Council of Medical and Scientific Affairs has

recently discussed the idea of a national apheresis

registry that would track use and form a knowledge base for development of well-controlled studies (32). On a smaller scale, the American Red

Cross has requested its regional blood services to

register all apheresis patients at the onset of treatment and report treatment methods and results

upon completion (1.21).

A second issue, which arises where conditions

of use have been sufficiently standardized, is the

lack of well-designed research studies and the need

for such undertakings. There have been at least

two obstacles preventing the accumulation of

valid evidence of safety and efficacy: the ethics

of providing sham apheresis or conventional therapy for control group patients, and the high costs

of such trials. Long hours of sham apheresis procedures, while possibly inflicting on control group

patients some of the same side effects of apheresis

as treatment group patients, has led to questions

of the ethical implications of such trials. Furthermore, in life-threatening or severely debilitating

situations, doctors feel they cannot ethically deny

apheresis therapy to control group patients.

The obstacle of costs of well-designed studies

has been partially offset by a recent infusion of

Government and foundation funding. Should

costs continue to be a problem, one alternative

might be to have third-party payers, including

Medicare, selectively reimburse for therapeutic

apheresis in return for clinical data. If implemented properly, this alternative could substantially increase the quality of information

available for public and private reimbursement

coverage decisions. Evidence of the technology’s

cost effectiveness could result in yielding substantial budgetary savings. Even if the results of such

trials were disappointing, they could lead the way

to unexpected advances in research (47).

57
58 ● Health Technology Case Study 23: The Safety, Efficacy, and Cost Effectiveness of Therapeutic Apheresis

Because of the promise of apheresis for certain

disease complications, this technology would appear to be a particularly choice candidate for such

a policy course. In such conditions as Goodpasture’s syndrome, for example, effective alternative therapies are very limited and the disease

is frequently fatal. Because apheresis has been

claimed effective, selective reimbursement could

be of great utility from both research and clinical

standpoints.

There would be problems in implementing this

alternative (see e.g., 104), primarily concerning

the legal and ethical implications of selectively

reimbursing for health care. It seems clear, however, that third-party payers could use this approach to encourage less costly and more effective forms of treatment. In the case of Medicare,

too, elements of the Public Health Service could

be involved in developing research protocols and

in interpreting research evidence from the resulting experiments.

A recent precedent exists for third-party payer

participation in clinical trial funding for apheresis.

Five Midwestern State or local Blue Goss/Blue

Shield groups and other third-party payers have

agreed to reimburse five centers involved in a randomized clinical trial of apheresis for multiple

sclerosis. Both the investigational procedure and

a sham procedure are covered. Medicare and the

State Medicaid groups, on the other hand, are not

participating, but administrative and other research costs of the trial are being funded through

a National Institutes of Health grant (97).

The Arthritis Foundation and the National Multiple Sclerosis Society are also sponsoring a

meeting (to be held in July 1983) at which they

hope to develop proposals for third-party payer

participation in funding other clinical trials.

Representatives of both private and public insurers will be participating (97).

A third issue is the possibly transitional nature

of this technology. Some major new hardware developments are now undergoing clinical tests.

These use adsorption columns and membranes

that work like molecular sieves. When a specific

fraction whose removal is desired can be identifed,

an adsorption column containing an antibody to

that fraction can remove it from the plasma as

it passes through. Another method, resembling

hemodialysis, passes the blood across a membrane

with a specific antibody attached to it. A third

technique uses a membrane filter to remove fractions of a specific molecular weight (80).

These advances in equipment may, in the

course of the next decade, be reinforced or even

overshadowed by advances in basic biomedical

research or in emerging parallel developments

such as biotechnology. The National Cancer Institute, and the National Heart, Lung, and Blood

Institute, for example, are currently supporting

strategies for the separation of complex blood proteins. Advanced separation technologies could

make it possible to index most human proteins.

Once proteins are displayed and distinguished

from one another, investigators might then tease

out individual functions and relate them to the

DNA code. Other activities could include the

detection of abnormal protein patterns in disease

states (e.g., leukemia), and the corresponding production of preventive or neutralizing elements

(e.g., monoclinal antibodies) to these noxious or

damaging processes (53,60).

In the final analysis, such a state of scientific

and technological flux has important policy implications. Therapeutic apheresis, as a medical intervention, falls into a category of medical technologies classically referred to as half-way

technologies (133). These are generally treatments

directed at correcting the effects of a disease or

palliating them. It has been pointed out and illustrated repeatedly in the literature and research

community that such measures are less satisfactory and more costly than so-called definitive

technologies, which effectively prevent or control

a disease or condition (e.g., poliomyelitis vaccine).

As Robbins (116) and numerous others have asserted, “where alternatives exist, resources should

be directed so as to encourage the development

of definitive technologies as opposed to half-way

measures.” To the extent that such alternatives

can be identified, considerable attention should

be given to the possibility of devoting resources

to their development. Indeed, one of the critical,

ongoing policy issues in medicine is how to establish the most rational and productive balance

between development and support of half-way

technologies and that of basic research toward

definitive technologies.
Appendixes
Appendix A.— Health Program Advisory Committee

and Acknowledgments

HEALTH PROGRAM ADVISORY COMMITTEE

Sidney S. Lee, Chair

Michael Reese Hospital and Medical Center

Stuart H. Altman*

Florence Heller School

Brandeis University

Carroll L. Estes

Department of Social and Behavioral Sciences

School of Nursing

University of California, San Francisco

Rashi Fein

Department of Social Medicine and Health Policy

Harvard Medical School

Melvin A. Glasser

Health Security Action CouncilCommittee for National Health Insurance

Patricia King

Georgetown Law

Joyce C. Lashof

Center

School of Public Health

University of California, Berkeley

Margaret Mahoney

The Commonwealth Fund

Frederick Mosteller

Department of Health Policy and Management

School of Public Health

Harvard University

Mitchell Rabkin*

Beth Israel Hospital

Boston, Mass.

Dorothy P. Rice

Department of Social and Behavioral Sciences

School of Nursing

University of California, San Francisco

Richard K. Riegelman

George Washington University

School of Medicine

Walter L. Robb

Medical Systems Operations

General Electric

Milwaukee, Wis.

Frederick C. Robbins

Institute of Medicine

Rosemary Stevens

Department of History and Sociology Science

University of Pennsylvania

● Until April 1983.

61
62 ● Health Technology Case Study 23: The Safety, Efficacy, and Cost Effectiveness of Therapeutic Apheresis

ACKNOWLEDGMENTS

The development of this case study was greatly aided by the advice and review of a number of people in

addition to the Advisory Panel for the assessment of Medical Technology and Costs of the Medicare care Program

and the Health Program Advisory Panel. The case study director and OTA staff would like to express their appreciation especially to the following individuals:

Cheryl Anderson, Advocacy International, Ltd.

Jack M. Anthony, Travenol Laboratories, Inc.

Thomas Asher, Immunogenetics, Inc.

Robert Berenson, Washington, D.C.

Eugene Berkman, Tufts New England

Medical Center

Gary F. Brown, Seattle, Wash.

Meredith F. Buco, Blue Cross/Blue Shield

Association

Maria Charest, Arthur D. Little, Inc.,

Cambridge, Mass.

Arthur A. Ciarkowski, Food and

Drug Administration

Vincent Ciuryla, E. I. du Pent de Nemours & Co.,

Inc.

P. P. Clymer, Office of Technology Assessment

Robert M. Collins, Cobe Laboratories, Inc.

Dennis Cotter, Office of Health Technology

Assessment

W. Palmer Dearing, Blue Cross/Blue Shield

Association

Vincent T. DeVita, Jr., National Cancer Institute

Allen J. Douma, American Medical Association

Frances Edmondson, Travenol Laboratories, Inc.

Lenny Friedman, American Red Cross

W. Bradford Gary, Travenol Laboratories, Inc.

Murray Goldstein, National Institute of

Neurological and Communicative Disorders

and Stroke

Max I. Hamburger, State University of New York

at Stony Brook

Steven Heyse, National Institute of Arthritis,

Diabetes, and Digestive and Kidney Disease

Terry Hollis, Blue Cross/Blue Shield of

Massachusetts

Douglas W. Huestis, University of Arizona

John Verrier Jones, Dalhousie University,

Nova Scotia, Canada

Richard Landfield, Goodell, Landfield, Becker,

Green & Martingale, Washington, D.C.

Claude Lenfant, National Heart, Lung, and

Blood Institute

Joshua Levy, Immunogenetics, Inc.

L. M. Magner, E. I. du Pent de Nemours & Co.,

Inc.

Guy M. McKhann, Johns Hopkins Hospital

Donald Myers, RMR Health and Hospital

Consultants, Inc.

Terri Louise Nally, American Chemical Society

Nan Newell, Office of Technology Assessment

Robert K. Oldham, National Cancer Institute

Robert W. Reilly, American Blood Resources

Association

J. Gerald Sandier, American Red Cross

Phillips L. Scoville, Scoville Associates,

Greenville, S. C.

Ira D. Singer, Project Hope

Glenda Sweeney, American Red Cross

Garry Vibert, Parker-Hannifin Corp.

Donald Young, Health Care Financing

Administration
Appendix B.—Apheresis for Hemolytic-Uremic Syndrome

Prepared for OTA by: Paul M. Wortman, Ph. D.

Hillary Murt, M.H.S.A.

In collaboration with: Bruce Friedman, M.D.

The most prominent feature of hemolytic-uremic

syndrome (HUS) is renal microangiopathy, which is

characterized by endothelial damage in glomerular

capillaries and renal arterioles. The event which initiates this endothelial damage is unknown although

some authors have suggested that endotoxin is a prime

candidate (71). The damaged endothelial cells become

swollen, leading to renal ischemia and decay of kidney

function and two secondary hematologic events—red

cell destruction (hemolytic anemia) and a dramatically reduced level of circulating platelets (thrombocytopenia). The former results from mechanical damage to red cells passing through the damaged vessels.

The reduced platelet count results not only from

trauma but also localized intravascular coagulation

(and platelet consumption) occurring in the damaged

vessels.

An alternative and more recent hypothesis cites

decreased formation of PGI2

, (prostacyclin) as the

precipitating event leading to the full-blown clinical

manifestation of the syndrome (instead of a toxic agent

such as endotoxin). The finding of PG12 deficiency in

adults and children with HUS supports this concept

(11). In this case, the loss of PGI2, causes localized

platelet aggregation in renal vessels and vascular

obstruction. Traumatic red cell destruction (hemolytic

anemia) is a corollary of the development of the

microthrombi which partly occlude the vascular

lumens (84).

Finally, Seger, et al. (126), have suggested that HUS

is a polyetiologic syndrome with neuraminidase being the culprit agent in some cases, particularly among

children suspected of having pneumococcal infections,

as this agent can produce lesions in all three cell

systems (red blood cells, platelets, and endothelial

cells).

The hemolytic-uremic syndrome shares a number

of features, including vascular endothelial damage,

with thrombotic thrombocytopenic purpura (TTP). In

fact, HUS has been considered by some clinicians to

be a variant of TTP, this being supported by similar

overlapping clinical and pathologic characteristics and

the possibility of similar precipitating events. There

is no objective method at present to distinguish HUS

from TTP, although in the case of the former, the kidney is typically the main and often only target organ,

children are primarily affected, and the prognosis is

generally much better (71). These authors believe,

however, that a clinical diagnosis of one or the other

conditions must be made because the treatment differs and in HUS, depends on the management of the

complications associated with renal failure.

Plasma exchange (PE) was first administered as a

therapy for TTP in 1959 by Rubenstein and others

(84). Rapid and sustained recovery was observed after

two exchange transfusions with fresh whole blood to

an n-year-old patient.

Taft and Baldwin (132) noted that centers which

have experience with five or more patients diagnosed

with TTP and treated with PE are reporting survival

rates in the 60- to 80-percent range. Plasma exchange

is now being advocated as a potential therapy for

treating HUS because of the suspected etiological

similarity between the syndrome and TTP. Apheresis

is viewed as being potentially helpful in removing a

toxic agent (e.g., endotoxin, neuraminidase) or replacing a missing factor, possibly a physiological inhibitor

of platelet aggregation. In the latter case, Beattie, et

al. (11), and Misiani, et al. (84), have both suggested

that PE using normal plasma replaces a missing factor needed for stimulating PGI2 production by vascular

endothelium.

Specification of Treatment

Only eight reports (including two letters to the editor

and one abstract) have been published in the English

medical literature on the effectiveness of plasma exchange in the management of HUS. These eight communications account for 11 patients diagnosed with

HUS ranging in ages from 11⁄2 to 59 years who were

treated as an ancillary therapy with corticosteroids,

antiplatelet drugs, or heparin. * Moreover, in seven

● Beattie, et al. (11), report on a 3%-year-old boy diagnosed with HUS.

The patient was initially treated with aspinn and dipyrimadale (S mg/kg/day)

and his condition gradually improved. Plasma exchange was not initiated

until 10 days later when the patient was readmitted to the hospital with recurrent symptoms of HUS. The authors do not indicate whether any drug therapy

was administered during the second episode, so it is assumed that PE was

the only therapy administered. The article by Taft and Baldwin (132) focuses

primarily on the treatment of patients diagnosed with TTP. They only briefly mentioned two patients with HUS who were treated with apheresis and

do not provide full case histories.

63
64 ● Health Technology Case Study 23: The Safety, Efficacy, and Cost Effectiveness of Therapeutic Apheresis

cases hemodialysis or peritoneal dialysis was performed concurrently with plasma exchange.

It appears that apheresis is not the sole treatment

regimen of HUS and thus the particular impact on patient health may be hard to determine. Apheresis is

commonly embedded within a more comprehensive

treatment regimen including a variety of drugs, some

form of dialysis, and blood or platelet transfusions.

Several authors (84,132) have mentioned the difficulty

in evaluating the efficacy of each treatment approach

alone since different forms of therapy have typically

been employed in combination. Misiani, et al. (84),

for example, are concerned with separating the beneficial effects of PE from antihypertensive drugs in

treating HUS, whereas Taft and Baldwin (132) emphasize the need to evaluate the relative contributions

of ancillary therapies such as corticosteroids and antiplatelet drugs to the successful recovery of PE-treated

patients.

Despite the fact that a sizable proportion of HUS

patients are treated with some form of dialysis, none

of the authors point out the possible confounding effects of hemodialysis and peritoneal dialysis performed

concurrently with plasma exchange. It should be noted

that dialysis may provide beneficial effects independent of apheresis. In the case of hemodialysis, all patients are heparinized during dialysis. Heparin, an anticoagulant drug, exerts an antithrombotic effect.

Recall that thrombotic occlusions of capillaries and

arterioles have been implicated in the pathogenesis of

HUS. Thus, hemodialysis (which necessarily includes

the administration of heparin) may be partly responsible for inhibiting the formation of microthrombi in

the glomerular capillaries and thereby increasing renal

blood flow.

Heparin was also administered to one HUS patient

in the absence of hemodialysis, which suggests that

clinicians recognize the potential efficacy of using

heparin therapy alone for treating HUS. Parnes, et al.

(106), report on two small series of HUS patients

treated with only heparin; mortality rates of 9 and 50

percent were recorded. In each series, about 30 percent of the patients completely recovered; the remaining underwent chronic dialysis.

In the case of either hemodialysis or peritoneal dialysis, it may also be postulated that the removal of unspecified substances of low molecular weight may

ameliorate the symptoms of HUS, if the substances

that are removed are responsible for the development

of the vascular lesions.

It is important to draw a distinction between plasma

exchange and plasma infusion. In the former case,

plasma is removed and replaced by a colloid solution,

commonly albumin, fresh frozen plasma, or simple

donor plasma. Although the plasma replacement in

early cases was initiated only for purposes of expansion of the intravascular volume, later authors suggested that the administration of fresh frozen plasma

had an independent therapeutic effect. This led some

investigators to administer it alone with apheresis; this

is described in the literature as plasma infusion. The

beneficial effects of PE may be confounded when plasma infusion is also administered as part of the treatment regimen. Obviously, both methods have the advantage of replacing the missing plasma factor, if, in

fact, that is the underlying cause of HUS. However,

PE may provide the additional advantage of removing other possible etiological agents, the products of

damaged red blood cells, and other hypothetical platelet aggregating substances. In short, when these two

forms of therapies are both administered during a

relatively short period of time as in the case of two

HUS patients described in the literature (84) it becomes

difficult, if not impossible, to attribute any measure

of success to one therapy or the other.

It is conceivable that some form of adjuvant drug

therapy or dialysis is required in conjunction with

apheresis to successfully treat patients with HUS. That

is to say, clinicians may view PE as a necessary but

not sufficient form of treatment to restore normal

physiological functions. When other forms of therapy

are used in addition to PE, particularly drug therapy,

there still is the problem of operationalizing the treatment when the concomitant therapies vary widely

across cases (e.g., the use of heparin with or without

platelet inhibitors). When there is differential improvement by type of drug used, the integrity of the treatment is called into question. It may be the case that

the synergistic effects of apheresis and drug therapy

may vary according to the dosage and regimen of the

particular drug used.

Plasma exchange therapy itself varies widely with

respect to the number of exchanges performed and the

volume of plasma removed at each exchange process.

Table B-1 shows that the number of PEs performed

for each episode of HUS ranges from one to eight exchanges for the 11 patients diagnosed with HUS. In

two of the studies, the frequency of plasma exchange

appears to be dictated by the platelet response (spontaneous increment v. lack of increment), and the level

of serum LDH activity or creatinine levels. In one

study, however, the frequency of plasma exchange in

another study depended on the resolution of neurologic symptoms (sO). As best as can be determined

from table B-1, the volume of plasma removed at each

exchange is variable. However, the discrepancy in the

volume of plasma removed at each exchange across

patients may be due to the fact that 7 of the 11 pa-
App. B—Apheresis for Hemolytic-Uremic Syndrome ● 65

Table B-1 .—Apheresis Experience Among Patients Diagnosed With Hemolytic-Uremic Syndrome

Range of plasma Range of

Study exchanges plasma volume

reference Number of Age range performed removed per Types of replacement

number patients of patients per episode exchange fluids used

1 31⁄2 yrs. 2 1,000 ml Fresh frozen plasma

1::::::::::::: 2 7 yrs. 3 Unknown Whole blood

5 . . . . . . . . . . . . . 2 54-56 yrs. 1 3,000 ml Fresh frozen plasma

6 . . . . . . . . . . . . . 1 21 yrs. 5 3,000 ml Fresh frozen plasma and

normal saline

7 . . . . . . . . . . . . . 2 19-22 mo. 1,500 ml-2,350 ml Whole blood

8 . . . . . . . . . . . . . 1 8 yrs. 8 1,500 ml Albumin, fresh frozen plasma

9 . . . . . . . . . . . . . 2 2-7 yrs. 1-6 27 ml/kg-89 ml/kg Whole blood, fresh

frozen plasma

10 . . . . . . . . . . . . . 1 37 yrs. 4 Unknown Unknown

SOURCE: Office of Technology Assessment, 1983.

tients undergoing PE were children, who have smaller

blood volumes. Table B-1 also shows that whole blood

and fresh frozen plasma are the two most common replacement fluids used in the process of plasma exchange for patients with HUS. Human serum albumin

was used as a replacement fluid in only one case and

the authors noted that there was no improvement after

three exchanges, suggesting that no circulating agent

perpetuated the condition. Plasma exchange was then

performed with fresh frozen plasma, which was followed by a prompt recovery in the platelet count (131).

The absence of explicit and detailed protocols for

performing plasma exchange poses a major problem

in the evaluation of the effectiveness of apheresis

therapy. However, given the rare occurrence of HUS

in the population, it comes as no surprise that not

enough information has been accumulated on the use

of plasma exchange to develop such protocols.

Misiani, et al. (84), suggest that at the present time

it is impossible to define individual PE requirements

since both the patient’s and donor’s plasma may differ with respect to the plasma factor (e.g., PGI2

) concentrations. Those authors recommend apheresing a

full volume at the initial exchange, followed by onehalf the initial amount daily until full hematologic

remission is obtained. The literature on TTP, on the

other hand, is considerably more extensive and consequently, a set of treatment guidelines or protocols

has recently been proposed by Taft and Baldwin (132).

They have developed a clinical scoring system (including necrologic evaluation) to evaluate the day-today severity of the disease, which maybe used to determine the frequency of PE. Relying on five clinical

criteria (i.e., platelet count, serum LDH, total

bilirubin, creatinine, and necrologic status) a score is

calculated to determine whether therapy should be

continued. Since several investigators have suggested

that HUS is a variant of TTP, it is conceivable that

such a scoring system modified slightly to take account

of the clinical manifestations specific to HUS could be

used to determine the appropriate frequency and volume of PE.

Outcome Measures

A recurring critical issue in any attempt to analyze

the effectiveness of a medical innovation is the selecting of appropriate endpoints for evaluating the success or failure of the innovation. In many instances,

outcome measures are either lacking, not specified, or

ill-defined in the written reports. For example, one

study of HUS reports that the patient “showed improvement” after the PE was initiated, without defining precisely what improvement means (135).

It appears that on, the whole, nonspecification of

outcome measures is less of a problem when evaluating

the effectiveness of plasma exchange for patients with

HUS. While it is noteworthy that none of the eight

studies provide a discussion that specifically focuses

on the kinds of outcome measures that should be used

to evaluate apheresis for HUS, there does appear to

be some consensus in the literature on the array of

clinical indicators that are reported pre- and post-PE.

Table B-2 shows, for example, that all eight studies

reported whether or not their patients underwent

chronic dialysis and their mortality experience. However, the length of followup during which mortality

data were collected varies across studies, which may

limit the usefulness of directly comparing mortality

rates, Furthermore, seven of the eight studies reported

creatinine or BUN levels (i.e., indicators of renal insufficiency) and six studies indicated platelet counts.

All six indicators displayed in table B-2 should be considered to be objective outcome measures. That is to

say, none of these measures is likely to be influenced
66 ● Health Technology Case Study 23: The Safety, Efficacy, and Cost Effectiveness of Therapeutic Apheresis

Table B-2.—Variability in Effectiveness of Plasma Exchange Therapy for Hemolytic-Uremic Syndrome as Expressed

in Selected Outcome Measures (all outcome measures relate to past plasma exchange period)

Outcome measures

Patients with Patients for

Patients with Patients with Patients with eventual decline whom chronic

Study increment in eventual remission of in serum creatinine dialysis was

reference Number of platelet decline neurologic or BUN (renal initiated

number patients count in serum LDH signs improvement) or continued Mortality

1/1

NA

2/2

1/1

NA

1/1

212

1/1

NA

NA

2/2

NA

NA

NA

2/2

NA

NA

1/1

NA

NA

NA

NA

NA

NA

0/1

1/1

1/2

1/1

0/2

1/1

212

1/1

1/1

0/1

1/2

0/1

2/2

0/1

0/2

0/1

0/1

0/1

1/2

0/1

2/2

0/1

0/2

0/0

NA-Not available.

SOURCE: Office of Technology Assessment, 1983.

by expectations of the physician or patient concerning the efficacy of treating HUS with apheresis.

These measures clearly represent endpoints that are

evaluated at different times during a given episode of

HUS. It may, in fact, be convenient to make a distinction between the more general measures of health

status relating to HUS (e.g., chronic dialysis, mortality), which represent the sum total of many influences

and the more sensitive and specific hematologic, biochemical, and clinical signs and symptoms (e.g., platelet count, creatinine, BUN, serum LDH levels, and

neurological status) that often occur rapidly following plasma exchange. The former may be called ‘longterm” outcomes, whereas the latter may be termed “immediate” outcomes.

When an outcome measure such as mortality is used

to evaluate the effectiveness of apheresis therapy for

HUS, the benefits of apheresis may be substantially

understated. Plasma exchange may, for instance, bring

about a temporary improvement in the patient’s clinical status, but other intervening factors may ultimately cause the patient’s death. Most clinicians, however,

would probably agree that the ultimate objective of

apheresis therapy is to increase the likelihood of survival, which suggests that survival (or mortality) is an

important outcome measure of the efficacy of apheresis

and should not be disregarded.

The need for chronic dialysis, on the other hand,

may be a more appropriate outcome measure for determining the ultimate success of plasma exchange in the

treatment of HUS, since renal failure is a major element of the syndrome. Chronic dialysis was deemed

necessary for 4 of the 11 patients listed in table B-2

(two of whom later died) which represents a 36-percent

failure rate when dialysis is used as the sole measure

of the effectiveness of PE therapy.

Finally, changes in hematologic and biochemical parameters such as platelet count, serum LDH, creatinine, and BUN levels may also be used to evaluate

the effectiveness of apheresis therapy. The difficulty

with using these measures, however, is that patients

may show improvement in one or all of those parameters yet still require long-term dialysis (e.g., patients

in studies 1 and 5). In short, the “immediate” outcome

measures may be necessary but insufficient indicators

of the efficacy of plasma exchange. Perhaps these

measures and the end points of chronic dialysis and

mortality could be combined in some way as co-measures. The problem of combining multiple evaluation

criteria and assessing the significance of the results is

a difficult one. For example, researchers may choose

to assign different weights to each outcome measure

which would lead to disagreement and perhaps a lack

of consensus on the effectiveness of PE in treating

HUS.

Patient Selection

In seven of the eight studies, PE therapy was initiated when patients diagnosed with HUS did not respond to either hemodialysis or peritoneal dialysis or

other conventional therapies including corticosteroids,

antiplatelet drugs, or heparin. In other words, apheresis was performed on these patients as a last resort

therapy when there were no other effective alternative

therapies and death was the likely outcome. Since only

the “worst cases” of HUS appear to be selected for

apheresis therapy, it is possible that the effectiveness

of plasma therapy is underestimated, depending on

which outcome measure is used. If PE is initiated in

the later stages of the disease (i.e., when end-stage

renal disease is inevitable), the beneficial effects of
App. B—Apheresis for Hemolytic-Uremic Syndrome ● 67

apheresis maybe dramatically reduced if chronic dialysis is the end point used for evaluating the effectiveness of the treatment.

Evaluation of the Evidence

The eight communications that have appeared in the

literature during the past 3 years describing the effectiveness of apheresis in treating patients with HUS

present data on a total of 11 patients, but each case

is described individually. Only one of the communications suggests that PE has limited effectiveness on the

disease process (11). However, the authors in this article add that the clinical benefit may have been compromised because PE was performed during a recurrent phase of the illness which is recognized as being

associated with poor prognosis. The remaining seven

studies are almost uniformly favorable in suggesting

that apheresis contributes to clinical improvement,

although there is no explanation provided about which

measures are used to gauge this improvement. Several

authors add the caveat that PE be initiated during the

early stages of the disease in order to realize its full

benefit (132). Parries, et al. (106), caution that PE alone

is associated with complications (e.g., hepatitis) and

that these risks should be weighed against the potential benefits of apheresis.

What can be said about the “scientific soundness”

of the data on which the conclusion that PE is efficacious is based? Scientific soundness is defined here

as the adequacy and the credibility of the available information for reaching a consensus. First, in the case

of evaluating the use of PE therapy for treating HUS,

it is quite clear that the newness of this particular application of the technique is associated with a small

and incomplete research base. With only 11 patients,

there is insufficient data on which to make a recommendation to endorse this procedure. Second, the credibility of the evidence is open to question because of

the quality of research used in all eight studies; these

case studies do not include any comparison groups.

The major problem with the case-study approach (and

other pretrial studies) is that they are subject to a variety of competing alternative explanations for the observed effects of the therapy. Interpreting the evidence

becomes even more problematic when the potential affects of apheresis therapy are confounded by other

therapies that are used concomitantly with plasma exchange. Apheresis was the single therapy used in only

two case studies; one patient completely recovered and

the other patient underwent chronic dialysis because

of continued deterioration of renal function (11,106).

Finally, it is unclear as to which criteria (e.g., outcome measures) should be used in evaluating the effectiveness of the therapy. There are too few cases to

determine whether there is high concordance between

the “immediate” outcomes (e.g., platelet counts, LDH,

creatinine, and BUN levels) and the “long-term” outcomes (e.g., chronic dialysis, mortality). If these

measures turn out to be discordant, some method will

have to be developed to combine these multiple evaluative criteria in order to arrive at the recommendation.
Appendix C.—Apheresis for Inhibitors to Factor Vlll

Prepared for OTA by: Paul M. Wortman, Ph. D.

Hillary Murt, M.H.S.A.

In collaboration with: Bruce Friedman, M.D.

Factor Vlll Antibodies

Apheresis, and more specifically, plasma exchange

(PE), has been investigated as a potential therapy for

patients with antibodies or inhibitors to Factor VIII

during the past 10 years. Factor VIII is essential to

achieve hemostasis (i.e., permit normal blood clotting

and end bleeding). For that reason, patients with classic

hemophilia have been particularly at risk from complications associated with the development of Factor

VIII antibodies. It has been estimated that as many as

20 percent of such patients may develop this condition. Factor VIII inhibitors can also arise spontaneously in other patients. This so-called idiopathic or acquired inhibitor to Factor VIII can occur in women in

their first year after childbirth, persons with rheumatoid arthritis, the elderly, and persons suffering a variety of other disorders.

The major concern in these situations has been to

return Factor VIII to normal or effective levels. Treatment typically involved immediate and continued

doses of human Factor VIII concentrate. This treatment often failed since it did not remove existing antibodies in the blood and frequently appeared to stimulate the production of more antibodies. To deal with

these complications a variety of alternative treatments

has been investigated. One of these has involved the

use of apheresis with or without Factor VIII. The following sections summarize the available scientific research reporting on the use of PE in treating patients

with antibodies to Factor VIII.

Literature Reviews

Twenty articles were located and retrieved from a

MEDLARS search of the research literature. Four of

these articles did not deal specifically with cases involving Factor VIII, five were in a foreign language

(two in Russian, two in German, and one in Hungarian), one article was a duplicate copy of another,

and one contained the same case information as

another by the same authors. Of the foreign language

articles, the two in Russian were excluded, the one in

Hungarian also was published in English and that article was included in our review; the two German studies were read. One of the German articles did not deal

with Factor VIII and the other presented a very brief

case drawn from 210 patients and also was not included in this review.

There remained nine articles to review after the

various exclusions were made. The articles were all

case studies involving from one to six patients. Five

studies reported treating a single patient; two had two

patients; one had three, and another had six. Of the

18 patients in these nine studies, 10 had classic

hemophilia, seven idiopathic Factor VIII antibodies,

and one had von Willebrand’s disease. The patients

generally faced a life-threatening situation. Thirteen

had severe bleeding and three required or were recovering from surgery. The patients ranged in age from

3 to 77 and generally had either low levels of Factor

VIII or high levels of Factor VIII inhibitor reported

prior to treatment.

68
App. C—Apheresis for Inhibitors to Factor VIII ● 69

Specification of Treatment

Although apheresis was employed in all of these

studies, the actual definition or specification of treatment varies widely from one report to another (see

table C-1). First, the number of PEs vanes widely from

just 1 (109,143) to 15 (129). The modal number of PEs

was three (occurring in six of the 18 patients) with

another four receiving two exchanges. The volume of

plasma actually exchanged also differed widely from

one study to the next, ranging from 500 to 6,000 ml

per exchange. The replacement fluid also varied. Although in seven studies fresh frozen plasma was used,

other fluids included albumin, gelatin, plasma protein,

and saline (or plasma expander). It should be noted

that in most patients who were severely compromised

fresh frozen plasma was used. The treatment also

varied in duration, lasting from 1 day to 6 weeks.

Perhaps most troublesome in determining the appropriate treatment regimen is the use of immunosuppressants such as azathioprine and cyclophosphamide

in conjunction with apheresis. Five of the eight studies

used one of them simultaneously with PE and two had

tried it before using PE. Nevertheless, there is a great

difference of opinion on the value of such therapy

despite its confounding with apheresis. One study

(129) claims that “immunosuppression has not been

shown to be effective and may well interfere with

wound healing and increase susceptibility to infection. ”

However, another study (111) concludes that “a combination of specific immune suppression and intensive . . . (apheresis) . . . may be the best form of

treatment in patients with acquired idiopathic factor

VIII inhibitors and life-threatening bleeding.” The

resolution of these conflicting claims and the separation of the two treatments (PE and immunosuppression) poses some difficulties in so few studies.

The study by Pintado, et al. (111), contains the best

discussion of possible alternative treatments. In that

study one elderly patient with idiopathic or acquired

Factor VIII inhibitor was given six plasma exchanges

over a 2-week period. These researchers reviewed the

previous literature and concluded that “spontaneous

remission of the immune response” (i.e., termination

of production of Factor VIII antibodies) was “unlikely.” Instead, they feel that the remission was due to

the combined use of immunosuppressants and “antigenic load” (i.e., human Factor VIII concentrate).

Treatment with Factor VIII concentrate poses an additional problem in determining the efficacy of apheresis. As noted in the introduction, Factor VIII supplementation is viewed as the primary treatment with

apheresis an adjunct to improve its efficiency. The use

of Factor VIII was, in fact, reported in all nine studies

encompassing 16 of the 18 patients treated. However,

in one study (37) involving two patients, this treatment was evidently discontinued just prior to apheresis

because of a rise in inhibitor level in one patient and

an adverse reaction (to a porcine derivative) in the

other. Similarly, in the study by Piller, et al. (109),

one of three patients was treated with Factor VIII concentrate just prior to apheresis. While the inhibitor

level was reduced from 1.3 to 0.5, p/ml, the goal of

this study was its complete neutralization and an increase in Factor VIII. In the remaining two patients

(who were not in a life-threatening situation) apheresis

using Factor VIII-free solutions was tried in an attempt

to prevent the “rapid increase” in inhibitor activity.

In both cases there was a “less rapid” return of inhibitor

activity to its previous level (and, in one case, a “considerably higher” level). The authors conclude that inhibitor levels can be lowered through “repeated . . .

(apheresis) . . . at intervals of about one month. ”

The Piller, et al. (109), study did not employ immunosuppressants concurrently in conjunction with

apheresis (although one patient received prior treatment with azathioprine and Factor VIII with cyclophosphamide “without success”). If the hypothesis of

Pintado, et al. (111), is correct, then antibodies would

continue to be produced requiring regular PE. As noted

Table C-2.—Effectiveness of Apheresis for Factor Vlll Inhibitors

Immediate Followup

Factor Vlll Factor Vlll

Study reference number Hemostasis inhibitor (μ/ml) inhibitor (μ/ml)

1 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . — 1.2 0.8

2 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes 36 8

3 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes 1-8 0-1

4 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . — O-4.8 0-17

5 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes — o

6 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes — o

7 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes 12 0

8 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes —

9 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes 0-1 5-47

SOURCE: Office of Technology Assessment, 1983.

98-822 0 - 83 - 6 : QL 3
70 ● Health TechnoIogy Case Study 23: The Safety, Efficacy, and Cost Effectiveness of Therapeutic Apheresis

this is exactly the conclusion of Piller, et al. (109).

Moreover, the two studies with the greatest number

of PEs did not use immunosuppressants. In the study

by Slocombe, et al. (129), noted above, one of the two

patients received 15 PEs exchanges along with varying doses of Factor VIII. Similarly, Cobcroft, et al.

(23), performed nine apheresis treatments on a patient

(who had previously had unsuccessful immunotherapy). One can only speculate on whether as many exchanges would have been required had immunosuppressants been employed concurrently. In both studies,

however, there is little justification provided for additional exchanges beyond the first two.

In summary, the modal regimen in the research studies involved two or three apheresis treatments in conjunction with both immunosuppressants (typically

cyclophosphamide) and Factor VIII concentrate (from

humans). Two hypotheses seem tenable from these

studies. First, immunosuppressants may stop the production of antibodies as Pintado, et al. (111), claim,

with the apheresis quickly removing existing antibodies. And second, apheresis using Factor VIII-free

solutions such as gelatin or saline may slow the return

of the inhibitor activity as Piller, et al. (109), maintain. The two treatment therapies are clearly not independent and could be combined. At present there

is a need for more systematic research on the most appropriate treatment for patients presenting with Factor VIII antibodies.

Results of Treatment

The results of the treatment just described in the nine

studies reviewed are presented in table C-2. Both shortterm or immediate results and long-term findings are

indicated. For 16 of the 18 patients at risk due to severe

bleeding or surgery the immediate clinical results were

uniformly successful. In all cases hemostasis was

achieved and the patient fully recovered from the acute

episode. One should note, of course, that cases of clinical failures are much less likely to be submitted or accepted for publication.

The measures of Factor VIII inhibitor (in ~/ml) and

Factor VIII (in percent normal) are not consistently

reported in the text. Where possible this information

was recorded or interpolated from tables and figures.

These figures indicate a less than consistent pattern of

results. In almost half the patients (i.e., 8 of 18) the

inhibitor level falls below 2 @ml at followup; while

in 9 of the patients reported, the inhibitor level is 8

μ/ml or greater. The inhibitor data for one patient

(129) were not available, but were probably very low

given the Factor VIII level of 75 percent.

Eight of the nine patients with poor long-term results

are from just two studies (109,143). The Piller, et al.,

study differed from all the others in that its sole objective, as noted earlier, was the long-term reduction

in the Factor VIII inhibitor level. This study did not

employ Factor VIII therapy along with immunosuppressants in the two failed cases (although one had

received them earlier). It should be noted that shortterm control was achieved and the authors conclude

that one could “treat severe hemorrhages immediately by only administering Factor VIII or by combining

one . . . (apheresis) . . . run with replacement therapy.”

The other six patients, one-third of the total from

all of the studies, with poor long-term or “secondary

rise” in the inhibitor level, were treated by Wensley,

et al. (143). In this case, apheresis combined with

human Factor VIII concentrate produced an initial lowering of the inhibitor level to permit hemostasis and

healing. The authors recommend this combined therapy as a better alternative to using “significant quantities” of Factor VIII alone.

As noted in the previous section, the impact of immunosuppressants should be considered. Neither of

these two studies reported the concurrent administration of immunosuppressants to patients. On the other

hand, five of the six patients treated with immunosuppressants had followup inhibitor levels of 1 @ml or

less.

Evaluation of the Evidence

In conclusion, it is important to ask what one can

infer from these nine studies. To do this, it is useful

to consider the quality of the research evidence provided. A number of points should be considered in

reaching an overall assessment.

First, the studies are all pretrial clinical reports generally of one patient (i.e., the five articles). There were

no clinical trials comparing a number of patients systematically treated by a number of well-defined therapies. In fact, other than references to some prior treatment regimen there is no comparative information

available.

Second, as an earlier section noted, there is no

agreed upon treatment for patients with inhibitors to

Factor VIII. While apheresis is used and endorsed in

all nine studies, the treatment is more complex than

that. Other concurrent therapies are described with

varying results and the number of PEs also differed

from study to study. While a number of possible hypotheses were examined, the evidence is far from con-
App. C—Apheresis for Inhibitors to Factor VIII ● 71

elusive on what is the best method to treat this condition.

Third, the goals of the studies also differed. Most

involved acute, life-threatening situations, usually

episodes of severe bleeding. In those cases, short-term

resolution of the problem was sought and generally

achieved. In a few other studies, longer term solutions

to the anti-Factor VIII were attempted with varying

results. Here too, there are possible treatment combinations that need to be further investigated.

Finally, with so few patients in so few studies one

must consider the issue of sample bias. It would only

take a few reports of a few patients with differing or

negative results to alter one’s notion of the efficacy of

apheresis in this situation. For this reason the evidence

can only be viewed as preliminary and provocative.

It is far from persuasive.

Apheresis in combination with other therapy is only

an emerging technology for treating patients with Factor VIII antibodies. There is a need for more careful

study and specification of the treatment and its effects

—both of immediate and longer duration. There are

a number of questions that need to be answered before

its efficacy is established. If, as is likely, apheresis continues to be employed in life-threatening situations,

then physicians should be encouraged to undertake

more systematic study of the treatment. This could include a number of therapeutic alternatives systematically applied to a series of patients, perhaps in a

controlled trial.

In conclusion, it should be noted that some experts

believe all the treatment combinations described above

are not effective. In particular, PE is viewed as a

stopgap measure, at best, because (as the literature indicates) the antibody titer rapidly increases post exchange. For these reasons current interest has focused

on bypassing the blockade of the Factor VIII inhibitor

by administering new agents that contain a mixture

of clotting factors, including activated Factor VIII.

Given the availability of these new agents, such treatment may be the therapy of choice for patients with

high titers of Factor VIII antibodies.
Appendix D.—Apheresis in Guillain-Barre Syndrome

Prepared for OTA by: Richard K. Riegelman, M. D., Ph. D.

Introduction

Guillain-Barré syndrome (GBS) (65,119,148) is an

acute polyneuropathy. It begins in a restricted area of

the body, most often distally, and then spreads or

ascends to involve many muscle groups. The rate and

extent of progression vary widely. Many patients recover spontaneously without life-threatening progression. Some become severely paralyzed within a few

days while in others the disease worsens slowly and

insidiously over a period of several days or even

weeks. The extent of paralysis varies widely. Sensory

and autonomic nervous system involvement can also

occur. In the most severely involved individuals, control of blood pressure and breathing maybe affected

requiring a respirator and intensive care management.

Progression of weakness usually ceases less than 4

weeks after onset. Spontaneous recovery usually

begins within 2 to 4 weeks after progression stops.

Recovery is usually gradual, but abrupt spontaneous

recovery has been documented.

With current intensive care management under the

most ideal conditions the mortality can be reduced to

5 percent or less. Prognosis for complete recovery is

good, with about 85 percent of patients restored to

normal function. The remaining usually have only

mild residual deficits.

The etiology of GBS remains unknown. Cases have

been associated with injection of foreign protein, cat

scratches, dog bites, transfusions, and immunizations,

including rabies vaccine and the widely publicized association with the 1976 influenza vaccine program.

Rumpl, et al. (119), have summarized the evidence

as of 1981 for an immunologic mechanism as follows:

Experimental allergic neuritis has shown striking similarity with the disease in humans. The immune pathogenesis of GBS was further supported by the finding of

complement fixing antibodies, of precipitating antibodies against trypsinized white matter extracts and of

myelinotoxin serum antibodies of the IgM class in patients with GBS. Cellular hypersensitization to peripheral nervous antigen presented by circulating immunoblasts and lymphocytes supported the role of cellular

mechanisms in pathogenesis.

The rationale for the use of plasma exchange (PE)

in GBS is based on the presence of serum antibodies

which can be removed by PE.

Brettle, et al. (15), first reported the successful use

of PE in acute GBS in 1978. An abrupt and dramatic

improvement was seen in this case. This report was

published shortly after Hughes, et al. (63), reported

a poor response to steroids in a controlled clinical trial

of acute GBS. With evidence against the use of steroids

established in a controlled clinical trial and with

evidence of a dramatic improvement with plasma exchange, many centers throughout the world began to

experiment with and report their results of PE therapy.

The existing literature includes many case reports

and small series of cases in which apheresis or more

specifically PE was used in the treatment of acute GBS.

In reviewing this literature one must appreciate several factors repeatedly emphasized by the authors and

critics.

1.

2.

3.

4.

5.

As an experimental therapy initial use of the therapy was not standardized. The timing, quantity, duration, and type of PE varied considerably.

In some patients the therapy was used concurrently with steroid treatment and in others after

steroids had failed. Some patients were treated

after extended respirator and intensive care therapy while others were treated in an effort to avoid

the need for such care.

The measures of assessment of outcome also varied enormously. Some investigators reported obvious and at times dramatic clinical improvements while others reported changes in nerve conduction tests and immunological changes which

preceeded or were unassociated with a clinical

response.

The reported studies are all case reports without

any concurrent control groups, blinding, randomization, or other techniques used in controlled clinical trials.

The documentation of adverse effects was not

systematic and may have been biased by the tendency to report successful uses of a new therapy.

The natural history of acute GBS with its tendency for spontaneous and occasionally abrupt improvement makes the interpretation of therapy

related results more difficult.

Despite these difficulties much has been learned from

the initial studies and reports on the use of PE in GBS.

The following section summarizes the reported evidence on efficacy.

72
App. D—Apheresis in Guil!ain Barré Syndrome • 73

Efficacy

The reported individual cases repeatedly refer to

striking or dramatic change which occur within minutes to hours after plasma exchange.

One report (134) stated: “the improvement after the

exchanges was so abrupt and striking that it induced

us to believe that the plasma exchanges were essentially responsible for this development. Particularly in

our case with ventilator insufficiency and bulbar

palsy, which worsened day by day, the course of the

disease seemed to have been reversed by plasma exchange inducing an immediate amelioration. The response was quicker in those nerves which had deteriorated the latest, which is in accordance with clinical

experience in cases of spontaneous recovery.”

Other cases of dramatic improvements after plasma

exchange includes the following:

Littlewood and Bajada (77) report: “On day 8 of our

patient’s illness respiratory vital capacity fell to 1.41

and was accomplished by complete ophthalmoplegia

and iridopligia. A dramatic improvement in vital capacity followed the first session and was subsequently maintained.” Similarly, Corachan, et al. (27), report

a case of: “ . . . dramatic improvement after . . .

(apheresis) . . . “ Levy, et al. (76), report that “clinical

improvement was dramatic” in a patient with chronic

relapsing disease.

Not all investigators have reported success. Cook,

et al. (26), reported a series of five patients only one

of whom had a “significant clinical improvement. ”

Maisey and Olczak (78) reported two patients who

failed to respond to PE. Gross, et al. (45), have argued

that Maisey’s use of 1.5 liters per day of plasma exchange was “small compared with those used by other

operators for the same disease and in other disease

processes.” They further argue that one would not expect all cases to respond. They write: “Cases of inflammatory polyneuropathy probably constitute a heterogeneous group and it would be surprising if every patient proved to benefit from plasma exchange.”

Several larger series have also been recently reported. Rumpl, et al. (119), reported eight cases of successful treatment with PE. They report: “Recovery was

abrupt in all cases after the first PEs. Improvement was

more marked, when . . . (apheresis) . . . was performed on three successive days with plasma exchanges of 2.0-3.01 each . . . . Recovery seemed to

be delayed in cases when plasma exchanges were reduced to 0.5-1.51 each and were spread over several

days or weeks, even when the number of plasma exchanges was increased.”

Durward, et al. (33), reported their experience with

six cases all of whom improved to some degree after

PE. They conclude “Our experience to date (11 incidents in six patients) is of recovery beginning or accelerating immediately after plasma exchange . . . .

We started exchanges fairly early-usually about one

week after onset —and exchanged more than 10—1 on

each occasion (except in case 3). ”

Dau, et al. (31), report on 13 patients with acute

GBS who underwent 2 to 3 weeks of PE with 4 or 5

exchanges of 4 liters. Seven patients, all of whom were

still progressing or stable “stopped progressing on the

day of the first . . . (apheresis) . . . and had discernible clinical improvement within 48 hours.” Among the

other patients two continued progressing, three were

already slowly improving and apheresis “did not seem

to accelerate recovery.” In these patients apheresis was

started “relatively late after disease onset .“ In the last

patient there was progressive deterioration. The report

concluded that factors associated with a good outcome

were:

1. Institution of apheresis early in the course of the

illness.

2. Normal evoked muscle action potential.

3. Little electromyographic evidence of denervation.

4. Age less than 50 years.

Schooneman, et al.’s (123), series of 10 patients with

acute GBS is the only reported series in which no patients received steroids and in which a control group

was attempted. In addition, the authors performed extensive neurological testing before and after each exchange. Respiratory impairment was assessed by clinical examination and blood gas determinations.

In 9 of their 10 cases patients showed improvement

within 24 hours after the first exchange. The authors

believe that “the progressive phase of the disease was

halted.” They term their results “spectacular.” In comparing their 10 patients to 258 historical control patients with GBS they conclude that apheresis appeared

to shorten the duration of paralysis, reduce the need

for tracheotomy, and shorten the hospital course.

They did not demonstrate reduced mortality since one

patient died in each group. They also did not demonstrate or claim that these patients represented comparable study and control groups.

Safety

Plasma exchange carries inherent risks in all patients. Samtleben, et al. (120), reporting on 100 consecutive PE procedures, observed allergic reactions to

albumen in 10 percent, hypocalcemic symptoms in 6

percent, and vasovagal reactions in 5 percent. Other

side effects have included massive extracorporeal blood

clotting, hypercoagulation states with vascular thrombosis, hemorrhagic tendencies, changes in serum lipid
74 ● Health Technology Case Study 23: The Efficacy, and Cost Effectiveness of Therapeutic Apheresis

fractions, cardiac arrhythmias, and pulmonary emboli

(93).

Rumpl, et al. (119), reported that in their experience

with plasma exchange for GBS, cardiovascular problems, coagulation difficulties, and allergic reactions

made it necessary to interrupt PE and influenced the

amount of exchanged plasma.

Patients with severe GBS may have an unstable

autonomic nervous system predisposing them to problems with blood pressure control and cardiac arrhythmias. The need to perform the procedure on

respirator dependent patients may further complicate

PE.

In light of these considerations Mayr, et al. (81),

who have successfully used PEs in GBS, conclude:

“The considerable risks and high technical requirements may limit this therapy to the severe course of

Guillain-Barré syndrome.”

Need for Controlled Clinical Trials

A controlled trial is not a trial of a treatment. It is

a trial of a specific means of administering a therapy;

thus it requires agreement on the timing, extent, and

duration of therapy.

The performance of a controlled clinical trial should

be preceded by enough research to establish an agreed

upon method for administering the therapy. In addition, before going to the expense of a well-performed

controlled clinical trial, it is important that preliminary

evidence exists of the effectiveness and additional benefit of the treatment. These two prerequisites to a controlled clinical trial have been adequately fulfilled by

the existing literature.

Despite the controversy in the reported literature

over the efficacy and safety of PE in GBS, both the

advocates and the skeptics appear to agree on the need

for controlled clinical trials. A sampling of their comments should demonstrate this point.

Irvine and Tibbles (64) in their report of an apparently successful treatment with exchange transfusions conclude: “In the future it will be important to

document failures as well as success to place this treatment in its proper perspective. It is likely that the

organization of a prospective controlled trial of this

costly form of management will be necessary. ”

During 1981 a series of letters appeared in the British

Medical Journal reporting dramatic improvement, evidence of subtle response, and cases without measurable

improvement. All three reports agreed on the need for

a controlled trial. The group (78) reporting no response

wrote: “If anecdotal reports are relied on, publication

bias ensures that apparently successful results dominate the literature. ” The group (62) reporting success

wrote: “ . . . a controlled trial of plasma exchange is

necessary in acute inflammatory polyradiculoneuropathy before its value can be assessed. Since patients

with this condition begin to improve after a variable

time after the onset of symptoms and usually recover

completely, it is not surprising that each new treatment has been hailed with enthusiasm on the basis of

anecdotal reports.” The group (33) reporting subtle

responses concurred, stating: ‘These data only reemphasize the need for a controlled clinical trial,

especially in the early phase, in order to delineate the

role of plasma exchange in acute Guillain-Barré syndrome.”

In their advocacy of their forthcoming controlled

clinical trial Asbury, et al. (10), wrote in the October

1980 issue of Neurology that apheresis of “an acutely

ill patient with respiratory depression and autonomic

instability is not a benign procedure. Until this study

is completed anecdotal reports of the efficacy

of . . . (apheresis) . . . in the Guillain-Barre syndrome

should be interpreted with caution. At present, it is

not possible to state the therapeutic role

that . . . (apheresis) . . . plays for this disease,”

Controlled Clinical Trials in Progress

In December 1980, the National Institute of Neurological and Communicative Disorders and Stroke

funded a 3-year multiple site cooperative study of

apheresis treatment of acute GBS (87).

The primary study question is: Does apheresis effect a significant beneficial change in the early course

of severely ill patients with GBS? Secondary study

questions include the following:

1.

2 .

3 .

Are there clinical, epidemiologic, laboratory, or

electrodiagnostic factors associated with a good

outcome of GBS? If so, how does apheresis interact with these factors?

Is there a subgroup of patients with GBS for

whom apheresis can be expected to be of value

and a subgroup for whom it cannot?

Can apheresis reduce the incidence of long-term

complications (assessed at 6 months) in the 15 to

20 percent of GBS patients destined to have some

lasting deficits?

The study uses generally accepted criteria for the

diagnosis of GBS. Patients must be within 30 days of

onset of definitive neuropathic symptoms. They must

require a walker or support to walk 5 meters or be

more severely affected. Steroid treatment is not given

to study patients. The quantity and timing of the PE

are consistent with that reported for successful uses

of PE in GBS.
App. D—Apheresis in Guillain Barré Syndrome ● 75

The study protocol provides standard methods for

assuring randomization, informed consent, termination, monitoring of followup, and statistical analysis.

The study is designed to include about 240 patients.

This number is adequate to provide an 80-percent

chance of demonstrating a statistically significant improvement if apheresis actually provides a 50-percent

improvement over conventional therapy. As of July

1, 1982, 102 patients had been enrolled in the study.

An interim analysis of the data is planned when approximately 120 patients have been entered into the

study. The interim analysis is designed to determine

whether the study should continue. This analysis will

consider the following three possibilities:

1.

2 .

3 .

The evidence is overwhelming that the apheresis

patients are doing better, and if the study were

to continue with little or no advantage to the exchange protocol over the second half of the study,

a statistically significant difference would still

exist.

the exchange protocol patients are doing worse

or no better than the other patients and continuation of the study could not, even with an extreme

reverse of results in the second half, demonstrate

a beneficial effect of apheresis.

Neither extreme exists.

The endpoints considered in this analysis will be measures of clinical improvement 4 weeks after entry into

the study as well as time spent on a respirator. If the

interim report reaches conclusion 1 or 2, the study will

be stopped and presumably the results released and

reported. Otherwise the study will continue and the

results presumably will not be released by the National

Institutes of Health (NIH).

The NIH study appears to be adequately designed

to answer the basic questions regarding efficacy of

apheresis. The results should largely determine

whether evidence exists for moving PE from an experimental status to that of a conventional therapy for

A second randomized controlled clinical trial is currently underway in Great Britain (87). This study also

includes patients who require support to walk 5 meters

or who are more severely affected. The findings on

the first 19 randomized patients were reported in May

1982. A “decided trend in favor of plasma exchange

was noted at 4 weeks after randomization which did

not reach statistical significance. ”

NIH will not currently release preliminary results

of the American study. The interim analysis should

be completed by early 1983, but unless the results of

the interim analysis clearly answer the efficacy question, a full report may not be available until 1984.

Conclusions

1 .

2.

3.

4.

5.

Case reports and small-scale, mostly uncontrolled

trials provided suggestive evidence that plasma exchange may be efficacious for some patients with

acute GBS.

Because of the low mortality and good prognosis

for most patients with Guillain-Barré syndrome, the

safety of the procedure and indications for its use

should be delineated prior to nonexperimental use

of plasma exchange in GBS.

The conditions for use of plasma exchange in acute

Guillain-Barré syndrome have been sufficiently

standardized to enable a controlled clinical trial of

the procedure.

The potential cost saving and potential for shortened disability make well-designed controlled studies of this therapy important.

Controlled studies of the efficacy, safety, and indications for plasma exchange in acute GBS are currently in progress. These studies should be adequate

to provide data which address the essential clinical

questions. Until the results of these studies are

available, the use of plasma exchange in GBS should

be considered an experimental procedure.

acute GBS.
Appendix E.—The Cause and Pathological Development

of Autoimmune Diseases*

The cause and pathological development of autoimmune diseases are thought to be due to several mechanisms, each having varying importance in different

diseases. These mechanisms are: inactivation reactions,

cytotoxic reactions, immune complex deposition, anaphylaxis, and delayed hypersensitivity.

With inactivation reactions, autoimmune antibodies

are directed against molecules that are receptors or

mediators for important physiological functions. For

example, people with myasthenia gravis have antibodies directed against neurotransmitter receptors on

muscle membranes, and thus the conduction of electrical impulses between nerve and muscle is disturbed.

In diseases in which cytotoxic antibodies are thought

to play a role, antibodies are directed against molecules

on the surface of cells, and reactions between the antibodies and antigens result in the killing of the cells

through complement mechanisms or clearance by

lymphoid tissues. This can lead to depletion of sets of

cells required for vital functions, such as platelet loss

in idiopathic thrombocytopenic purpura.

In many diseases, deposition of immune complexes

in tissues is thought to be the mechanism for the

destructive lesions observed. These immune complexes

may consist of antibodies and viral antigens, cancer

antigens or other antigens. In these diseases, the complexes are of such a nature or in such great amounts

that they saturate the normal clearing system in lymphoid tissues (or these clearing systems are deficient

secondary to the underlying disease). Deposition of the

complexes in vessel walls, in structures of the kidney,

and joint spaces leads to inflammation due to the activation of complement or cellular immune responses.

Vasculitis, glomerulonephritis and arthritis, for example, can be the result.

Anaphylaxis refers to the release by antigen stimulation of immediately reacting inflammatory agents by

tissue cells which have antibodies directly on their surfaces. Severe anaphylactic reactions are life threatening. Diseases that are manifested by anaphylactic reactions include food allergies, insect allergies, and

asthma.

Finally, there are diseases transmitted by cellular immune mechanisms, referred to as delayed hypersensitivity reactions. In this case, specifically, sensitized

lymphocytes infiltrate tissues and cause destruction.

Often circulatory antibodies participate in the process

as well. Examples of this disorder include viral hepatitis

and graft rejection.

● This appendix is condensed from Frost & Sullivan, Inc., in-Vivo Hemodetoxification and Hemoprocessing Markets in U. S., New York, June 1981.

76
Appendix F.—American Red Cross Bibliography

This appendix contains a Therapeutic Apheresis Bibliography that was compiled by the

American Red Cross and is distributed to American Red Cross regional blood services to facilitate

access to current information on therapeutic apheresis by specific disease categories.

The bibliography is divided into two sections. The first section contains 1,241 citations that

comprised the apheresis literature as of May 1982. The second section is a supplement that adds

778 references through January 1983 to the original list.

References in both sections are listed by reverse chronological order and grouped by specific

disease categories. Some articles may be cited in more than one category if their content warrants multiple listings. Texts, symposia, and review articles (sec. XVII) may also contain information pertinent to specific diseases, but some of these summary publications may not be listed

by disease category.

77
No. VU: Liver Disease

No. 1:

A.

: :

D.

E.

/-

No. II:

A.

B.

c.

D.

E.

F.

G.

H.

L

No. Ill:

A.

B.

c.

D.

E.

No. IV:

A.

B.

c.

No. V:

A.

: :

D.

E.

No. W:

A.

B.

Neurological Disorders

Myasthenia Gravis

Multiple Sclerosis

RefSum’s Disc se ? Guillair+Barre Syndrome

Miscellaneous: Polyneuropathy, Motor Neuron Disease, Amyotrophic

Lateral Sclerosis

Blood Diseases

Hemo~ilia

Autoimmme Hemolytic Anemia

Aplastic Anemia

Immme Ttrombocytopenic Purpura

Ttrombotic Ttrombocytopenic Purpura, Hemolytic Uremic Syndrome

Sickie Cell Disease

Leukemiaj Myeloproliferative Syndrome, S&zary Syndrome

Ttrombocytosis

Miscellaneous

Malignant Paraproteinemias

Hyperviscmsity Syndrome “

Macroglobulinemia

Multiple Myeloma

Cryoglobulinemia

Miscellaneous

Renal Diseases

GoodPasture’s Syndrome

Glomerulonephritis

Miscellaneous

Connective Tissue Disorders

Systemic Lupus Erythematosus

polyarteritis Nodosa - Wegener’s Granuloma

Rheumatoid Arttiitis

Raynaud’s Syndrome

Miscellaneous

Transplantation

Renal

Bone Marrow

A.

B.

Hepatitis, Hepatic Coma

Miscellaneous

No. VIII: Hemolytic Disease of the Newbocn

No. Ix: Cancer

No. X: Skin Diseases

A.

B.

c.

Pemphigus Vulgaris

Eryttrocyte Autosensitization

Miscellaneous

No. X1: Lipid Disorders (Hyperlipidemia)

No. XII: Immmological Disorders

A.

B.

Irnmumdeficiency

Irnmtne Complex Disease

No. XIII: “Miscellaneous Diseases

A.

B.

c.

D.

:

G.

Thyroid Storm

Pulmonary Edem~ Aduit Respiratory Distress Syndrome

Hypertensim

Poisoning

Asthma

Crohn% Disease

Miscellaneous

No. XIV: Clinical Reactions, Complicatiuls

No. XV: Technical Aspects

No. XVL Alternative Methodologies

No. XVII: Texts, Symposia

.

*l’his Case Study has used the term “apheresis” throughout its contents for the

purpose of consistency. However, the term “pheresis” is used by the American

Red Cross with the same meaning.
AMERICAN RED CROSS BLOOD SERVICES

Therapeutic Pheresis Bibliography No. 1: Neurological Disorders

A. Myasthenia Gravis

Anchie T: Plasm apheresis as a treatment for myasthenia gravis. J Neurosurg Nurs

13:23-27, 1981.

Dau PC: Response to plasmapheresis and immunosuppressive drug therapy in sixty

myasthenia gravis patients. Ann NY Acad Sci, in press.

Dau PC, Denys EH: Plasmapheresis and immunosuppressive drug therapy in the

Eaton-Lambert syndrome. Ann Neurol, in press.

Goulon M, et al: Treatment of myasthenia gravis by plasma exchange and

immunosuppressors. Rev Med Interne 1:213-216, 1981 (English abstract).

Hawkey CJ, et al: Plasma exchange and immunosuppressive drug treatment in

myasthenia gravis: No evidence for synergy. J Neurol Neurosurg Psychiatry

44:469-475, 1981.

Kornfeld P, Ambinder EP, Mittag MW, Bender AN, Papatestas AE, Genkins G:

Plasmapheresis in myasthenia gravis. Plasma Ther 2:127-133, 1981.

Kornfeld P, et al: Plasmapheresis in refractory generalized myasthenia gravis.

Arch Neurol 38:478-481, 1981,

Lang AE, et al: Plasma exchange therapy for severe penicillamine-induced

myasthenia gravis. 3 Rheumatol 8:303-307, 1981.

Miller RG, et al: Antibody-negative acquired myasthenia gravis: Successful

therapy with plasma exchange. Muscle Nerve 4:255, 1981.

Newsom-Davis J, Hawkey C, Vincent A: Plasma exchange in the treatment of

myasthenia gravis. In Borberg H, Reuther P (eds): “Plasma Exchange Therapy.”

Stuttgart: Georg Thieme Verlag, 1981, pp 180-185.

Reuther P, Wiebecke D, Fateh-Moghadam A, Besinger U, Mertens HG: The role of

plasma exchange in the treatment of myasthenia gravis. In Borberg H, Reuther P

(eds): “Plasma Exchange Therapy.” Stuttgart: Georg Thieme Verlag, 1981, pp

186-193.

Scadding GK, Havard CWH: Pathogenesis and treatment of myasthenia gravis. Br

Med J 283:1008- 1012, 1981.

Toyka KV, Besinger UA, Heiniger K, Samtleben W, Hein D, Fateh-Moghadam A,

Gurland HJ, Grabensee B: Myasthenia gravis: The pathogenic role of antibodies to

acetylcholine receptor and the effect of antibody depletion. In Borberg H, Reuther

P (eds): “Plasma Exchange Therapy.” Stuttgart: Georg Thieme Verlag, 1981, pp

172-179.

ARC Blood Services

Bibliography

TPB I-2

Wysenbeek AJ, Smith JW, Krakauer RS: Plasmapheresis 11: Review of clinical

experience. Pl=ma Ther 2:61-71, 1981.

Campbell WW Jr, et al: Plasma exchange in myasthenia gravis: Electrophysiological studies. Ann Neurol 8:584-589, 1980.

Carter B, et al: Anti-acetylcholine receptor antibody titres in the sera of

myasthenia patients treated with plasma exchange combined with immun~

suppressive therapy. J Neurol Neurosurg Psychiatry 43:397-402, 1980.

Dau PC: Plasmapheresis therapy in myasthenia gravis. .Muscle Nerve 3:468-482,

1980.

Gerlag K, et al: Successful treatment by plasmapheresis of respiratory insufficiency in myasthenia gravis. Cfin Neurol Neurosurg 82:237-243, 1980.

Johns TR, Sanders D: Plasmapheresis in myasthenia gravis. Plasm apheresis

WWkshop sponsored by Muscular Dystrophy Association, New York University,

April 1980.

Lisak RP, Abramowitz O, .khotland DL: Plasm apheresis in myasthenia gravis.

Pla.smapheresis Workshop sponsored by Muscular Dystrophy Association, New York

University, April 1980.

Pollard 3D, Basten A, Hassall 3E, Kronenberg H, CobCroft R, Dawkim R: Current

trends in the management of myasthenia gravis: Plasmapheresis and immunosuppressive therapy. Aust NZ J F&XI 10:212-217, 1980.

Reuther P, Wiebecke D, Boske A, Mertens HG: Plasma exchange in myasthenia

gravis and other neurological disease. Heidelberg: Springer, 1980 (in press).

Riley TL, Monagle WP: Antireceptor-antibody decline without improvement after

plasm apheresis in myasthenia gravis. AM Intern ,Med 92:713, 1980.

%wntleben W, Besinger UA, Toyka KV, Fateh+iogharlam A, Brehm G, Gurland HJ:

P1=ma-separation in myasthenia gravis: A new method of rapid plasma exchange.

Klin Wochenschr 58:47-49, 1980.

Sanders DB: Plasm apheresis in myasthenia gravis. Sixth International Conference

on Diseases of the L&iotor Unit, Key Biscayne, Florida, June 1980.

Tokya KV, Augspach R, Besinger UA, Grabensee B: Treatment of myasthenia

gravis and Guillain-Barre’ syndrome with plasma exchange. In Sieberth HG (cd):

“Plasma Exchange. Plasmapheresis - Plasm aseparationo” Stuttgart: F. K.

Schattauer Verlag, 1980, pp 289-296.

Behan PO, Shakir RA, Simpson 3A, Burnett AK, AlIan TL, Haase G: Plasmaexchange combined with immunosuppressive therapy in myasthenia gravis. Lancet

2:438-440, 1979.

Blount M, Kinney AB, Stone .M: Plasma exchange in the management of

myasthenia gravis. Nurs Clin North Am 14:172- 176, 1979.
ARC Blood Services

Bibliography

TPB I-3

Dau PC (cd): “Plasmapheresis and the Immunobiology of Myasthenia Gravis.”

Boston: Houghton Mifflin, 1979.

Dau PC, Lindstrom 3M, Cassel CK, Clark EC: Plasmapheresis in myasthenia gravis

and polymyositis. In Dau PC (cd): “P1asmapheresis and the Immunobiology of

Myasthenia Gravis.” Bcaston: Houghton Mifflin, 1979, pp 229-247.

Kornfeld P, Ambinder EP, Papatestas AE, Bender AN, Genkins G: Plasmapheresis

in myasthenia gravis: Controlled study. Lancet 2:629, 1979.

Lisa; RP, Abramsky O, Schotlad DL: Plasmapheresis in the treatment of

myasthenia gravis: Preliminary studies in 21 patients. In Dau PC (cd): “Plasmapheresis and the Immunobiology of Myasthenia Gravis.” Boston: Houghton Mifflin,

1979, Pp 209-215.

Newsom-Davis 3: Plasma exchange in myasthenia gravis. Plasma Ther 1:17-31,

1979.

Newsorn-Davis J, Vincent A: Combined plasma exchange and immunosuppression

in myasthenia gravis. Lartcet 2:688, 1979.

Newsorn-Davis 3, Wilson SG, Vincent A, Ward CD: Long-term effects of repeated

plasma exchange in myasthenia gravis. Lancet 1:464-468, 1979.

Pinching A3, Peters DK, Newsorn-Davis 3: Plasma exchange in the investigation

and treatment of myasthenia gravis. Plasma Ther 1:29-32, 1979.

Plasmapheresis for myasthenia gravis. Med Lett Drugs Ther 21:64, 1979.

Reuther P, Wiebecke D, Hertel G, M“ske A, Mertens HG: Treatment of myasthenia

gravis with plasmapheresis. Dtsch ,Med Wochenschr 104:1806-1810, 1979.

Dau PC, Cassel CK, Denys EH, Shev E& Spitler LE: Plasmapheresis for

myasthenia gravis. Lancet 1:457, 1978.

Howard JF Jr, Sanders DB, Johns JR: The role of plasma exchange therapy in

myasthenia gravis. Haemonetics Research Advanced Component Seminar, Boston,

1978.

Jacobs P, Dubovsky D, Ferguson A: Plasmapheresis and myasthenia gravis. Br Med

3 1:177, 1978.

Keesey 3: Caution on plasm apheresis for myasthenia gravis. N Engl J Med

298:1029, 1978.

Lisak RP, Schotland DL: Symposium on therapeutic controversies. Myasthenia

gravis. Plasmapheresis in the treatment of myasthenia gravis. Trans Am Neurol

Assoc 103:292-302, 1978.

LNewsom-Davis 3, Pinching A3, Vincent A, Wilson SG: Functicm of circulating

antibody to acetylcholine receptor in myasthenia gravi~ Investigation by plasma

exchange. Neurology 28:266-272, 1978.

ARC Blood Services

Bibliography

TPB I-4

Newsom-Davis J, Vincent A, Wilson SG, Ward CD, Pinching AJ, Hawkey C:

Plasmapheresis fcr myasthenia gravis. ~ Engl J Med 298:456, 1978.

Dau PC, Lindstrom 3M, Cassel CK, Denys EH, Shev EE, Spitler LE: Plasmapheresis

and immuios~pressive &ug therapy in myasthenia gravis. N Engl 3 Med

297:1134- 1140, 1977.

Finn R, Coates PM: Plasma exchange in myasthenia gravis. Lancet 1:190-191,

1977.

Havard CWH: Progress in myasthenia gravis. Br Med 3 2:1008-1011, 1977.

Pinching A3, Peters DK, Newsom-Davis 3: Plasma exchange in myasthenia gravis.

Lancet 1:428-429, 1977.

Pinching RJ, Peters DK, Newsom-Davis 3: Remission of myasthenia gravis

following plasma exchange. Lancet 2:1373-1376, 1976.

B. Multiple Sclerosis

Masland W, Gicaono GF: Lymphocytapheresis in multiple sclerosis. In “Third

AMua.1 Symposium on Apheresix Current Concepts and Future Trends.” Skokie,

IL: American Society fcc Apheresis, 1981 (abstract).

Rosen AD, Hamburger MI: Plasmapheresis in multiple sclerosis: Effect on the

visual evoked potential. Plasma Ther 2:239-242, 1981.

Valbonesi M, Garelli S, Mosconi L, Zerbi D, Celano 1: Plasma exchange in the

management of selected neurological diseases. Plasma Ther 2:13-18, 1981.

Vukovich DM, Vaithianathan T, French A: Lymphocytapheresis in multiple

sclerosis - a pilot study. In “Third AMUd Symposium on Apheresis: Current

Concepts and Future Trends.” Skokie, IL: American Society for Apheresis, 1981

(abstract).

Dau PC, Petajan JH, Johnson KP, Partitch HS, Bernstein .MB: Plasmapheresis in

multiple sclerosis: Preliminary findings. Neurology (NY) 30:1023- 1028, 1980.

Giordano GF, Wallace BA, ,Masland W, Ketchel S3, Tilmann K, Holl%d K:

Lymphocytapheresis as a therapeutic modality in muitiple sclerosis: A preliminary

repxt. In “Second Annual Apheresis Symposium: Current Concepts and Future

Trends.” Skokie, IL: American Society for Apheresis, 1980, pp 25-37.

Khatri Bo, ,McQuillen .MP, Kiethe SM, Hussey C, Cook A: Plasmapheresis in

multiple sclerosis: Correlation of clinical improvement with increased suppressor

cell activity in peripheral blood. AM Neurol 8:1 14, 1980.

Plasmapheresis for multiple sclerosis. Int IMed Alert 2:65-66, 1980.

Stefoski D, Schauf CL, Davis FA, et al:

Clinical observations and effects on serum

rology 30:362-363, 1980.

Plasmapheresis in multiple sclerosis:

neuroelectric blocking factor. Neu-
ARC Blood Services

Bibliography

TPB 1-5

ARC Blcad Services

Bibliography

TPB I-6

vanden Noort S, Waksman BH: Plasma exchange: Aid to therapy of multiple

sclerosis. Neurology 30:1 111, 1980.

Weiner HL, Dawson DM: Plasmapheresis in multiple sclerosis: Results of a

preliminary study. Neurology 30:1029- 1033, 1980.

Dau PC, Petajan 3H, 3ohnson KP, Panitch HS, Bornstein MR: Plasmapheresis and

immunosuppressive drug therapy in multiple sclerosis. Neurology 29:573, 1979.

/-

Schauf CL, Stefcski DA, Davis FA, McLeod BC: The applica~lon of plasmapheresis

to multiple sclerosis. Plasma Ther 1:33-42, 1979.

C. Refsum’s Disease

Gibberd FB: Heredopathia atactica polyneuritiformis (Refsum’s disease) and its

mamgement with plasma exchange. Plasma Ther 1:17-26, 1980.

Karnanabroo D, Harnest U, Feldman H, Assman G, van de Loo J: Herodopathia

atactica polyneuritiformis (Refsum’s disease) treated by diet and Iarg&volume

plasma exchange. In Sieberth HG (cd} “Plasma Exchange. Plasmapheresis -

PlasmaSeparation.” Stuttgart: F. K. Schattauer Verlag, 1980, pp 297-299.

Moser HW, Braine H, Pyeritz RE, Unman D, Murray C, Asbury AK: Therapeutic

trial of plasmapheresis in Refsurn disease and in Fabry disease. Birth Defects

16:491-497, 1980.

Gibberd FB, Billimoria JD, Page NG, Retsas S: Heredopathia atactica polyneuritiformis (Refsum’s disease) treated by diet and plasma-exchange. Lancet 1:575-

578, 1979.

Penovich PE, Hollander 3, Nusbacher 3A, Griggs RC, McPherson 1: Note on

plasma exchange therapy in Refsum’s disease. In Kark RAP, Rosenberg RN, Schut

A3 (eds): “Advances in Neurology:’ Vol 21. New York: Raven Press, 1978, PP

151-153.

Lmdberg A, Lilja LG, Ltmdberg PO, Try K: Heredopathia atactica polyneuritiformis (Refsum’s disease). Experience of dietary treatment and plasmapheresis.

Eur Neurol 8:309-324, 1972

D. Guillain-Barr~ Syndrome

Augspach R, Toyka KV, Padus W, Hein D, Grabensee B: Plasma exchange in

chronic Guillain-Barr~ syndrome. In Borberg H, Reuther P (eds): “Plasma

Exchange Therapy.” Stuttgart: Georg Thieme Verlag, 1981, pp 208-209.

Durward WF, et al: Plasma exchange in Guillain-Barr~ syndrome. Br Med J (Chn

Res) 283:794, 1981.

Gross MLP, Sweny P, Legg N3: Successful plasmapheresls in ,Miller-Fisher

syndrome. Br Med J (Clin Res) 282:1394, 1981.

Irvine AT, Tibbles J: Treatment of Fisher’s variant of Guillain Barr: syndrome by

exchange transfusi~. 3 Can Sci Neurol 8:49-50, 1981.

Littlewood R, Bajada S: Successfd plasmapheresis in the ,MiUer-Fisher syndrome.

Br ,Med 3 282:778, 1981.

Maisey DN, Olczak SA: Successful plasmapheresis in the ,Miller-Fisher syndrome.

Br Met! 3 (Clin Res) 282:1159, 1981.

.Mayr U, Rumpl E, Hackl JM, Gerstenbrand F : Treatment of Guillain-Barr~

syndrome by plasma exchange. In Borberg H, Reuther P (eds): “Plasma Exchange

Therapy.” Stuttgart: Georg Thieme Verlag, 1981, pp 199-204.

Reuther P, Rauterberg EW, Hempel K, .Mertens HG: Plasma exchange in relapsing

Guillain-Barre syndrome. In Borberg H, Reuther P (eds): “Plasma Exchange

Therapy.” Stuttgart: Gecrg Thieme Verlag, 1981, pp 206-207.

Rumpl E, et- al: Treatment of Guillain Barr: syndrome by plasma exchange. 3

Neuroi 225:207-217, 1981.

Schooneman F, Janet C, Streiff F, Gerard, A, Dureux 3B, Canton P, Roche G,

Aubrun P: Plasma exchange in GuUain-Barre syndrome: Ten cases. Plasma Ther

2:117- 121, 1981.

Successful pl=mapheresis in the tMiller-Fisher syndrome. Br LMed J (Clin Res)

282:2055, 1981.

Valbonesi M, Garelli S, IMcaconi L, Zerbi D, Celano I: Plasma exchange in t~

management of selected neurological diseases. Plasma Ther 2:13-18, 1981.

Asbury A, Fisher R, McKhann GM, Mobley W, Server A: Guillain-Barre syndrome:

Is there a role for plasmapheresis? Neurology (NY) 30:1 112, 1980.

Corachan M,,Talonu T, Oldfield E, Kaven 3, Flynn P: Treatment of acute severe

Guillain-Barre syndrome by plasmapheresis. Papua New Guinea Med 3 23:146-147,

1980.

Rail D, Stark R, Swash (M, Newlanfl A: Improvement in nerve condition after

plasma exchange for Guillain-Barre syndrome. 3 Neurol NeurosMg Psychiatry

43:1 147, 1980. CZ

Ropp~r AH, Sttaharti B, Huggins CE: Improvement in 4 patients with acute GullainBarre syndrome after plasma exchange. Neurology 30:361, 1980.

Tokya KV, Augspach R,, Besinger UA, Grabensee B: Treatment of myasthenia

gravis and Guillain-Barre syndrome with plasma exchange. In Sieberth HG (cd):

“Plasma Exchange. Plasm apheresis - PlasmaseFation.” Stuttgart: F.K.

Schattauer Verlag, 1980, pp 289-296.

Valbonesi M, ,Mosconi L, Garelli S, Zerbi D, Celano I: Successf~ treatment by

plasma exchange in GuiUain-Barre’ syndrome with immune complexes. Vox Sang

38:181-184, 1980.
ARC Blood Services

Bibliography

TPB 1-7

Levy RL, Newkirk R, Ochoa 3: Treatment of chronic Guillain-Barre’ syndrome by

plasma exchange. Lancet 2:741, 1979.

Levy RL, Newkirk R, Ochoa J: Treating chronic relapsing Guillain-Barr~ syndrome

by plasma exchange. Lancet 2:259-260, 1979.

E. Miscellaneous: Polyneuropathy, Motor Neuron Disease,

Amyotrophic Lateral Sclerosis

Dau P: Plasm apheresis in autoimmune necrologic diseases. In “Third AMI.Ial

Symposium on Apheresis: Current Concepts and Future Trends.” Skokie, IL:

American Society for Apheresis, 1981 (abstract).

Dau PC, Lindstrom JM, Denys EH: Plasmapheresis in necrologic disorders. In

Nemo G3, Taswell H (eds): “Proceedings of the Workshop on Therapeutic

Plasmapheresis and Cytapheresis, April 1979.” W=hington, DC: U.S. Department

of Health and Human Services, 1981, pp 169-197.

Dyck P3: Controlled trial of pkrna exchange on inflammatory demyelineating

neuropathy: Preliminary report. In “Third Annual Symposium on Apheresis:

Current Concepts and Future Trends.” Skokie, IL: American Society for

Apheresis, 1981 (abstract).

Maas AIR, Busch HFM, van der Heuf C: Plasma infusion and plasma exchange in

chronic idiopathic polyneuropathy. N Engl 3 Med 305:344, 1981.

Cook 3D, Tindall RAS, Walker J, et al: Plasma exchange as a treatment of acute

and chronic idiopathic autoimmune polyneuropathy: Limited success. Neurology

30:361-362, 1980.

Dechy H, et al: Plasmapheresis in the management of peripheral neuropathy in

dysglobulinemia and collagen disease. Rev Med Interne 1:219, 1980.

Keleman J, Hedlund H, Orlin 3B, Berkrnan EM, Munsat TL: Failure of partial

plasma exchange (PPE) and immunasuppression to effect the course of lower motor

neuron disease. Transfusion 20:649, 1980.

Mark B, Hurwitz BJ, Olanow CW, Fay 3W: Plasmapheresis in idiopathic inflammatory Polyradiculoneuropathy. Neurology 30:361, 1980.

Olarte MR, Schoenfeldt RS, McKiernan G, Rowlancl 1P: Plasmapheresis in

arnyotrophic lateral sclerosis. Ann Neurol 8:644-645, 1980.

Schauf CL, Antel 3P, Arnason BG, Davis FA, Rooney MW: Neuroelectric blockin

activity and plasmapheresis in arnyotrophic lateral sclerosis. Neurology (NY7

30:101 1-101,3, 1980.

Server AC, Stein SA, Braine H, et al: Experience with plasma exchange and

cyclophosphamide in the treatment of chronic relapsing inflammatory polyradiculoneuropathy. Neurology 30:362, 1980.

ARC Blood Services

Bibliography

TPB I-8

Si.lani V, Scarlato G, VaUi G, Marconi M: Plasma exchange ineffective in

amyotrophic lateral sclerosis. Arch Neurology 37:51 1-513, 1980.

Tokya KV, et ah Plasma exchange in pcdyradict.doneuropathy. Ann Neurol 8:205-

206, 1980.

Fowler H, Volpe M, Marks G, Egolf C, Dau PC: Recovery from chronic progressive

polyneuropathy after treatment with plasma exchange and cyclophosphamide.

Lancet 2:1193, 1979.

Monstad I, Dale I, Petlund CR, Sjaastad O: Plasma exchange in motor neuron

disease. A controlled study. J Neurol 221:59-66, 1979.

Norris FH Jr, Denys EH, Mielke CH: Plasmapheresis in amyotrophic lateral

sclerosis. In Dau PC (ed~ “Plasmapheresis and the Immunobiology of IMyasthenia

Gravis.” Bcston: Houghton IMifflin, 1979, pp 258-264.

Server AC, Lefkowith J, Braine H, McKhann GM: Treatment of chronic relapsing

inflammatory polyradictdomeuropathy by plasma exchange. Ann Neurol 6:258-261,

1979.

Vanderheyden 3E, Kennes B, Bain H, Hubert C, Neve P: Plasma exchange in acute

polyneuropathy. Acta Clin Belg 34:246, 1979.

.

Brettie RP, Gross M, Legg N3, Lockwood MC, PaUis C: Treatment of acute

polyneuropathy by plasma exchange. Lancet 2:1 100, 1978.

Elliott HL, McDougall AI, Hwe G, Curnming RLC, Gardiner RHE, Fell GS:

Plasmapheresis in the treatment of dialysis encephalopathy. Lancet 2:940-941,

1978.

Monstad I, Dale 1, Dethund CF, Sjaastaf O: Plasmapheresis in motor neurone

disease (MND): A controlled study. Acta Neurol Scand 57: Suppl 67:270-271, 1978.

Norris FH Jr, Denys EH, Mielke CH: Plasmapheresis in arnyotrophic lateral

scierosis. .Muscle Nerve 1:342, 1978.

Casper 3T, Varma RR, Lewis ID, et al: Exchange transfusica in Reye’s syndrome

with saline-washed red blocd cells. Transfusion 16:130-134, 1976. .>

Strauss RA, Kling TF, Levinsohn IMW, et al: Facilitation of exchange transfusions

with .Scribner shunts in Reye% syndrome. Am J Surg 131:772, 1976.
AMERICAN RED CROSS BLOOD SERVICES

Therapeutic Pheresis Bibliography No. II: Blcmd Diseases

ARC Blcmd Services

Bibliography

TPB II-2

A. Hemophilia

Erskine JG, Burnett AK, Walker ID, Davidson JF: Plasma exchange in nonhaemophiliac patients with inhibitors to factor VIII. Br Med J 283:760, 1981.

Slocombe GW, Newland AC, Colvin MP, Colvin BT: The role of intensive plasma

exchange in the prevention and management of hemorrhage in patients with

inhi~tors to Factor VIII. Br J Haematol 47:577-585, 1981.

R~ve\z T, M&yus 3, Goldschmidt B, Hars~yi V: Combined plasmapheres]s and

immunosuppression in hemophilia in a patient with antibodies. Orv Hetil 121:1753-

1754, 1980.

R&e~z T, M~tyus 3, Goldschmidt B, Hars~yi V: Control of Iife+threatening

bleeding by combined plasmapheresls and immunosuppressive treatment in a

hemophiliac with inhibitors. Arch Dis Child 55:641-643, 1980.

Schwerdtfeger R, Hinth G: Repeated intensive plasma exchange in a patient with

high levels of factor VIII inhibitor. In Sieberth HG (cd): “Plasma Exchange.

Plasmapheresis - Plasmaseparation.” Stuttgart: F. K. Schattauer Verlag, 1980, pp

323-326.

Spero 3A, Lewis JH, Hasiba U, Pierce 3M: Plasma exchange in preparation of mild

!actor IX deficient hemophiliacs for surgical procedures. Plasma Ther 1:19-22,

1980.

Wensley RT, Stevens RF, Burn AM, Delamore IW: Plasma exchange and human

factor VIII concentrate in managing hemophilia A with factor VIII inhibitors. Br

[Meal 3 281: 1388-1389, 1980.

CobCroft R, Tamagnini G, Dormandy KM: Serial plasmapheresis in a hemophiliac

with antibodies in FVHL 3 Clin Pathol 30:763-765, 1977.

iMibashan RS: (Management of patients with inhibitors: Replacement therapy

(including plasmapheresis). In “Workshop on Inhibitors of Factors VIH and IX.”

Vienna: Verlag, 1977, p 64.

Pineda AA, Brzica SM, Taswell HF: Continuous- and semicontinuous-flow bl~d

centrifuge systems: Therapeutic applications with plasma-, platelet-, Iympha-, and

eosimpheresis. Transfusion 17:407-416, 1977.

Tilz GP, Teubl I, Kopplhuber CH, Vollmann H, Lanzer G: Therapeutische

Plasm aphese: Eineneue Form der symptomatischen Therapic. Med Klin 71:1952-

1957, 1976.

Oon C3, Hobbs JR: Clinical applications of the continuous flow blood separator

machine. Clin Exp Immutol 20:1-16, 1975.

Stacher A, H&cker P, Pitterman E: Einsatzmoglischkeiten und Ergebuisse der

Anwendung eines Zellseparators in der Hamatologic. Wien Lied Wochensch

125:35-44, 1975.

Pittermann E, HUcker P, Lechner K, Stacher A: Plasmaphereses with the

continuous flow blood cell separator in the treatment of macroglobulinaemia,

multiple myelom+ hemophilia and hyperlipidaemia. In Goldman 3M, Lowenthal

RM (eds): “Leukocytes: Separation Collection and Transfusion.” London:

Academic Press, 1974, pp 576-577.

Edson JR, McArthur JR, Branda RF, LMccullough 33, Chou SN: Successful

management of a subdural hematoma in a hemophiliac with an anti-factor VIII

antibody. Blood 41:1 13-122, 1973.

Danilov 1P, Ivanov EP, Margolin AZ: Effect of exchange plasmapheresis on the

blood-coagulation m~hanism in hemophilia. Vestn Khir 106:1 17-121, 1971.

Fischer M, Krenn 3, Lechner K, Steinbereithner K, Vonkilch E: The importance of

plasma-pheresis during intensive postoperative care in hemophilia. Anaesthesist

17:72-76, 1%8.

Abduliaev GM, Mailer AR, Kozhevnikov IN: On the use of plasma obtained by the

plasmapheresis method in hemophilia A. Probl Gematol Pereliv Krovi 11:15-19,

1966.

Borucki DT, Peterson CA: Plasmapheresis in hemophilia utilising angle head

centrifugation, a new parameter in blood component therapy. Proceedings IOth

Congress International Society Blood Transfusion, Stockholm, 1965, pp 1210-1213.

B. Autoimmune Hemolytic Anemia

Besa EC, Ray PK, Swami VK, IdicuUa A, Rhoads 3E, Bassett 3G, Joseph RR,

Cooper DR: Specific immunoadsorption of IgG antibody in a patient with chronic

Iymphocytic-leukemia and aut-immune hemolytic-anemia - a new form of therapy

fcr the acute critical stage. Am 3 Med 71:1035- 1040, 1981.

Bernstein ML, Schneider BK, Naiman 31: Plasma exchange in refractory acute

autoimmune hemolytic anemia. 3 Pediatr 98:774-775, 1981.

Garelli S, M=coni L, Valbones ,M, Schieppa G, Navassa G: Plasma-exchange for a

hemolytic crisis due to autoimmune hemolytic-anemia of the IgG Warm type. Blut

41:387-391, 1980.
ARC Blood Services

Bibliography

TPB H-3

Herrera A, Bernard 3F, Vroclans M, Dhermy D, Renoux M, Bolvin P: Intensive

plasm apheresis and erythropheresis, an emergency treatment of superacute autoimmune anemia. Nouv Presse Med 9:317, 1980.

Klein HG, Faltz 11, McIntosh CL, Appelbaum FR, Deisseroth AB, Holland PV:

Surgical hypothermia in a patient with a cold agglutinin: Management by plasma

exchange. Transfusion 20:354-357, 1980.

Orliw2JB, Berkman EiM, Matloff DS, Kaplan MM: Primary biliary cirrhosis and cold

autoimm une hemolytic anemiw Effect of partiaf plasma exchange. Gastroenterology 78:576-578, 1980.

Patten E, Reuter FP: Evans’ syndrome: Possible benefit from plasma exchange.

Transfusion 20:589-593, 1980.

Ruberto G, Gulinatti L, Pellegrino S, Ascari E: Plasmapheresis in the treatment of

autoimmune haemolytic anaemias. Haematologica 64:759-765, 1979.

Gilcher RO: Plasma exchange in immune and autoimmune diseases. Haemonetics

Research Institute, 1978.

Weleba K: The use of plasma exchange in AHA. Haemonetics Advanced

Component Seminar, Boston, 1978.

Nieburg PI, Stockman 3A III: Rapid correction of anemia with partial exchange

transfusion. Am 3 Dis Child 131:60, 1977.

Patten E, Reuter FP, Castle R, Mercer C: Evan’s syndrome: Benefit from plasma

exchange. American Association of Blood Banks 30th AMual Meeting, 1977,

Abstract S-34.

Taft EG, Propp RP, Sullivan SA: Plasma exchange for cold agglutinin hemolytic

anemia. Transfusion 17:173-176, 1977.

C. Aplastic Anemia

Messner HA, Fauser AA, Curtis 3E, Dotten D: Control of antibody-mediated pure

red-cefl aplasia by plasmapheresis. N Engl 3 Med 304:1334-1338, 1981.

Fitchen 3H, et al: Antibody-mediated aplastic anemia with recovery after

exchange plasmapheresis. Am 3 Med (in press), 1980.

Fitchen 33, Cline LMJ, Saxon A, Golde DW: Serum inhibitors of hematopoiesis in a

patient with aplastic anemia and systemic lupus erythematosus: Recovery after

exchange plasm apheresis. Am J Med 66:537, 1979.

Messner HA, Fauser AA, Curtis JE, et al: Control of pure red cell aplasia by

repeated plasm apheresis. Blood 54:71 A, 1979.

Marmont AM, Damasio EE, Bacigalupo A, Giordano D, Rose E, Reali G, Gay A,

Dagna-Bricarelli F, Brema F, Carelloam Santini G: A to O bone marrow

transplantation in severe aplastic anemia: Dynamics of blood group conversion and

demonstration of early dyserythropoiesis in the engrafted marrow. Br J Haematol

36:51 1-518, 1977.

ARC Blood Services

Bibliography

TPB 11-4

D. [mmme Thrombocytopenic Purpura

Buskard NA, Grossman L, Shematek G: Plasma exchange for the treatment of

immune thrombocytopenia. In Borberg H, Reuther P (eds): “Plasma Exchange

Therapy.” Stuttgart: Georg Thieme Verlag, 1981, pp 220-223.

LeRoux G, Pourriat 3L, Lapan&y C, Aufeuvre JP, LeFoch A, Baudelet 3,

Lortholary P: Post-transfusion R~rpura. Report of a case: Treatment by plasma

exchange and transfusion of PI negative platelets. Rev Fr Transfus Immunohematol 24:21 1-219, 1981.

Marder VJ, Nusbacher J, Anderson FW: One-year follow-up of plasma exchange

therapy in 14 patients with idiopathic thrombocytopenic pmpura. Transfusion

21:291-298, 1981.

Taft EG: Apheresis in platelet disorders. Plasma Ther 2:181-209, 1981.

Taft EG: Plateletpheresis in the treatment of thrombocythemia. In Nemo GJ,

Taswell H (eds): “Proceedings of the Workshop on Therapeutic Plasmapheresis and

Cytapheresis, April 1979.” Washington, DC: U.S. Department of Health and

Human Services, 1981, pp 85-99.

Blum SF, Lessig IMA: Plasmapheresis in quinidine purpura. ~ssma Ther 1:65, 1980.

Weir AB, Peon M-C, ,McGowan EI: Plasma exchange in idiopathic thrombocytopenic purpura. Arch Intern ,Med 140:1 101-1103, 1980.

Branda RF: Plasma exchange in the treatment of immune thrombocytopenia.

Plasma Ther 1:43-48, 1979.

Buskard NA, Shematak G, Grossman L, et al: Failure of plasma exchange to

improve immune thrombocytopenia. Blood 54:108a, 1979.

Novak R, Willim= 3: Plasmapheresis in catastrophic complicaticm of idiopathic

thrombocytopenic purpura. J Pediatr 92:434, 1979.

Nusbacher J, Marder VJ, Anderson FW: Long-term follow-up of 15 patients with

idiopathic thrombocytopenic pupura (ITP) treated by plasma exchange. ,~ransfusion 19:666-667, 1979.

Branda RE, Tate DY, ~McCullough JJ, Jacob HS: Plasma exchange in the treatment

of fulminant idiopathic (autoimmune) thrombocytopenic purpura. Lancet 1:688-

690, 1978.

Gandolfo GM, Afeltra A, Ferri GM: Plasmapheresis for thrombocytopenia. Lancet

1:1095, 1978.

Gilcher RO: Plasma exchange in immune and autoimmune diseases. Haemonetics

Research Institute, 1978.
ARC Blood Services

Bibliography

TPB II-5

ARC Blood Services

Bibliography

I TPB II-6 mNJ Al

o

I

al cd

I

. .

43

r’

w

Larison 3, Fatteh MM: Plateletpheresis as a preventive measure to complications

of asymptomatic cases of idiopathic thrombocythemia. J Med Assoc GA 67:296-

297, 1978.

Marcler V3, Nusbacher J, et al: Results of plasma exchange in six patients with

idiopathic thrombocytopenic purpura (ITP): A mixed bag. Blood (suppl) 52:167,

1978.

McLepd BC, W u KK, Knospe W H: Plasmapheresis in thrombocytopenia. Clin Res

26:7(1A, 1978.

Novak R, WiUimas 3: Plasmapheresis in catastrophic complications of idiopathic

thrombocytopenic pupura. 3 Pediatr 92:434-436, 1978.

Okuno T: Phsrnapheresis fm ttrombocytopenia. Lancet 1:1095, 1978.

Patten & Reuter FP, Castle R, Mercer C: Evans’ syndrome: Benefit from plasma

exchange. Transfusion 18:383, 1978.

Weir AB Jr, Peon MC, McGowan Ek Plasma exchange f m idiopathic tlrombcytopenic pwpura. Lancet 2:689, 1978.

Gofodetsk~ VM, Pashkov W, Rogova EM: Replacement therapy in acute nonimmune thrombocytopeni~ Ter Arkh 48:127-130, 1976.

Howard JE, Glassberg AB, Perkim? HA: Post-transfusion thrombocytopenic purpur= A case report. Am J Hematol 1:339-34A 1976.

Abramson N, Eisenberg PD, Aster RH: Poattransfusion purpura: Immmologic

aspects and therapy. N Engl J Med 291:1163, 1974.

Cimo PL, Aster RH: Post-transfusion purpura: Successful treatment by plasma

exchange. N Engl 3 Med 287:290-292, 1972

Berglund G: Plasma tramfusion of six Childen with idiopathic thrombocytopenic

pupura. Acta Pediatr 51:523, 1962.

E. Ttrombotic Thrombocytopenic Wrpura, Hemolytic Uremic Syndrome

Beattie T], Murphy AV, Willoughby MLN, MaChin S3, Defreyn G: Plaamapheresis in

the haemolytic-uraemic syndrome in children. Br Med 3 282:1667-1668, 1981.

Byrnes 33: Plasma infusion in the treatment of thrombotic thrombocytopenic

purpura. Semin Thromb Hemmtas 9:9-14, 1981.

Case DC 3r: Plasma therapy fcx thrombotic thrombocytopenic purpura. Blood

58:409, 1981.

Chen Y-C, McLeod B, Hall ER, WU KK: Accelerated prostacyclin degradation in

thrombotic thrombocytopenic purpura. Lancet 2:267-269, 1981.

Cooper MR, et al: Intensive plasma exchange in thrombotic thrombocytopenic

purpura (lTP). NC Med J 42:403-404, 1%1.

Crain SM, Choudhuy AM: Thrombotic thrombocytopenic purpura. JAMA

246:1243-1246, 1981.

Frankel AE, Rubenstein MD, Wall RT: Ttrombotic thrombocytopenic purpura:

Prolonged coma with recovery of necrologic function with intensive plasma

exchange. Am J Hematol 10:387-390, 1981.

Gottschall JL, Pisciotta AV, Darin J, Hussey CV, Aster RH: Thrombotic

thombocytopenic ~rpura: Experience with whole blood exchange transfusion.

Semin Thromb Hemoatas 7:25-32, 1981.

Kohn D, et al: Tlrombotic ttrombocytopenic purpura with a subacute course:

Remission after steroids and high-dose plasma exchange. Isr J Med 17:283-285,

1981.

Myers T3: Treatment of tl’rorrdmic ttrombocytopenic purpura with combined

exchange plasmapheresis and anti-platelet agents. Semin Thromb Hemostas 7:37-

42, 1981.

Sweny P, ● t al: Plasrnapheresis in the haemolytic-uraemic syndrome in children.

Br Med J (Clin Res) 282:2137, 1981.

Taft EG, Baldwin ST: Plasma ● xchange transfusion. Semin Ttromb Hemostas 7:15-

21, 1981.

tiowski RM, Hewlett 3S, LWas F: Plasmapheresis in the treatment of thrombotic thrombocytopenic pmpura. Clin Res 28:306A, 1980.

Harden LB, Gluck RS, Salcedo JR: Simultaneous hemodialysis and exchange

transfusion in hemolytic uremic syndrome. Cf.in Pediatr 19:640-642, 1980.

MaChin SJ, Defreyn G, Chamone DAF, Vermylen 3: Plasma 6-keto-PGF1 levels

after plasma exchange in thrombotic thrombocytopenic purpura. Lancet 2:661,

1980.

McLeod BC, Wu KK, Knospe WH: Plasmapheresis in thrombotic thrombocy{&enic

pupura. Arch Intern Med 140:1059-1060, 1980.

l~isiani R, Trevisan F, Lkiarchesi D, Bertani T, Remuzzi G, tMeCCa G: Plasmapheresis and plasma infusion in the treatment of hemolytic-uremic syndrome. In

Remuzzi G, Mecca G, de Gaetano G (eds): ‘7-lemostasis, Prostaglandins and Renal

Disease.” New York: Raven, 1980, pp 423-431.

Myers T3, Wakem CJ, Ball ED, Tremont S3: Thrombotic thrombocytopenic

pmpur~ Combined treatment with plasmapheresis and antiplatelet agents. Ann

Intern Med 92:149-155, 1980.

Rossi EC, del Greco F, Kwaan HC, Lerman BB: Hemodialysis-exchange transfusion

for treatment of thrombotic thrombocytopenic purpura. 3AMA 244:1466- 1468,

1980.
ARC Blood Services

Bibliography

TPB II-7

Sacher RA: Plasmapheresis in TTP-clearance of immune complexes. Transfusion

20:118-119, 1980.

Seger R, Joller P, Baerlocher K, Kenny A, Dulake C, Leumann E, Spierig M, Hitzig

W1-k Hemolytic-uremic syndrome associated with neurarninidase-producing micr~

organisms: Treatment by plasma exchange. Helv Paediatr Acta 35:359-367, 1980.

Vialtel P, Chenais F, Dechelette E, Elsener M, Bayle F, Cordonnier D: Adult

hem~ytic uremic syndrome treated with plasma exchange. Plasma Ther 1:51-54,

1980.

Walker BK, Balks SK, Martinez 3: Plasma infusion fcf thrombotic thromb

cytopenic pupura during pregnancy. Arch Intern Med 140:981-983, 1980.

Yogore MG, Chawla MS, Kasprisin DO: Plasma exchange in a case of ttrombotic

thrombocytopenic pmpura and suspected acute systemic lupus erythematoaus.

Plasma Ther 1:23-25, 1980.

AUoatti S, et al: Use of hemofiltration in ‘difficult’ uremic patients. Minerva

Nefrol 26:365-374 1979 (English abstract).

Bukowski RM, Hewlett 3S, Reimer RR, ● t al: Plasmapheresis in the treatment of

thrombotic thrombocytopenic pqmra (TTP). Blood 54: Suppl 1, 235a, 1979.

Byrnes 33, Khurana M: Treatment of ttrombotic thrombocytopenic purpura with

plasma. N Engl J Med 297:1386-1389, 1979.

Okuno T, KOSOVa L: Plasrnapheresis for ttwombotic thrombocytopenic purpura

(TTP). Transfusion 19:342-344, 1979.

Plasma exchange in tlrombotic ttrombocytopenic purpura. Lancet 1:1065-1066

(editorial), 1979.

Ryan PF, Cooper 1A, Firkin K: Plasrnapheresis in the treatment of ttrombotic

thrombocytopenic pupurw A report of five cases. Med 3 Aust 1:69-72, 1979.

Stern R, Cornell C3 Jr, Beck R, Smith RE: Ttrombotic thrombocytopenic purpura:

Failure of plasma infusion and antiplatelet agents. Ann Intern Med 90:989, 1979.

Taft EG: Thrombotic ttrombocytopenic purpura and dose of plasma exchange.

Blood 54:842-849, 1979.

Vialtel P, Chenais F, Dechelette E, Bayle F, Couderc P, Cordonnier D: Adult

hemolytic uremic syndrome successfully treated with plasma exchange. Kidney Int

15:453, 1979.

Vialtel P, Chenais F, Dechelette E, Bayle F, Couderc P, Cordonnier D: Hemolyticuremic syndrome of adults successfully treated with massive plasmapheresis

(proceedings). J Urol Nephrol (Paris) 85:331-332, 1979.

Yang C, Nussbaum M, Park H: Timxnbotic ttrombocytopenic purpura in early

pregnancy: Remission after plasma exchange. Acta Haematol 62:112-116, 1979.

ARC Blood Services

Bibliography

TPB II-8

Abramson N: Treatment for thrombotic thrombocytopenic pt.rpur~ Plasma,

vincristine, hemodidysis and exchange transfusims. N E@ 3 Med 298:971-972,

1978.

Araell 3, Beaser RS, Pechet L: Tkombotic ttrombocytopenic purpura fails to

respond to fresh frozen plasma infusion. Ann Intern Med 89:647-648, 1978.

Bukowski RM, Hewlett 3S, King 3: Plasrnapheresis in ttrombotic thrombocytopenic

pmpura (TTP). Blood 51:561, 1978.

Bymes 33, Khurana M: Treatment fw tlrombotic ttrombocytopenic purpura:

Plasma, hernodialysis and exchange transfusions. N Engl J Med 298:291, 1978.

Hanzlick RL, Shah NT, Senhauser DA: Treatments fcr thrombotic thrombocytopenic ptrpura, plasma, vincristine, hernodialysis and exchange transfusions.

N Engl J Med 298:971, 1978.

Reiss R, Shah V, Kalter R, Panlilio A: Plasmapheresis in ttrombotic thrombocytopenic pupura (TTP). Blood 51:560-561, 1978.

Rossi EC, del Greco F: Treatment of ttrombotic tlrombocytopenic purpura with

hemodialysis and exchange transfusion. N Engl J Med 298:974 1978.

Taylor I-L, Gal K: TTP treated with therapeutic pheresis. Transfusion 18:599,

1978.

Bukowski RM, King 3W, Hewlett 3S: Plasmapheresis in the treatment of

thrombotic thrombocytopenic ptrpura Blood 50:413-417, 1977.

Fisher WB: Exchange transfusion in acute ttrombotic ttrombocytopenic purpura:

Case repon. Milit Med 142:789-790, 1977.

Pisciotta AV, Garthwaite T, Darin 1, Aster RH: Treatment of tlrombotic

thrombocytopenic pvpura by exchange transfusion. Am J Hematol 3:73, 1977.

Bukowski RM, Hewlett 3S, Harris JW, Hoffman GC, Battle JD Jr, Silverblatt E,

Yang k Exchange transfusions in the treatment of thrombotic thrombocytopenia

purpura. Semin Hematol 13:219-232, 1976.

Pisciotta AV, Garthwaite T, Darin 3, et al: Treatment of thrombotic tl&mcytopenic pwpura Semin Hematol 13:219-232, 1976.

Rubenstein MA, Kagan BM, MacGillviray MH, Reuben M, Sacks H: Unusual

remission in a case of thrombotic thrombocytopenic pmpura syndrome following

fresh blood exchange transfusions. AM Intern tMed 51:1409-1419, 1959.

F. Sickle Cell Disease

Fullerton JAW, Philippart AI, Sarnaik S, Lusher JM: Preoperative exchange

transfusion in sickle celi anemia. J Pediatr Surg 16:297-300, 1981.
ARC Blood Services

Bibliography

TPB II-9

ARC Blood Services

Bibliography

TPB II-10

Goldfinger D: Erythrocytapheresis in the management of sickle cell disease. In

“Third AMual Symposium on Apheresis: Current Concepts and Future Trends.”

Skokie, IL: American Society for Apheresis, 1981 (abstract).

Haruda F, et al: Rapid resolution of crganic mental syndrome in sickle cell anemia

in response to exchange transfusion. Neurology 31:1015- 1016, 1981.

Kleinman R, Thompson-Breton R, Breen D, Hurvitz C, Goldfinger G: Exchange red

blo~. cell transfusion in a pediatric patient with severe complications of sickle cell

anemia. Transfusion 21:443-446, 1981.

Nagey DA, Garcia 3, Welt Sk lsovolumetric partial exchange transfusion in the

management of sickle cell disease in pregnancy. Am 3 Obstet Gynecol

141:403-407, 1981.

Rossof AH, McLeod BC, Holmes AW, Fried W: Intrahepatic sickling crisis in

hemoglobin SC disease. Management by partial exchange transfusion. Plasma Ther

2:7-11, 1981.

Davis K, Thorp D, Taylor A, Dart G, Taylor A: Red cell exchange in sickle cell

disease. Plasma Ther 1:27-32, 1980.

Key TC, Horger EP, Walker EM, Mitchum EN: Automated erythrocytopheresis for

sickle cell anemia during pregnancy. Am J Obstet Gynecol 138:731, 1980.

Klein HG, Garner R3, Miller DM, Rosen SL, Stathm NJ, Winslow RM: Automated

partial exchange transfusion in sickle cell anemia. Transfusion 20:578-584, 1980.

Miller DM, Wimlow RM, Klein HG, Wilson KC, Brown FL, Statham NJ: Improved

exercise performance after exchange transfusion in subjects with sickle cell

anemia. Blood 56:1127-1131, 1980.

Sheehy TW, Law DE, Wade Bi-k Exchange transfusion for sickle cell intrahepatic

cholestasis. Arch Intern Med 140:1364-1366, 1980.

Keeling MM: Experiences with red blood cell exchange in sickle cell disorders in

pregnancy. In “First AMual Apheresis Symposium: Current Concepts and Future

Trends.” Chicago: American Red Cross Blood Services, 1979, pp 97-102.

Kleinrnan S, Thompson-Breton R, Rifkind S, et al: Exchange red blood cell pheresis

in the management of compli=tions of sickle cell anemia. Haemonetics Research

institute Advance Component Seminar, Boston, 1979.

Rifkind S, Waisman 3, Thompson R, Goldfinger D: RBC exchange pheresis fcr

priapism in sickle cell disease. 3AMA 242:2317-2318, 1979.

Davey R3, Espcaito DJ, 3acobsen R3, Corn M: Partial exchange transfusion as

treatment for hemoglobin SC disease in pregnancy. Arch Intern Med 138:937, 1978.

Lanzowsky P, Shende A, Karayalcin G, Kim YJ, Abelli AM: PartisJ exchange

transfusion in sickle cell anemia. Am 3 Dis Child 132:1206- 1208, 1978.

Kernoff LM, Botha MC, Jacobs P: Exchange transfusion in sickle cell disease using

a continuous-flow blood cell separator. Transfusion 17:269-271, 1977.

Morrison 3C, Wiser WL: The use of prophylactic partial exchange transfusion in

pregnancies associated with sickle cell hemoglobulinopathies. Obstet Gynecol

48:516-520, 1976.

Perkim RP: Partial exchange transfusion in a pregnant patient with sickle cell

anemia. Obstet Gynecol 48:22 -24S, 1976.

Green M, Hall RJC, Htmtsman RG, Lawson A, Pearson TC, Wheeler CG: Sickle

cell crisis treated by exchange transfusion: Treatment of two patients with

heterozygous sickl~cell syndrome. 3AMA 231:948-950, 1975.

Morrison JC, Whybrew WD, Bucovaz ET: Use of partial exchange transfusion

preoperatively in patients with sickle cell hemoglobinopathies. Am 3 Obstet

Gynecol 132:59-63, 1973.

Brody 31, Goldsmith MH, Park SK, Soltys HD: Symptomatic crises of sickle cell

anemia treated by limited ● xchange transfusion. Ann Intern Med 72:327-330, 1970.

Buckle AER, Price TML, Whitrnore DN: Exchange and simple transfusion in sickle

cell diseases in pregnancy. Postgrad Med J 45:722-725, 1969.

Ricks P Jr: Further experience with exchange transfusion in sickle cell anemia and

pregnancy. Am 3 Obstet Gynecol 100:1087-1091, 1968.

Anderson R, Czssell M, Mullinax GL, Chaplin H: Effect of normal cells on

viscosity of siclcbcell blood In vitro studies and report of six years’ experience

with a prophylactic program of “partial exchange transfusion.” Arch Intern !Med

111:286, 1963.

G. Leukemi4 Myeloproliferative Syndrome, Se’my Syndrome

Bongiovanni LMB, Katz RS, Tom=zewski JE, Ziselman EM, Goldwein ,MI, Wurzel

HA: Cytapheresis in a patient with Sezary syndrome. Transfusion 21:332-334,

1981.

Cuttner J, Meyer R3, Ambinder EP, Greenberg ML, Button G, HollaHU 3F:

Leukapheresis in acute myeloblastic leukemia. In Nemo GJ, Taswell H (eds):

“Proceedings of the Workstxip on Therapeutic Plasmapheresis and Cytapheresis,

April 1979.” Washington, DC: U.S. Department of Health and Human Services,

1981, pp 29-43.

Durkalec 3, et al: Repeated Ieukapheresis in a pregnant woman with myelocytic

leukemia. Pol Tyg Lek 36:449-450, 1981 (English abstract).

Graubner M, et al: Discontinuous cell separation as depletion therapy in chronic

Ieukemias. Onkologie 4:162-167, 1981 (English abstract).

Imamura N, Okada K, Karamoto A: Recommendation of Ieukapheresis as well as

combination chemotherapy of adult T-cell leukemia. Transfusion 21:471, 1981.
ARC Blood Services

Bibliography

TPB 11-11

Karp DD, et ak Chronic granulocyte leukemia with respiratory distress. Efficacy

of emergency Ieukapheresis. Arch Intern Med 141:1353-1354, 1981.

Klose H3, et al: Initial treatment of acute childhood leukemia with extreme

Ieukocytosis by blood exchange transfusion - theological aspects. Klin Padiatr

193:172-176, 1981 (English abstract).

M&l A, et al: Plasmapheresis in patients with leukaemia, multiple myeloma and

imm$me complex diseases. Haematologia (Budap) 14:49-56, 1981.

Shende A, Festa R, Honigman, Lanzkowsky P: Exchange transfusion as a treatment

for hyperleukocytosis, anemia, and metabolic abnormalities in patients with

leukemia. J Pediatr 98:852, 1981.

v

Baidurin SA, Khoroshko ND, Polianskaia AM, Kalinin NN, Pashitin AN: use o f

Ieukopheresis in chronic myeloleukemia. Sov Med 10:55-58, 1980.

Cohen 3, et al: Plasma exchange in treatment of leuCocytoclastic vasculitis. 3 R

Soc Med 73:457-460, 1980.

Goldfinger D, Capostagno V, Lowe C, Sacks H3, Gatti RA: Use of long-term

Ieukapheresis in the treatment of chronic Iymphocytic leukemia. Transfusion

20:450-454, 1980.

Hamblin T, Gordon J, Stevenson F, Stevenson G: Reduction of blocking factor to

immunotherapy by plasma exchange. In Sieberth HG (edh ‘

f

Plasma Exchange.

Plasmapheresis - Piasmaseparation.m Stuttgart: F. K. Schattauer Veriag, 1980, pp

387-391.

Harrer S, H6cker P, Pittermann E: Rapid regression of papilledema under

leukapheresis therapy in chronic myelosis (author’s transl). Klin Monatsbl Augenheilkd 176:823-825, 1980.

Hester 3: Cytopheresis in the management of leukemia. In “Second Amual

Apheresis Symposium: Current Concepts and Future Trends.” Skokie, IL: American Society for Apheresis, 1980, pp 111-116.

Karnen BA, Summers CP, Pearson HA: Exchange transfusion as a treatment for

hyperleukocytosis anemia, and metabolic abnormalities in a patient with leukemia.

3 Pediatr 96:1045-1046, 1980.

Lane TA: Continuous-flow Ieukapheresis for rapid cytoreduction in leukemia.

Transfusion 20:455-457, 1980.

M&i A, FiJst G, Hars&yi V, Natonek K, Poros A, Szabo’ J, Holl& SR: Plasmapheresis in patients with leukaemia, multiple myeloma and immune complex

diseases. Acta Haematol Pol 11:165-171, 1980.

Orlin 3B, Berkmm EM: Improvement of platelet function following plateletpheresis in patients with myeloproliferative diseases. Transfusion 20:540-545,

1980.

ARC Blood Services

Bibliography

TPB II-12

Revuz J, Mannoni P, Touraine % Long-term disease free, survival of S&y

syndrome obtained by leukapheresis. 3 Invest D~atol 74:448, 1980.

Winkelman RK, Pineda A: Leukapheresis for S&WY syndrome. In %cond AMUSLI

Apheresis Sympoaium: Current Concepts and Future Trends.n Skokie, IL: American Society for Apheresis, 1980, pp 83-89.

BaUas SK, Kiesel JK: Leukapheresis for hyperviscosity. Transfusion 19:787, 1979.

C-pentieri U, Patten EV, Chamberlain PA, Young AD, Hitter MIL Leukapheresis in

a 3-year-old child with Iymphoma in leukemic transfccmation. J Pediatr 94:919-

921, 1979.

Cooper IA, Ding 3C, Adarns PB, Quim MA, Brettell M: Intensive Ieukapheresis in

the management of cytopeniaa in patients with chronic Iymphocytic leukaemia

(CLL) and Iymphocytic lymphoma= Am J Hematol 6:387-398, 1979.

Cutmer J, Meyer RJ, Ambinder EP, Greenberg ML, Button G, Holland 3F:

Therapeutic leukapheresis in acute myelogenous Ieukemi& [n “First Amual

Apheresia Symposium: Current Concepts and Future Trends:’ Chicago: American

Red Cross Blood Services, 1979, pp 127-143.

Fay JW, Moore JO, Logue GLj Huang AT: Leukopheresis therapy of leukemic

reticu.loendot~liosis (hairy cell leukemia). Blood 54:747-749, 1979.

Bell R, Sullivan JR, Hurley TH, D’Apice AJ, Kincaid-Smith R Some uses of the

contimous flow blood separator in the myeloproliferative syndrome. Aust NZ 3

Mad 8:433-435, 1978.

CapIan SN, Coco FV, Berkman EM: Management of chronic myelocytic leukemia in

pregnancy by cell pheresis. Transfusicm 18:120-124, 1978.

Eisenstaedt RS, Berkman EM: Rapid cytoreduction in acute leukemia Management of cerebral Leukostasis by cell pheresis. Transfusion 18:113-115, 1978.

Goldfinger D, Capostagno V, et al: Long-term leukapheresis as therapy for chronic

Iymphocytic leukemia. Transfusion 18:625, 1978.

Greenberg ML, Ambinder EP, Grant S, Meyer R3, Paster J: A cytokinetic effect of

Ieukapheresis in leukemic patients. Cell Kinetics Society 2nd AMUd ~eting,

1978.

Meyer RJ, Cuttner 3, Truog P, Ambinder EP, Holland 3F: Therapeutic leukopheresis of acute myel-monocytic leukemia in pregnancy. Med Pediatr Oncol

4;77-83, 1978.

Taft EG, et al: Leukapheresis in the management of high count Ieukemi&

Transfusion 18:625, 1978.

Capostagno V, KUZ L, Gatti RA, Goldfinger D: Effect of a three phase

Ieukapheresis program fff the management of chronic Iymphocytic leukemia.

Blood 50:216, 1977.
ARC Blood Services

Bibliography

TPB II-13

ARC Blood Services

Bibliography

TPB II-14

Glaser E: Separation and filtration of granulocytes and other substances which

have qualities that contribute to the therapy of Ieucosis. Bilt Hematol Transfuz

5:31-36, 1977.

Kawashima K, Ueda R: Leukapheresis of patients with acute leukemia and chronic

myelogenous leukemia. Rinsho Ketsueki 18:620-626, 1977.

Kobayashi S: Leukapheresis. A. Treatment of chronic myelogenous leukemia.

Rim@ Ketsueki 18:615-620, 1977.

Lowenthal RM: Chronic Ieukaemias: Treatment by Ieucapheresis. Exp Hematol 5:

kIpji 73-84, 1977.

Meyer RJ, et al: Effect of Ieukapheresis on remission induction with chemotherapy

in patients with acute myelocytic leukemia (AML). Blood 50 (Suppl 1):199, 1977.

Stirling ML, Parker AC, Keller A3, Urbaniak S2: Leukapheresis for papilloedema in

chronic granulocytic Ieukaemia. Br Merf J 2:676, 1977.

Forttny IE, Hadlock DC, Kennedy B3, Theologies, McCullough J: The role of

continuous flow centrifuge Ieucapheresis in the management of chronic lymphocytic leukemia. Br J Haematol 32:609-615, 1976.

Huestis DW, Price MJ, White RF, ●t al: Leukapheresis of patients with chronic gr~~qtic leukemia (CGL), using the Haemonetics blood processor. Transfusion

16:255-260, 1976.

Hadlock DC, Forttny IE, McCullough 3, Kennedy BJ: Continuous flow centrifuge

leucapheresis in the management of chronic myelogenous Ieukaemia. Br J

Haematol 29:443-453, 1975.

H6cker P, Pittermann E, Gobets M, Pawlowsky J, Flegel U, Stacher A: The use of

the cell separator in the treatment of leukemia. Folia Haernatol (Leipz) 102:283-

294, 1975.

Hocker P, Pitterman E, Gobets M, Sticher A: Treatment of patients with chronic

myeloid leukemia (CML) and chronic Iymphocytic leukemia (CLL) by leukapheresis

with a continuous flow blood cell separator. In Goldman JM, Lowenthal RM (eds):

“leukocyte= Separation Collection and Transfusion.” London: Academic Press,

1975, pp 510-518.

Huestis DW, Corrigan JJ Jr, Johnson HV: Leukapheresis of a five-year-old girl

with chronic granulocytic leukemia. Transfusion 15:489-490, 1975.

Lowenthal RM, Buskard NA, Goldman JM, Spiers AS, Bergier ‘N, Graubner M,

Galton DA: Intensive Ieukapheresis as initial therapy for chronic granulocytic

leukemia. Blood 46:835-844, 1975.

Edelson ~ F=ktor M, Andrews A, Lutzner M, Schein P: Successful management

of the Sezary syndrome: Mobilizatim and removal of extravascular neoplastic T

cells by Ieukapheresis. N Engl J Med 291:293-299, 1974.

H&ker P, Pittermann E, Gobets M, Haist B, Gazda M, Stacher A: Therapeutic,

functional and kinetic aspects of Ieukopheresis therapy in chronic lymphatic

leukemia. Blut 28:396-410, 1974.

Wheeler TG, McCredie KB, Freireich EJ, Daniels TV: [ncreased efficiency of

leukocyte collection from patients with chronic myelocytic leukemia. Transfusion

14:253-256, 1974.

Fcm.my IE, Crandall L, McCullough J, et al: Leukapheresis in the management of

chroNc leukemia. Minn Med 56:674-676, 1973.

Sakalova’ A; Ga%a’ S, Hrubi(ko M, G~ikovs’ J: Clinical utilization of plasmapheresis and cyclophoaphamide in the treatment of malignant Iymphoproliferative

processes. NeopIasma 20:335-339, 1973.

VaUejcs CS, McCredie KB, Brinin GM, Freireich EJ: Biological effects of

repeated Ieukapheresis of patients with chronic myelogenous leukemia Blood

42:925-933, 1973.

Curtis JE, Hemh EM, Freireich EJ: Leukapheresis therapy of chronic Iymphocytic

leukemia. Blood 39:163-174, 1972

Reich L, (YHara K, Stoeringer P, Clarkson B: Effect of massive Ieukapheresis on

proliferation in AML. Proc AACR 12:25, 1971.

Sm~ik S, Filon’ J: Plasmapheresis a an auxiliary method in the immtmotherapy of

chronic myelosis. Cas Lek Cesk 109:246-250, 1970.

Buckner D, Graw RG Jr, Eisel RJ, Henderson ES, Perry S: Leukapheresis by

continuous flow centrifugation (CFC) in patients with chronic myelocytic leukemia

(CML). Blood 33:353-369, 1%9.

Morse EE, Carbonne PP, Freireich EJ, Bronson W, Kliman A: Repeated 1eukapheresis of patients with chronic myelocytic leukemia. Transfusion 6:175, 1966.

Bierman HR, Marshall GJ, Kelly KH, Byron RL: Leukapheresis in m~. III.

Hematologic observations in patients with leukemia and myeloid metaplasia. Blood

21:164, 1963.

H. Thrombocytosis

Belloni M, Fabris F, Ongaro G, Girolami A: Therapeutic ttwombocytapheresis in a

case of thrombocytosis. Transfusion 21:229-230, 1981.

Taft EG: Apheresis in platelet disorders. Plasma Ther 2:181-209, 1981.
ARC Blood Services

Bibliography

TPB II-15

Taft EG: Piateletpheresis in the treatment of thrombocythemia. In Nemo GJ,

Taswell H (eds): “Proceedings of the Workshop on Therapeutic Plasrnapheresis and

Cytapheresis, April 1979.” Washington, DC: U.S. Department of Health and

Human Services, 1981, pp 85-99.

Beard MEJ, Blacklak HA, Varcoe AR: Control of tlrombocytosis by plateletpheresis using a cell separator. NZ Med J 91:136-138, 1980.

Taft EG: Management of ttrombccytosis. Transfusicm 20:235-236, 1980.

Goldfinger D, Thompson R, Lowe C, Kurz L, Belkin G: Long-term plateletpheresis

in the management of primary tlrombocyto+sis. Transfusion 19:336-338, 1979.

Orlin JB, Berkman EM: Plateletpheresis improves platelet function in myeb

proliferative disease. Transfusicm 19:667, 1979.

Goldfinger D, Kurz L, Lowe C, Thompson R, Belkin G: Failure of long-term

plateletpheresis to control primary tlrombocytosis. Transfusion 18:384, 1978.

Younger 3, Urnlas 3: Rapid reduction of platelet count in essential hemorrhagic

ttrombocythemia by discontinuous flow plateletpheresis. Am J Med 64:659-661,

1978.

Goldfinger D, Ktrz L, Lowe C, Thompson R, Belkin G: Failure of long-term

plateletpheresis to control primary thrombocytosis. American AsaocI“ation of Blood

Banks 30th Amual Mteting, 1977, Abstract $-39.

Taft EG, Babcock RB, Scharfman WB, Tartaglia AP: Plateletpheresis in the

management of ttwmbocytoais. Blood 50:927-933, 1977.

Greenberg BR, Watson-Williams E3: successful control of life-threatening thrornbocytoais with a blood processor. Transfusim 15:620-622, 1975.

Miller DS, Rundles RW, Silver DC: Hemorrhagic thrornbocythemisu Rapid

plateletpheresis by continuous flow blood cell separation. Clin Res 19:426A, 1971.

Colman RW, Sievers CA, Pugh RP: Thrombocytopheresi= A rapid and effective

approach to ttrombocytosis. 3 Lab Clin Med 68:389-399, 1966.

L Miscellaneous

Bada HS, Korones SB, Fitch CW: Reversal of altered cerebral hemodynamics by

plasma exchange transfusion in polycythemia Clin Res 29494A, 1981.

Chirnside A, et al: Coagulatiut abnormalities following intensive plasma exchartge

on the cell separator. Il. Effects on factors 1, II, V, VII, Viii, 1X, X and

antittrombin 111. Br 3 Haematol 48:627-634, 1981.

Erskine 3G, Burnett AK, Walker ID, Davidson JF: Plasma exchange in nonhaemophiliac patients with inhibitors to factor VIII. Br Med 3 283:760, 1981.

ARC Blood Services

Bibliography

TPB II-16

Gleich G3, Pineda AA, SoIley GO, Taswell HF: Cytapheresis for procurement of

eoainophils and for the treatment of diseases associated with eosinophilia. In Nemo

G3, Tasweil H (edsb “Proceedings of the Wcrkshop on Therapeutic Plasmapheresis

and Cytapheresis, April 1979.” Washington, DC: U.S. Department of Health and

Human Services, 1981, pp 73-79.

Quietzsch D, et al: Therapeutic plasmapheresis in the treatment of plasmacytoma.

Z Gexamte Inn Med 36:308-310, 1981 (English abstract).

Sciuicker KT: Exchange transfusion and ABO erythroblastosis. Crit Rev Clin Lab

Sci 14:21, 1981.

Anderson E, SkOv F, Hippe E: A case of cold haemoglobinuria with later

sarcoidosis. Treatment with plasmapheresis and immuncauppression. Scand J

Haematol 24:47-50, 1980.

Ladisch S, Ho W, Hartman G: Treatment of familial erythophagocytic lymphohistivtosis (FEL) by repeated plasma exchange. Clin Res 28:105A, 1980.

Taft E, Becker H, Hammer C, Sullivan S, Baldwin S: Apheresis in platelet disease

states. In Kasprisin DO, Vaithianathan T (edah “Proceedings of the Second AMUd

Apheresis Symposium/l Chicago, Mi&America Red Cross/Michael Reese Research

Foundation/Rush Presbyterian-St. Luke% Medical Center, 1980, pp 138-153.

Blackiock HA, Cleland JR, Tan P, Piilai VM: The hypereosinophilic syndrome and

Ieukapheresis. Ann Intern Med 91:650-651, 1979.

Gor@etstiy VM, Buachidze LN, Paahkov W, Labetskaia IA, Fomim 11: Blood

components in the treatment of myelotoxic agranulocytcisis and thrombopenia. Ter

Arkh 51*3-89, 1979.

Panlilio AL, Reiss RF: Therapeutic plateietpheresis in thrombocythemia. Transfusion 19:147-15Z 1979.

Scharfman WB, TiUotson JR, Taft EG, Wright E: Plasmapheresk for menim

gococcernia with disseminated intravascular coagulation. N Engl J Med 300:1277-

1278, 1979.

Cundall JR, Moore WH, Jenkins DE: Erythrocyte exchange in paroxysmal nocturnal

hemoglobunuria prior to cardiac surgery. Transfusion 18:626, 1978.

Landwehr DM, Evans PS, et al: Removal of immwte complexes by plasmapheresis

in patients with subacute bacterial endocarditis. Proc Int Cong Nephrol, Abstract

D33, 1978.

Ellrnan L, Lhdiller L, Rappepcct 3: Leukapheresis therapy of a hyperecasinophilic

disorder. JAMA 230:1004- 1005, 1974.

Vesel~ V: Erythro@eresis-contribution to the treatment of polycythemia Vnitr

Lek 19:183-189, 1973.

Gutnik RB: Plasmapheresis in the treatment of erythremia. Ter Arkh 40:1 16-118,

1968.

Fullerton WT, Turner AG: Exchange transfusion in treatment of severe anaemia in

pregnancy. Lancet 1:75, 1962.
AMERICAN RED CROSS BLOOD SERVICES ARC Blood Services

Bibliography

Therapeutic Pheresis Bibliography No. III: Malignant TPB III-2

Paraproteinemias

A. Hyperviscosity Syndrome

Ballas SK, Kiesel JK: Leukapheresis for hyperviscosity. Transfusion 19:787, 1979.

Buskard NA: Blood flow studies in the hyperviscosity syndrome before and after

plasma exchange. In Borberg H, Reuther P (eds): “Plasma Exchange Therapy.”

Stutt@t: Georg Thieme Verlag, 1981, pp 89-94.

Nusbacher 3: Plasmapheresis in the treatment of hyperviscosity syndrome and

paraproteinemia. In Nemo G3, TasweU H (eds): “Proceedings of the Workshop on

Therapeutic Plasmapheresis and Cytapheresis, April 1979.11 Washington, DC: U.S.

Department of Health and Human Services, 1981, pp 105-118.

Isbister 3P, Biggs 3C, Penny R: Experience with large volume plasmapheresis in

malignant paraproteinaemia and immune disorders. Aust NZ J Med 8:15*164,

1978.

Radovic M, Duric D, Trajkovi B, Radojicic B, Pekic B, Tomasevic R, Duji A:

Myeloma serum hyperviscosity syndrome treated with plasmapheresis. Med Pregl

30:471-476, 1977.

Loughrey JR, Meyer RL: Plasmapheresis in hyperviscpsity syndrome-a better

way? 3AMA 229:1211, 1974.

B. Macroglobulinemia

Reynolds WA: Late report of the first case of plasmapheresis for Waldenstr8m’s

macroglobulinemia. 3AMA 245:606-607, 1981.

Waldenstr6m JG: Plasmapheresis-bloodletting revived and refined. Acta Med

Scand 208:1-4, 1980.

Barbolla L, Fern&lez MN: Plasmapheresis in the treatment of Waldenstrtfm’s

macroglobulinaemia. Sangre (Bare) 23:334-34A 1978.

Buskard NA, Galton DA, Goldman 3M, Kohner EM, Grindle CF, Newman DL, Twinn

KW, Lowenthal RM: Plasma ● xchange in the long-term management of

Waldenstr&m’s macroglobulinemia. Can Med Assoc 3 117:135-137, 1977.

Plasmapheresis in macroglobulinaemia. Lancet 2:807-808 (editorial), 1977.

Russell 3A, Roy 3L, Powhes RL: Plasma exchange in malignant paraproteinaernias.

Exp Haematol 5:Suppl 1, 105-116, 1977.

.

Grindle C3F, Buskard NA, Newman D: Retinal blood flow changes following

plasrnapheresis in patients with Waldenstr6m’s macroglobulinaemia. Second, lnternatiawl Symposium on Leukocyte Separation and Trartsf usion. Abstract N7, 1976.

Sakalov: A, G&a’ S, Hrubi~ko M, Pokorn~ G, Mayer J: Follow up of certtin

immmological indicators in the treatment of plasrnacystoma with cyclophospharnide in combination with plasmapheresis. N-plasma 22:63-67, 1975.

Pittermann E, H6cker P, Lechner K: Stacher A: Plasmaphereses with the

continuous flow blood cell separator in the treatment of macroglobulinaemia,

multiple myelomz hemophilia and hyperlipidaemia. In Goldman 3M, Lowenthal

RM (eds): ‘Leukocytes Separation Collection and Transfusion.’t London:

Academic Press, 1974, pp 576-577.

Reich L, Feizi T, Winchester R, Wechsler B, Walzer P, Wright P: Effects of large

scale plaarnapheresis performed on patients with macroglobulinemi& Proc Am

Assoc Cancer Res 14:68, 1973.

Powles R, Smith C, Kohn 3, Hsmilton FG: Method of removing abnormal protein

rapidly from patients with malignant paraproteimemias. Br Med J 3:664-667,

1971.

Mokeeva RA, Zhuravlev VS: Effect of intensive plasmapheresis on the “syndrome

of increased viscosit~’ and blood coagulation system in Walden$trUm% macroglobulinemia). Probl Gematol Pereliv Krovi 14:8-16, 1%9.

Lawson N$ Ncaanchuk 3S, Oberman HA, Meyers MC: Therapeutic plasmapheresis

in treatment of patients with Waldenstrt5m’s macroglobulinemia. Transfusion

8:174-178, 1968.

Moulinier 3, ~vantie X, iMesnier F: Therapeutic ● ffects of phsrnapheresis in

Waldenstrdm% disease. J Med Bord 144:129> 1300, 1967.

Godal HC, Borchgrevink CF: The effect of plasmapheresis on the hemostatic

function in patients with macroglobu.linaernia Waldenstr6m and multiple myeloma.

Scand J Lab Clin Invest 17:Suppl 84, 133-137, 1965.

Mokeeva RA, Rutberg RA, Chemyak VYa, et ah Use of plasmapheresis in

macroglobulinemic reticulcais (WaMenstr&m’S disease). Fed Proc (transl SWPI)

25:153-156, 1965.

solomon A, Fahey JL: Plasmapheresis therapy in macroglobuliwmia. AM Intern

Med 58:789-800, 1963.

Skwg WA, Adams WS, Colmrn JW: Metabolic balance study of plasmapheresis in a

case of Waldenstr6m’s macroglobulinemi~ Blood 19:425, 1962.

Schwab PJ, Fahey 3L: Treatment of Waldenstrtfm’s macroglobulinemia by plasmapheresis. N Engl 3 Med 263:574-579, 1%0. Schwab PJ, Okun E, Fahey JL: Reversal

of retinopathy in Waidenstr6m’s macroglobulinemia by plasmapheresis. A report of

two cases. Arch Ophthalmol 64:515-518, 1%0.

Schwab P3, Okun E, Fahey 31: Reversal of retinopathy in Waldenstr6m’s macroglobulinemia by plasmapheresis. A report of two cues. Arch Ophthalmol 64:515-

518, 1%0.

Skoog WA, Adams WS: Plasm apheresis in a case of Waldenstr?fm’s m=rglobinaemia. Clin Res 7:96, 1959.
ARC Blood Services

Bibliography

TPB III-3

ARC Blood Services

B;&;o;;phy

C. Multiple Myelorna

Betourne C, Buge A, Dechy H, Dorra M, Dournon E, Rancurel G: The treatment of

peripheral neuropathies in a case of IgA myeloma and one of mixed cryogl~

bulinaemia Repeated plasmapheresis. Nouv Presse Med 9:1369-1371, 1980.

Blank HJ, Brinkmann OH, Junge-HUlsing G: Plasmapheresis An ● ffective procedure’fcr paraproteinemia coma. Dtsch Med Wochenschr 105:13%, 1980.

Mod A, et al: Plasmapheresis in patients with Ieukaemia, multiple myeloma and

immme complex diseases. Haematologia (Budap) 14:49-56, 1981.

Locatelli F, et ak Steroid pulses and plasmapheresis in the treatment of acute

renal failure in multiple myeloma. Proc Eur Dial Transplant Assoc 17:690-694,

1980.

Locatelli F, Pozzi C, Pedrini L, ● t al: Plasmapheresis and methylprednisolene

puhs in the treatment of acute renal failure in multiple myeloma. In Sieberth HG

(edh “Plasma Exchange. Plasmapheresis -Plasmaseparation.” Stuttgart: F. K.

Schattauer Verlag, 1980, pp 241-246.

M&l A, FClst G, Hars&nyi V, Natonek K, Poros A, Szabcf’ 3, Holl~ SIU Plasrnapheresis in patients with leukaemia, multiple myeloma and immune complex

diseases. Acta Haematol Pol 11:165-171, 1980.

Misiani R, Remuzzi G, Bertani T, Licini R, Levoni P, Crippa A, Mecca G:

Plasmapheresis in the treatment of acute renal failure in multiple myelonw Am 3

Med 66:684-688, 1979.

Sieberth HG, G16ckner W, Borberg H, Fohlmeister 3: Plasma separation in

Goodpasturels syndrome and multiple myelcma Proc Eur Dialysis Transplant Assoc

16:528, 1979.

Isbister 3P, Biggs JC, Penny R: Experience with large volume plasmapheresis in

malignant paraproteinaemia and immune disorders. Aust NZ J Med 8:154-164,

1978.

Rusdl 3A, Fitzharris BM, Corringham R, Darcey DA, Powles RL: Plasma

exchange v. peritoneal dialysis for removing Bence 3ones protein. Br Med 3 2:1397,

1978.

Fortmy IE, McCullough J: Plasma exchange by continuous flow centrifugation in

the management of acute renal failure of multiple myelorna. Minn Med 60:25-26,

1977.

Radovic M, Duric D, Trajkovi B, Radojicic B, Pekic B, Tomasevic R, Duji A:

Myeloma serum hyperviscosity syndrome treated with plaamapheresis. Med Pregl

30:471-4716, 1977.

Russell 3A, Toy 31, Powles RL: Plasma exchange in malignant paraproteinaemias.

Exp Haematol 5:Suppl 1, 105-116, 1977.

Feest TG, Buge PS, Cohen S1: Successful treatment of myeloma kidney by

diuresis and plasmapheresis. B; Med 31:503-504, 1976.

Hamblin TJ: Treatment of myeloma kidney. Br Med J 1:77Z 1976.

SakalOk A, G&ova’ S, l+rubi~o M, Pokor~ G, Mayer J: Follow-up of certain

immunologic indicators in the treatment of plasmacytoma with cyclophosphamide

in combinatia with plasmapheresis. Neoplasma 22:63-67, 1975.

Virella G, Preto RV, Graca F: Polymerised monoclinal IgA in two patients with

myelamatosis and hyperviscosity symkome. Br 3 Haematoi 30:479-487, 1975.

Loughrey JR, Meyer RL: Plasmapheresis in hyperviscosity syndrom~ better

way? JAMA 229:1211, 1974.

Pittermann E, H6cker P, Lechner K, Stacher A: Plasmaphereses with the

continuous flow blood cell separator in the treatment of macroglobulinaemia,

multi ie myelrxn~ haemo@ia and hyperlipidaemi~ In Goldman JM, Lowenthal

RM redsb ‘Leucocyte= Separation Collection and Transfuahm.n London:

Academic Press, 1970, pp 561-567.

Tuddenkm EGD, Whittaker 3A, Bradley “1, Lilleyman 3S, James DR: Hyperviscosity syndrome in IgA multiple myeloma Br 3 Haematol 27:65-76, 1974.

Revel L, Favr&GiUy J, Bryon PA, Guyon M, Fiere D: The treatment of oaseous

multiple mydomq possible value of plasmapheresis. Lyon Med 227:901-903, 1972.

Benninger GW, Krepa Sk Aggregatia phenomenon in an IgG multiple myelorna

resulting in the hyperviacoaity syndrome. Am J Mcd 51:287-294 1971.

Kopp WL, Bierne GJ, Burns ROt Hyperviscosity syndrome in multiple myelorm

Am 3 Med 43:141-146, 1967.

Tan B& Cleton F3, Beusekom GT van, Veltkamp 33, Rood 33 van: Plasmapheresis

treatment of hemorrhagic complications in a patient with multiple myeloma.

Folia Med Neerl 10:174-179, 1%7.

Godal HC, Borchgrevink CF: The effect of phsrnaphereais on the hemostatic

function in patients with macroglobulinaemia Waldenstrdm and multiple myeloma.

Scand J Lab Clin Invest 17:Suppl 84, 133-137, 1%5. M

D. Cryoglobulinemia

Bombardier S, Maggime Q, LtAbbate A, Bartolomeo F, Terri C: Plasma exchange

in essential mixed ayoglobulinemia Plasma Ther 2:101-109, 1981.

Kater L, Schuurman HJ: Immmobiology and clinical aspects of Cryoglobulinemia

Plasma Ther 2:83-99, 1981.

Berkman EM, Orlin JB: Use of plasm apheresis and partial plasma exchange in the

management of patients with ffyoglobulinemia. Transfusion 20:171-178, 1980.
ARC Blood Services

Bibliography

TPB III-5

Betoume C, Buge A, Dechy H, Dorra M, Dournon & Rancurel G: The treatment of

peripheral neuropathies in a case of lgA myelcsna and one of mixed cryogJobuIinaemia. Repeated plasmapheresis. Nouv Presse Med 9:1369-1371, 1980.

Cofdonnier D, Vialtel P, Chenais F, Jsannoel P, et al: Plasma exchange in 3 cases

of type II 1gM-lgG ayoglobulinaemia with severe membran~proliferative glomerulonephritis. In Sieberth HG (edh “Plasma Exchange. Pl=mapheresis -

Plaswtaseparation.” Stuttgart: F. K. Schattauer Verlag, 1980, pp 213-219.

Houwert DA, H-’ R3, Struyvenberg A, Kater L: Effect of plasmapkesk,

corticosteroids and cyclophosphamide in essential mixed polyclonal cryoglobulinemia associated with glomerulonephritis. In Sieberth HG (edk “Plasma

Exchange. Plasmapheresis - Plasmaseparation2’ Stuttgart: FK Schattauer Verlag,

1980, p 179-184.

Maggicre Q, L’Abbate A, Bartolaneo F, Misef cri V, Caccame A, Barbiano di

Belgiojoao G, Tarantino A, Colsmnti G: Cryopheresis in cryoglobulinemi~ Ric

Clin Lab 10:67, 1980.

McLeod BC, -etti R3: Plasmapheresis with retw of ayoglobulirwk!pleted

autologous plasma (ayoglobulinpheresia) in ayoglobulinemia Blood 55:866-870,

1980.

Vandelli L, Gaiani G, Ftrci L, et al: Control of clinical symptoms in mixed

essential uyoglobulinaemia with plasma ● xchange alone. In Sieberth HG (edh

“Plasma Exchange. Plasmapheresis - Plaamaseparation.” Stuttgart: F. K.

Schattauer Verlag, 1980, pp 221-223.

James MP, Kingston PJ: Essential monoclinal cryoglobuliraernh The use of

intermittent plasmapheresis to control cold induced symptoms. Clin Exp Dermatol

4:209-213, 1979.

Kater L, Mul N3A, Smeur 1, et al: Plasmapheresis as an adjuvant therapy in

systemic lupus erythernatcaus and in v=culitis associated with cryoglobulinemia.

San Francisco, XIV International Congress on RheumatolW, 1977, p 98.

& Miscellaneous

HaUer P, Werry H, Wrabetz-WUlke A: Plaamapheresis and functicm of tlw optic

nerve in IgM-paraproteinemia. In Borberg H, Reuther P (eds~ “Plasma Exchange

Therapy.” Stuttgart: Georg Thieme Verlag, 1981, pp 95-100.

Russell 3A: Treatment of paraproteinemias with plasma ● xchange. In Borberg H,

Reuther P (eds): “Plasma Exchange Therapy.” Stuttgart: Georg Thieme Verlag,

1981, pp 73-80.

AMERICAN RED CROSS BLOOD SERVICES

Therapeutic Pheresis Bibliography No. IV: Renal Diseases

A. GoodPasture’s Syndrome

Pussell BA, Lakwood CM, Bartolotti SR, Peters DK: Plasma exchange in immwte

complex disease and Goodpasture’s syndrome. In Nemo G3, Taswell H (eds):

“Proceedings of the Wcdtshop on Therapeutic Plasmapheresis and Cytapheresis,

April 1979.” Washington, DC: U.S. Department of Health and Human Services,

1981, PP 147-160.

Wysehbeek AJ, Smith JW, Krakauer RS: Plasmapheresis U: Review of clinical

experience. Plasma Ther 2:61-71, 1981.

Espinosa-Melendez E, Forbes RD, Hollomby D3, Ahuja 3, Katz MG: Goodpasture’s

syndrc+ne treated with plasmapheresis. Report of a case. Arch Intern Med

140:542-543, 1980.

Foidart 3B, Pirard Y, Foidart JM, DuBois CH, Mahieu PIU Evidence for a

polyclonal stimulation in GoodPasture’s syndrome. In Sieberth HG (edh ‘Plasma

Exchange. Pkrnapheresis - Plasmaseparation.” Stuttgart: F. K. Schattauer

Verlag, 1980, pp 3-7.

Loew H, Lockwood M, Witting Ctu Successful treatment of Goodpasture’s

syndrome by plasrnapheresis. In Sieberth HG (edk ‘Plasma Exchange. Plasmapheresis - Plasrnaseparation.” Stuttgart: F. K. Schattauer Verlag, 1980, pp 191-

193.

Matloff DS, Kaplan MM: D-penicillin-induced Goodpasttre’s-like syndrome in

primary biliary cirrhosis Successful treatment with plaamapheresis and immune

suppressives. Gastroenterology 78:1046-1049, 1980.

Pozo-Rodrigues R, et al: Idiopathic pulmonary haernoaiderosis treated by plaamapheresis. Thorax 35:399-400, 1980.

Siegler RL, Bond RE, Morris AH: Treatment of GoodPasture’s syndrome with

plasma exchange and immuncauppression. Clin Pediatr (Phila) 19:488-491, 1980.

Erickson SB, Kurtz SB, Donadio JV Jr, Honey KE, Wilson CB, Pineda AA: Use of

combined plasmapheresis and immunosuppression in the treatment of Goodpasture’s

syndrome. Mayo Clin Proc 54:714-720, 1979.

Finch RA, Rutsky EA, McGowan E, Wilson CB: Treatment of Goodpasture’s

syndrome with immtmos~pression and plasmapheresis. South Med 2 72:1288-1290,

1979.

Lakwood CM, Peters DK: The treatment of GoodPasture’s syndrome and

glomerulonephritis. Plasma Ther 1:19-27, 1979.

Mmk ZM, Skamene E: Goodpasture’s syndrome-effects of plasmapheresis. Clin

ExP lmmunol 36:244-249, 1979.
ARC Blood Services

Bibliography

TPB IV-2

Rosenblatt SG, Knight W, Bannayan GA, Wilson, CB, Stein JH: Treatment of

GoodPasture’s syndrome with plasrnapheresis. A case report and review of the

literature. Am J Med 66:689-696, 1979.

Sieberth HG, G16ckner W, Borberg H, Fohlmeister J: Plasma separation in

Goodpasture’s syndrome and multiple myelonm Proc Eur Dialysis Transplant Assoc

16:528, 1979.

Walker RG, @Apice AJF, Becker GJ, et al: Plasmapheresis in GoodPasture’s

syndrome with renal failure. Med J Aust 1:875-879, 1979.

Cove-Smith JR, McLcod AA, Blarney RW, Knapp MS, Reeves WG, Wilson CB:

Transplantation, immunoauppression and pkssmapheresis in GoodPasture’s syndrome.

Clin NephroI 9:126-128, 1978.

Johnson 3P, Whitman W, Briggs WA, Wilson CB: Plasmapheresis and immumsuppressive agents in antibasement membrane @kmdy-induced Goodpasture’s

syndrome. Am 3 Med 64:354-359, 1978.

McLeish KR, Maxwell DR, Luft F(2 Failure of plasma exchange and immtsmsuppression to improve renal function in GoodPasture’s syndrome. Clin Nephrol

10:71-73, 1978.

Misiani R, Bertani T, Licini R, Remuzzi G, Mecca G: Asphyxia in Goodpasmre%

syndrome Early treatment by immuncwppression and plasma exchange. Lancet

1:552, 1978.

Swanson CP, Robaon JS, Urbaniak SJ, Keller AJ, Kay AB: Treatment of

Goodpasturek disease by plasma exchange and immunosuppression. Clin Exp

Immtmol 32:233-242, 1978.

Kamanabroo D, Intorp HW, Samizadeh H, Loew H: Successful treatment of

Goodpasture’s syndrome with plasrnapheresis in combination with cyclophosphamide

and glucocoridoids. Verh Dtsch Ges IM Med 83:856-859, 1977.

Lang CH, Brown DC, Staley N, Johnson G, Ma KW, Border WA, Dalmasso AP:

GoodPasture’s syndrome treated with immumwqpression and plasma exchange.

Arch Intern Med 137:1076-1078, 1977.

Walker RG, d’Apice A3F, Becker GJ, Kincai&Smith P, Craswell PW: Pf&mapheresis in Goodpasture’s syndrome with renal failure. Med 3 Aust 1:875-879, 1977.

Lockwood CM, Rees AJ, Pearson TA, Evans DJ, Peters DK, Wilson CB: Immunosuppression and plasma exchange in the treatment of Goodpasture’s syndrome.

Lancet 1:711-715, 1976.

Rossen RD, Duff y J, McCredie KB, Reisberg MA, Sharp JT, Hersh EM, Eknyoyan G,

Suki WN: Treatment of GoodPasture’s syndrome with cyclophosphamide, prednisone and plasma exchange transfusions. Clin Exp Immunol 24:218-222, 1976.

Depner TA, Chaff in ME, Wilson CB, Gulyassy PF: Plasmapheresis for severe

Goodpasture’s syndrome. Kidney Int 8:409, 1975.

ARC Blood Services

Bibliography

TPB IV-3

Lockwood CM, Boulton-Jones 3M, Lowenthal RM, Simpaon IJ, Peters DK: Recovery from Goodpasti.re% syndrome after irnmtsmsqpressive treatment and

plasrnapheresis. Br Med J 2:252-254, 1975.

& Glomerulonephritis

Clark WF, et al: Monthly plasrnapheresis for systemic lupus erythematosus with

diffuse proliferative glomerulonephritis: A pilot study. Can Med Assoc J

125sf71- 174, 1981.

Lakwood CM: Plasma exchange in glofnerulonephritis. In Borberg H, Reuther P

(ectsk “Plasma Exchange Therapy:’ Stuttgart Georg Thieme Verlag, 1981, pp

155-160.

Nenov D, et al: Initial plasmapheresis treatment results in glomerulonephritis.

Vutr Boles 20:105-108, 1981 (English abstract).

Praga M, et al: Rapidly progressive glomerular disease treated with plasmapheresis. Med Clin (Bare) 77:33-36, 1981 (English abstract).

Solomon LR, ● t al: Reduction of post-transplant proteimria due to recurrent

mesangial proliferative (lgM) glomerubnephritis following plasma exchange. Clin

Nephrol 16:44-50, 1981.

Sommerlad KH, Leber HW, Rawer P, -Iz R, Graubner M, ScMftterle G: Plasma

exchange and irnmunosuppression in glomeruionephritis. In Borberg H, Reuther P

(eds): “Plasma Exchange Therapy.n Stuttgart: Georg Thieme Verlag, 1981, pp

161-167.

Warren SE, Mitas 3A 2d, Gcdbus SM, Swerdlin AR, Cohen IM, Cronin RE: Recovery

from rapidly progressive glomerulonephritis. Improvement after plasmapheresis and

immtrmst.ppression. Arch Intern Med 141:175-180, 1981.

Asaba H, Bergstr6m J, Bendz R, L6fquist B, et al: Plasma ● xchange with a

membrane plasma filter for treatment of glomerulonephritis. In Sieberth HG (edh

“plasma Exchange. Plasmapheresis - Plasmaseparation.” Stuttgart: F. K.

Schattauer Verlag, 1980, pp 207-211.

Asaba H, et al: Clinical trial of plasma exchange with a membrane filter in

treatment of crescentic glomerulonephritis. Clin Nephrol 14:60-65, 1980.

Boteila 3, Barbolla L, Sanz-Guajardo D, et al: Phsmapheresis treatment in diffuse

extracapillary glomerulonephritis without immune complexes or linear deposits. In

Sieberth HG (edk ‘Plasma Exchange. Plasmapheresis - Plasmaseparation.”

Stuttgart: F. K. Schattauer Verlag, 1980, pp 195-199.

Cordonnier D, Vialtel P, Chenais F, Mannoel P, ● t al: Plasma exchange in 3 cases

of type II IgM-IgG cryoglobulinaemia with severe membran-proliferative glomerulonephritis. In Sieberth HG (cd} c’Plasma Exchange. PlaSmaphereSi5 -

Plasmaseparation. Stuttgart: F. K. Schattauer Verlag, 1980, pp 213-219.

Freidman EA: Plasmapheresis fcr rapidly progressive glomerulonephritis: the

mystique of dramatic intervention. 3AMA 244:2446, 1980.
Houwert DA, Hen6’ RJ, Struyvenberg A,

corticosteroids and cyclophoaphamide

ARC Blood Services

Bibliography

TPB IV-4

Kater L: Effects of plasmapheresis (PP),

in essential mixed polyclonal cryoglobulinemia associated with glomerulonephritis. In Sieberth HG (cd):

Exchange.

“Plasma

Plasmapheresis - Plasm aseparation.” Stuttgart: F. K. Schattauer

Verlag, 1980, pp 179-183.

Lockwood CM, Peters DK: Plasma exchange in glomerulonephritis and related

vascuiitides. Ann Rev Med 31:167-179, 1980.

Lustenberger N, Neumann KH, MUller H-J, Etrlich HH, Stolte H: In vitro

characterization of phsrna exchange membrane and in VIVO application in rat

immute cnmplex glomsmlopathy. In Sieberth HG (edh “Plasma Exchange.

Plasmapheresis - PlasmaseparationJ’ Stuttgart: F. K. Schattauer Verlag, 1980, pp

225-230.

Rees AJ, Lockwood CM, Peters DK: Plasma exchange in the management of

rapidly progressive nephritis. In Sieberth HF (edk “Plasma Exchange. Plasmapheresis - Plasrnaseparaticn.” Stuttgart: F. K. Schattauer Verlag, 1980, pp 161-

167.

Riegger A3G, Liebau G, Steilner H, Roth W, Kochsiek K: Recovery of renal

function in oligo-anuric patients with rapidly progressive glomerulonephritis

(RPGN) after plasma exchange and immuma~re=i~. In Sieberth HG (edh

“Plasma Exchange. Plasmapheresis - Plasmaseparation2’ Stuttgart: F. K.

Schattauer Verlag, 1980, pp 207-211.

Sanz Guajardo D, Barbolla ML, Fern~dez 3, Gallego 3L, Anaya A, Botella J:

Plasmapheresis in the treatment of extracapillary gbrnerulonephritis. Med Clin

(Bare) 74:337-341, 1980.

Wing EJ, Brms FJ, Fraley DS, Segel DP, Adler S: Idectious complications with

plaamapheresis in rapidly progressive glomerulonephritis. 3AMA 244:2423-2426,

1980.

Ahmad S, Young JH, Striker GE, et al: Plasma exchange in rapidly progressive

glomerulonephrit!s (RPGN). Clin Res 27:91A, 1979.

Brtms FJ, Stachura 1, Adler S, et al: Effect of early pIasmapheresis and

immunosuppressive therapy on natural history of anti-glomerular basement membrane glen’mrulortep+witis. Arch Intern Med 139:372-375, 1979.

d’Apice AJF, Kincaid-Smith P : Treatment of glomerulonephritis by plasma

exchange. In Kincaid-Smith P, d’Apice AJF (eds): “Progress in Glomerub

nephritis.” New York: John Wiley & SonS, 1979.

Lockwood CM: Experience with plasm apheresis in glcsnerulonephritis and other

allergic diseases. In Dau PC (cd): “Plasmapheresis and the Immunobiology of

Myasthenia Gravis.” Boston: Houghton Mifflin, 1979, pp ‘175-185.

Lockwood CM, Peters DK: The treatment of Goodpasture% syndrome and

glwneruionephritis. Plasma Ther 1:19-27, 1979.

McKenzie PE, Taylor AE, Woodroffe A3, Seymour AE, Chn YL, Clarkn AR:

Plasmapheresis in glomerulonephritis. Clin Nephrol 12:97-108, 1979.

ARC Blood Services

Bibliography

TPB IV-5

Plasmapheresis and severe glomerulonephritis. Br Med J 1:434-435 (editorid),

1979.

Kinkaid-Smith P, d’Apice AJF: Plasmapheresis in rapidly progressive glomerulnephritis. Am 3 Med 65:564-566, 1978.

Becker G3, d’Apice A3F, Walker RG, Kincaid-Smith P: Plasmapheresis in the

treatment of glomerulonephritis. Med J Aust 2:693-696, 1977.

Landwehr DM, Evans PS, Fisher LM, et al: Removal of immme complexes by

plasmapheresis in glomerdonephritis with subacute bacterial endocarditis. Clin

Res 25:507, 1977.

Lockwood CM, Rees A3, Pussell B, Peters DK: Experience of the use of plasma

exchange in the mamgement of potentially fulminating glomerulonephritis and

SLE. Exp Haematol 5:SUPPI 1, 117-136, 1977.

Ravnskov U, Dahlback O, Messeter L: Treatment of glomerulonephritis with

drainage of the thoracic duct and plasmapheresis. Acta Med Scand 202:489-494,

1977.

Brtms F3, Stachura I, Adler S, Segel DP: Effect of early plasmapheresis and

immunosuppressive therapy on natural history of anti-glomerular basement membrane glomerulone~ritis: Repcct of a 22-month follow-up. Arch Intern Med 139:

372-374, 1976.

C. Miscellaneous

Cohen PC: Plasma exchange in a group of selected patients with renal disease. In

“Third AMUd Symposium on Apheresis: Current Concepts and Future Trends.”

Skokie, tL: American Society for Apheresis, 1981 (abstract).

Cohen J: Plasmapheresis, infection, and renal disease. JAMA 246:1545, 1981.

Frasca’ G, et al: Plasmapheresis in the treatment of immunological nephropathies.

G Clin Med 62:260-269, 1981 (English abstract).

Landini S, Coli U, Lucatello S, Bazzato G: Acute renal failure associated with

liver impairment treated by plasma-exchange. Proceedings of Symposium on Acute

Renal Failure. Tel Aviv, 1981, in press.

Lockwood CM: Plasma exchange in nephritis. Plasma Ther 2:227-234, 1981.

Lockwood M, Pusey C: Current status of plasma exchange in renal disease. In

“Third Annual Symposium on Apheresi= Current Concepts and Future Trends.”

Skokie, IL: American Society fof Apheresis, 1981 (abstract).

Morse EE, et al: Therapeutic plasm apheresis in patients with renal disease. AM

Clin Lab Sci 11:361-366, 1981.

Valbonesi M, Garelli S, Mcaconi L, Montani F, Camerone G: Plasma exchange and

combined immuncauppressive therapy in the management of severe renal damage

due to immune complex disease. Plasma Ther 2:139-142, 1981.
ARC Blood Services

Bibliography

TPB IV-6

Wing EJ, BWIIS FJ, Fraley DS, Segel DP, Adler S: Plasmapheresis, infection~ and

rend disease. IAMA 246:1545, 1%-l.

Liebau G, Riegger AJG, Steilner H,

patient with lupus nephritis and

Hoch&uck-Krankheiten 9:145, 1980.

Neilson EG, Phillips SM, Agus Z

neptritis. Lancet 1:264-265, 1980.

Rath W, Kochsiek K: Plasma exchange in a

severe nephrotic syndrome. Nieren and

Plasmapheresis in fulminating crescentic

Swaimon CP, Urbaniak SJ, Robson 3S: Plasma ● xchange in the successful

treatment of tig-induced renal disease. In Siebetth HG (edb Thsma Exchange.

Plasmapheresis - Plasmaseparaticm.n Stuttgart: F. K. Schattauer Verlag, 1980, pp

235-240.

Thysell H, Bengtsson U, Lindholm T, Bygren P, et al: Plasma exchange and pl=ma

filtration in renal disease. In Sieberth HG (edh “Plasma Exchange. Plasmapheresis - Plasmaseparation.N Stuttgart: F. K. Schattauer Verlag, 1980, pp 169-

174.

Vengelista A, et ah Effects of plasmapheresis in the ecute phase of immumcomplex nephropathy. Min=va Nefrol 27:567-570, 1980.

van den Berg CJ, Pineda AA: Plasma exchange in the treatment of acute renal

failure due to low molecular-weight dextran. Mayo Clin Proc 55:387-389, 1980..

Hmer D, Fim R, Goldsmith H3, ● t al: Plasmapheresis in fulminating crescentic

nephritis. Lancet 1:679, 1979.

Lockwood CM, W=lledge S, Nicholas A, Cotton C, Peters DK: Reversal of

impaired splenic function in patients with nephritis or vasctditis (or both) by plasma

exchange. N Eng J Med 300:524-530, 1979.

Reich LM, TurnbuU Am Combined renal and hepatic failur= The potential of

serial hemodialysis and massive exchange plasmapheresis. Curr Prob Cancer 4:18-

20, 1979.

Elliott HL, McDougall AI, H-e G, Cumming RLC, Gardiner RHE, Fell GS:

Plasmapheresis in the treatment of dialysis encephalopathy. Lancet 2:940-941,

1978. 4

Russell 3A, Fitzharris BM, Corringham R, Darcey DA, Powles RL: Plasma

exchange v. peritoneal dialysis for removing Bence Jones protein. Br Med J 2:1397,

1978.

Lockwood CM, Rees AJ, Pinching AJ, Pussell B, Sweny P, Uff 3: Plasma-exchange

and immunosuppression in the treatment of fulminating immun=omplex crescentic ne#uitis. Lancet 1:63-67, 1977.

Peters OK, Rees AJ, Lockwood CM: Plasma ● xchange in glanerular and related

aut-allergic diseases. Proc Eur Dial Transplant Assoc 14:409 -422j 1977.

Plasma-exchange in nephritis. Lancet 1:83 (editorial), 1977.

ARC Blood Services

Bibliography

TPB IV-7

Feest TG, Buge PS, Cohen S1: Successful treatment of myeloma kidney by

ditnsis and plasmapheresis. Br Med J 1:503-504, 1976.

Horisawa M, et al: Exchange transfusion in hepatorenal syndrome with liver

disease. Arch Intern Med 136:1135, 1976.

Nose’ Y, Malchesky PS, Castino F, Kc8hirw I, Scheucher K, Nokoff R: Improved

herndperfusion systems for renal/hepatic support. Kidney Int 10:S244, 1976.

Shafrir E, Brenne r T: Lipoprotein synthesis in hypoproteinemia of experimental

nephrotic syndrome and plasmapheresis. In Bianchi R, et al (edsb Tlama Protein

Twnover2’ Baltimore: University Perk Press, 1976, pp 343-355.

Buselmeier TJ, Merino G& Rodrigo F, et ak Diaiyzer-augmented whole blood and

plasma exchange f= patients with hepatic or hepatorenal failure. Crit Care Med

3:204, 1975.
AMERICAN RED CROSS BLOOD SERVICES

Therapeutic Pheresis Bibliography No. V: Connective Tissue Disorders

ARC Blood Services

Bibliography

TPB V-2

A. Systemic Lupus Erythematosus (SLE)

Abdou NI, Lindsley HB, Pollock A, Stechschulte DJ, Wood G: Plasmapheresis in

active systemic lupus erythematosu~ Effects on clinical serum, and cellular

abnormalities. Case report. Clin Immunol Immmopattwl 19:44-54, 1981.

Clark WF, et al: Chronic plasma exchange therapy in SLE nephritis. Clin Nephrol

16:20-23, 1981.

Clar~ WF, et al: Monthly plasmapheresis for systemic lupus erythematosus with

diffuse proliferative glomerulonephri tis: A pilot study. Can Med Assoc J

125:171 -174, 1981.

Parr y HF, et al: Plasma exchange in systemic lupus erythematosus. Am Rheum

Dis 40:224-228, 1981.

Rohkamm R, Przuntek H, Rockel A, Reuther P: Effect of plasma exchange in

systemic lupus erythematcsus with severe myopathy. In 8orberg H, Reuther P

(eds): “Plasma Exchange Therapy.” Stuttgart: Georg Thieme Verlag, 1981, pp

197-198.

Schlansky R, DeHoratius R3, Pincus T, Tmg Ks: Plasmapheresis in systemic lupus

erythematcsus: A cautionary note. Arthritis Rheum 24:49-53, 1981.

Verrier Jones J: Plasmapheresis in rheumatic disease - assessment of the impact

on Proce= and OUtCOltle. In ‘Third AMual Symposium on ApheresiS Current

Concepts and Future Trends.” Skokie, IL: American Society for Apheresis, 1981

(abstract).

Verrier Jones 3: Plasmapheresis in the treatment of systemic lupus erythematosus.

In Nemo GJ, Taswell H (edsh “Proceedings of the Workshop on Therapeutic

Plasmapheresis and Cytapheresis, April 1979.” Washington, DC: U.S. Department

of Health and Human Services, 1981, pp 221-229.

Wysenbeek A3, Smith 3W, Krakauer RS: Plasmapheresis II: Review of clinical

experience. Plasma Ther 2:61-71, 1981.

Hamblin I, Smith D: Plasma exchange as a long-term treatment of systemic lupus

erythematosus. In Sieberth HG (cd): “Plasma Exchange. Plasmapheresis -

Plasmaseparation.” Stuttgart: F. K. Schattauer Verlag, 1980, pp 185-189.

Hamblin T, Smith D: Plasma exchange as a long term treatment of systemic lupus

erythematosus. Nieren and Hochdruck-Krankheiten 9:142, 1980.

Hamblin T3, Smith DS, Steven MM: Plasma exchange in SLE. Lancet 1:882, 1980.

Hamilton WA, Vergani D, Bevis L, Tee DE, Zilkha KJ, Cotton LT: Plasma exchange

in SLE. Lancet 1:1249, 1980.

Liebau G, Riegger AJG, Steilner H, Rath W, Kochsiek K: Plasma exchange in a

patient with lupus nephritis and severe nephrotic syndrome. Nieren and

Hoch&uck-Krankheiten 9:145, 1980.

Meff ert H, B5hm F, Apostoloff E, Kramm H3: Plasmapheresis therapy in severe

lupus erythematcws D.N.A. serum antibodies and erythrocyte sedimentation rate

tm therapy control. Dermatol ,Monatsschr 166:331-335, 1980.

Plasma exchange in SLE. Lancet 1:688-689 (editorial), 1980.

Schlansky R, DeHoratius RJ, Pincus T, et al: Plasmapheresis therapy in systemic

lupus erythematosus (SLE). Clin Res 28:150A, 1980.

Yogore MG, Chawla MS, Kasprisin DO: Plasma exchange in a case of thrombotic

thrombocytopenic purpura and suspected acute systemic lupus erythematcaus.

Plasma Ther 1:23-25, 1980.

Young DW, Thompson RA, Mackie Pl+ Plasmapheresis in hereditary angioneurotic

edema and systemic lupus erythematosus. Arch Intern Med 140:127-128, 1980.

Fit&en 33, Clirte M3, Saxon A, Golde DW: Serum inhibitors of hematopoiesis in a

patient with aplastic anemia and systemic lupus erythematosus Recovery after

exchange pl=mapheresis. Am J Med 66:537, 1979.

Hubbard HC, Portnoy ~ Systemic lupus erythematosus in pregnancy treated with

phsmapheresis. Br J &rmatol 101:87-89, 1979.

Lindsley HB, Pollock A, Stechshulte DJ, et sI: P1asmapheresis (PL) in active

systemic lupus erythematosus (SLE): Effects on serum and cellular abnormalities.

Clin Ra 27:645A, 1979.

Molodenkov MN, Lopukhin IUM, Evseev NG, Shurkalin BK, Ageev SL: Plasmosorp

tion in the treatment of cold urticaria and systemic lupus erythematosus (a

preliminary report). Vestn Dermatol Verterol, pp 58-60, 1979.

Schildermans F, Dequeker 1, Van de Putte I: Plasmapheresis combined with

corticosteroids and cyclophosphamide in uncontrolled active systemic lupus erythematasus. J Rheumatol 6:687-690, 1979.

Terman DS, Buff aloe G, Mattioli C, Cook G, Tillquist R, Sullivan M, A)<m JC:

Extracorporeal immunoadsorption: Initial experience in human systemic lupus

erythematosus. Lancet 1:824-826, 1979.

Verrier Jones J, Cumming RH, Bacon PA, Evers J, Fraser ID, Bothamiey J, Tribe

CR, Davis P, Hughes GR: Evidence for a therapeutic effect of plasmapheresis in

patients with systemic lupus erythematosus. Q J Med 48:555-576, 1979.

Verrier Jones J, Fraser ID, Bothamley J, et al: Acute systemic lupus erythematosus: A therapeutic role fw plasmapheresis. Plasma Ther 1:33-41, 1979.

W~tzig V, Thiel W, Schreiber G: Plasmapheresis in the management of systemic

lupus erythematosus. Dermatol Monatsschr 165:305-307, 1979.
ARC Blood Services

Bibliography

TPB V-3

ARC Blood Services

Bibliography

TPB V-4

Gilcher RO: Plasma exchange in immune and autoimmune diseases. Haemonetics

Research Institute, 1978.

Houwert DA, Kater L, Struyvenberg A: Plasmapheresis, an aid in the treatment of

patients with active systemic lupus erythematosus? Ned Tijdschr Geneeskd

122:678-681, 1978.

Verrier 3anes 3 : Plasmapheresis in the management of systemic lupus erythematcaus. Muscle Nerve 1:339-340, 1978.

Verr~’= Jones 1, Robinson MF, Layfer LF, et al: Plasrnapheresis in SLE: Ccaelation of response with level of circulating immune complexes memured by Raji-cell

assay. Arttritis Rheum 21:567, 1978.

Kater L, Mul NJA, Smeur I, et al: Plasmapheresis as an adjuvant therapy in

systemic lupus erythematosus and in vasculitis associated with cryoglobulinemia.

San Francisco, XIV International Congress on Rheumatology, 1977, p 98.

Lockwood CM, Rees A3, Pussell B, Peters DK: Experience of the use of plasma

exchange in the management of potentially fulminating glomerulonephritis and

SLIL Exp Haematol 5:SUPP1 1, 117-136, 1977.

Moran CJ, Parry HF, Mowbray 3, Richards 3DM, Goldstone Al+ Plasmapheresis in

systemic lupus erythematosus. Br Med J 1:1573-1574, 1977.

Verrier Jones J, Fraser ID, Hughes G, et al: Therapeutic value of plasmapheresis in

systemic lupus erythematosus. San Francisco, XIV International Congress on

Rheumatology, 1977, p 98.

Verrier Jones J, Cumming RH, Bucknall RC, Asplin CM, Fraser ID, Bothamley F,

Davis P, Hamblin TJ: Plasrnapheresis in the management of acute systemic lupus

erythematosus? Lancet 1:709-711, 1976.

B. Polyarteritis Nodosa - Wegener’s Granuloma

Brubaker DB, Winkelstein A: Plasma exchange in rheumatoid vasculitis. Vox Sang

41:295-301, 1981.

Chalopin JM, Rifle G, Turc JM, Cortet P, Severac M: Immtmological findings

during successful treatment of HBsAg-associated polyarteritis nodosa by plasmapheresis alone. Br Med 3 280:368, 1980.

Chenais F, Debru JL, Baret L, Faure 3, Chalopin JM, Rifle G: Plasma exchange in

the treatment of polyarteritis nodosa. In Sieberth HG (edk “Plasma Exchange.

Plasmapheresis - Plasmaseparation.” Stuttgart: F. K. Schattauer Verlag, 1980, pp

285-288.

Suchy B-R, Nogai K, Sddey R, Wehnelt I, et al: Plasma exchange in a case of

Wegener’s granulomatosis. in Sieberth HG (ed~ “Plasma Exchange. Plasmapheresis - Plasmaseparation.” Stuttgart: F. K. Schattauer Veriag, 1980, pp 231-

234.

Valbonesi M, et al: Plasma exchange in management of a patient with diffuse

necrotizing cutaneous vasculitis. Vox Sang 39:241-245, 1980.

Hamblin T3, Oscier D: Polyarteritis presenting with thrombocytosis and palliated

by plasma exchange. Pfxtgrad &led J 54:615-617, 1978.

C. Rheumatoid Artlritis

Apheresis helps some arttritics - not ready for all. Med World News 22:42-43,

1981.

Apheresis in the treatment of rheumatoid arttritis. Washington, DC: National

Center for Health Care Technology Assessment Report Series, Volume 1, 1981.

Asanuma Y, Malchesky PS, Blumenstein M, Zawicki 1, Smith JW, $ayashima K, Kyo

A, Suzuki M, Shinagawa S, Krakauer RS, Calabrese L, Nose Y: Continuous

cryofiltration for rheumatoid artlritis. Artif Organs (accepted), 1981.

Bard H, et ah Rheumatoid polyarthritis and papular mucinosis with monoclinal

paraproteim Management with plaamapheresis. Rev Rhum Mal Osteoartic

48:359-365, 1981.

Brewer EJ, Nickeson RW Jr, Rossen RD, PersorI DA, Giannini EH, Milarn 3A:

Plasma exchange in selected patients with juvenile rheumatoid arthritis. J Pediatr

98:194-200, 1981.

Dubrovina NA, et al: Lymphocytapheresis in the treatment of rheumatoid

arthritis. Ter Arkh 53:125-13A 1981 (English abstract).

Evaluation of therapeutic apheresis fcc rheumatoid artlritis 1981. Rockville, MD:

Nationai Center for Health Care Technology, 1981.

From the NCHCT: Evaluatim of therapeutic apheresis fm rheumatoid arthritis.

JAMA 246:1053, 1981.

Goldfinger D, Wallace DJ, Klinenberg 3R: Plasrna-lymphocy tapheresis for the

treatment of rheumatoid arthritis. In Borberg H, Reuther P (eds): “Plasma

Exchange Therapy.” Stuttgart: Georg Thieme Verlag, 1981, pp 215-219.

Hamburger M: A critical assessment of the value of therapeutic apheresis in

rheumatoid arttiitis. In “Third AMUd Symposium on Apheresis: Current Concepts

and Future Trends.” Skokie, IL: American Society for Apheresis, 1981 (abstract).

Kanamono T, Iwata H, Yarnanaka N, Ohta K, Maeda K: Plasma separation using

various kinds of hemo-filters in rheumatoid arttr itis. [n “New” ,Membranes in

LMedical Treatment.” 2nd Tutzing Symposium on Chemical Engineering in ,Medicine, Munich, 1981.

Karsh 3, Klippel 3H, Plotz PH, Decker JL, Wright DG, Flye ,MW: Lymphapheresis

in rheumatoid arthritis: A randomized trial. Arthritis Rheum 24:867-873, 1981.
ARC Blood Services

Bibliography

TPB V-5

ARC Blood Services

Bibliography

TP13 V-6

Recommendations of the Arthritis Foundation and the American Rheumatism

Association on plasmapheresis in rheumatic disease. Atlanta, GA: Arthritis

Foundation, 1981.

Shiokawa Y, Yarnagata 3, Yuasa S, Shiozawa K: Plasma exchange for rheumatoid

arthritis using a new bag system. In Shiokawa Y, Abe T, Yamauchi Y (eds): “New

Horizons in Rheumatoid Arthritis.” Amsterdam: Excerpta ,Medica, 1981.

Smith JW, Asanuma Y, Kayashima K, Suzu$i M, Blumenstein M, Malchesky PS,

Krakauer R, Calabrese L, Shinagawa S, Nose Y: Rheumatoid arthritis treated by

membrane plasmapheresis with sequential plasma Cryofiltration for reUiOVdl of

macromolecules. Am Soc Artif Intern Organs 10:74, 1981.

Bletry O, Bussel A, Aubert L, Cabane 3, Herson S, Godeau P: The effect of plasma

exchange on the treatment of adult Still’s disease. In Sieberth HG (cd): “Plasma

Exchange. Plasmapheresis - Plasmaseparation.” Stuttgart: F. K. Schamauer

Verlag, 1980, pp 275-281.

Nickeson RW, Brewer EJ, Rossen RD, et al: Pl=ma exchange in juvenile

rheumatoid a~hritis. Atihritis Rheum 23:725, 1980.

RothweU RS, Davis P, Gordon PA, Dasgupta MK, YS_my KV, Russell AS, Percy 3S:

A controlled study of plasma ● xchange in the treatment of severe rheumatoid

artlritis. Arttritis Rheum 23:785-790, 1980.

Wallace D, Goldfinger D, Brachman M, et al: Therapeutic pheresis in the

management of rheumatoid arttritis (RA). Clin Res 28:77A, 1980.

Wallace D3, Goldfinger D, Thompson-Breton R, Martin V, Lowe CM, Bluestone R,

Klinenberg JR: Advances in the use of therapeutic pheresis for the management of

rheumatic diseases. Semin Arthritis Rheum 10:81-91, 1980.

Chenais F, Arvieux 3, Blanc D, Piton JL, Phelip X: Plasmaphereis in the treatment

of rheumatoid polyarthritis. Nouv Presse Med 8:2903, 1979.

Goldman 3A, Casey HL, IMcIlwain H, Kirby 1, Wilson CH Jr, Miller SB: Limited

plasmapheresis in rheumatoid arthritis with v=culitis. Arthritis Rheum 22:1 146-

1150, 1979.

Karsh 3, Wright DG, Klippel 3H, Decker IL, Deisseroth AB, Flye MW: Lymphocyte

depletion by continuous flow centritugation in rheumatoid arthritis: Clinical

effects. ArtlYitis Rheum 22:1055-1059, 1979.

Pheresis methods improve severe RA, but cost is a hurdle. Med World News

20(33):28, 1979.

Tennenbaum 3, Urowitz MB, Keystone EC, Dwosh IL, Curtis 3E: Leucapheresis in

severe rheumatoid arthritis. Ann Rheum Dis 38:40-44, 1979.

Wallace DJ, Goldfinger D, Gatti R, Lowe C, Fan P, Bluestone R, Klinenberg JR:

Plasmapheresis and lymphoplasmapheresiS in the management of rheumatoid arthritis. Arthritis Rheum 22:703-710, 1979.

Wright DG, Karsh 3, Fauci AS, et al: Leukapheresis to achieve lymphocyte

depletim and immunosuppression in rheumatoid art~itis (RA). Clin Res 27:339A,

1979.

Tennenbaum J, Dwosh IL, Burowitz M, et al: Severe rheumatoid arthritis

responsive therapy. San Francisco, XIV International Congress on Rheurnatoiogy,

1977, p 246.

Ro]a OG: Blood transfusim in rheumatoid arttritis. Lancet 2:1209- 121O, 1975.

Jasin Ha LoSpa.Uuto, Ziff M: Rheumatoid hyperviscosity syndrome. Am J ~Med

49:484-493, 1970.

Jaffe IA: Comparison of the effect of plasmapheresis and penicillarnine on the

level of circulating rheumatoid factor. Ann Rheum Dis 22:71-76, 1963.

D. Raynaud’s Syndrome

Verrier Jcmes 3, Clough 3D, Klinenberg JR, Davis P: Tl_= role of therapeutic

plasmapheresis in the rheumatic dise=es. 3 Lab Clin IMed 97:589-598, 1981.

Hamilton WAP, Dodds A3, Hancock 1ME3, Roberts VC, Vergani D, Cotton LT:

Circulatory improvement in Raynaud’s phenomenon following plasma exchange. [n

Sieberth HG (edk “Plasma Exchange. Plasmapheresis - Plasmaseparation.”

Stuttgart: F. K. Schattauer Verlag, 1980, pp 301-307.

Hamilton WAP, White J/M, Cotton LT: Plasma exchange in Raynaud’s phenomenon.

Lancet 2:475, 1980.

McCune MA, Pineda AA, W inkelman RK, Osmmdson P3: Controlled sK~Y of the

therapeutic effect of plasma exchange on scleroderma and Reynaud’s phenomenon.

Transfusion 20:649, 1980.

Zahavi J, Hamilton WAP, OReUly MJG, et al: Pl=ma exchange and platelet

!unction in Raynaud’s phenomenon. Thromb Res 19:85-93? 1980.

Dodds A3, O’Reilly iMJG, Yates CJP, Cotton LT, Flute PT, Dormandy” 3A:

Haemorrheological response to plasma exchange in Raynaud’s syndrome. Br .Med I

2:1186-1187, 1979.

O’Reilly M3, Talpca G, Roberts VC, White 3LM, Cotton LT: Controlled tria of

plasma exchange in treatment of Raynaud’s syndrome. Br Med J 1:1113-1115,

1979.

Zahavi J, Hamilton WAP, CYReilly ~MJG, Dubiel M, Cotton LT, Kakkar VV:

Plasmapheresis and platelet function in Raynaud’s syndrome. Thromb Haemost

42:338, 1979.

Acheson ED: Plasm apheresis in Raynaud’s disease. Lartcet 1:672, 1978.

Cotton LT: Plasm apheresis in Raynaud’s disease. Lancet 2:108, 1978.

Klinenberg JR, Wallace D: Plasm apheresis in Raynaud’s disease. Lancet 1:1310-

1311, 1978.
ARC Blood Services

Bibliography

TPB V-7

Talpm G, Cotton LT, White 3M: Plasrnapheresis in Raynaud% disease. Lancet

1:672, 1978.

Talpca G, Horrocks M, White JM, Cotton LT: Plasmapheresis in Raynaud’s disease.

Lancet 1:416-417, 1978.

E. Miscellaneous

Andm,son L, Ziter FA: Plasmapheresis via central catheter in dermatomyoaitis: A

new method for selected pediatric patients. 3 Pediatr 98:240, 1981.

Dau PC, Bennington 3: Plasmapheresis in childhood dermatomyositis. J Pediatr

98:237-240, 1981.

Hertzrnan A, Cooke CL, Rodriquez GE, Sharp D: Treatment of childhood mixed

connective disease with plasmapheresis. Clin Immunol Newsletter 2:142-144, 1981.

Verrier 3ones 3, Clough 3D, Klinenberg JR, et al: The role of therapeutic

plasmapheresis in the rheumatic diseases. J Lab Clin Med 98:589-598, 1981.

Brewer E3, Giannini EH, Rossen RD, et al: Plasma exchange therapy of a

childhood onset deqmammyositis patient. Arthritis Rheum 23:509, 1980.

Dequeker 3, Geusens P, Wielands L: Short and longterm ● xperience with

plasrnapheresis in connective tissue diseases. “Biomedicine 32:189-194, 1980.

Kamanabroo D, Lonauer G, Knob J: Plasmapheresis in the treatment of mixed

connective tissue disease. In Sieberth HG (edb Tlasrna Exchange. Plasmapheresis

- Plasmaseparation.n Stuttgart: F. K. Schattauer Verlag, 1980, pp 283.

Liebau G, Riegger A3G, Steilner H, Roth W, Kochsiek K: Plasma exchange in a

patient with lupus nephritis and severe nephrotic syndrome. Nieren and

Hockdruch-Krankkeiten 9:145, 1980.

Shiokawa Y, Yamagata 3: Plasmapheresis in treatment of rheumatic fever. 3pn

Circ J 44:797-800, 1980.

Verrier Jones 3: Therapeutic plasmapheresis in rheumatology. In “Second Annual

Apheresis Symposium: Current Concepts and Future Trends.”’ Skokie, Ils

American Society for Apheresis, 1980, pp 11-14.

Wallace 03, Goldfinger D, Thompson-Breton R, Martin V, Lowe CM, Bluestone R,

Klinenberg JR: Advances in the use of therapeutic pheresis fcr the management of

rheumatic diseases. Semin Arthritis Rheurn 10:81, 1980.

Yamagata J, Shiozawa K, Shiokawa Y: Therapeutic plasma exchange f- rheumatic

diseases. In Sieberth HG (edh “Plasma Exchange. P1asmapheresis - Plasmaseparation.” Stuttgart: F. K. Schattauer Verlag, 1980, pp 265-273.

Cardella C3: Plasma exchange-a new approach to immme modulatim in

rheumatic diseases. 3 Rheumatol 6:606-609, 1979.

ARC Blood Services

Bibliography

TPB V-8

Lockwood CM, Worlledge S, Nicholas A, Cotton C, Peters DK: Plasma exchange

reverses impaired splenic fwiction in nephritis and vasculitis. N Engl J Med

300:524-530, 1979.
AMERICAN RED CROSS BLOOD SERVICES

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Therapeutic Pheresis Bibliography No. Vl:

A. Renal

Adams MB, et al: Plasmapheresis in the treatment

re]ection. Transplant Proc 13(1 Pt 1): 491-494, 1981.

Blume KG, Spruce WE: Bone marrow transplantaticm

CH Jr (cd): “Apheresis Development, Applications,

New>ork: Alan R. Liss, 1981, pp 69-80.

Transplantation

of refractory renaf allograft

in acute leukemia. In Mielke

and Collection Procedures.”

Pease E: Plasmaleukapheresis halts graft rejection. 3AMA 246:1170, 1981.

Slapak M, et al: Renal transplant in a patient with major donor-recipient blood

group incompatibility: Reversal of acute rejection by the use of modified

plasmapheresis. Transplantation 31:4-7, 1981.

Allan TL, Briggs JD, Curnming RLC, et al: Plasma exchange in renal transplant

re~ection. In Sieberth HG (cd): “Plasma Exchange. Plasrna@eresis - Pl~rn~

separation.” Stuttgart: F. K. Schattauer Verlag, 1980, pp 247-250.

Cardella EJ, et al: A controlled trial evaluating intensive plasma exchange in renal

transplant recipients. Proc Eur Dial Transplant Assoc 17:429-434, 1980.

Cardella CJ, UldaU PR, Sutton DMC, et al: Effect and complications of intensive

plasma exchange in renal transplant recipients. In Sieberth HG (edh ‘Plasma

Exchange. Phsmapheresis - PlasrnaseparationJ’ Stuttgart: F. K. Sdattauer

Verlag, 1980, pp 251-255.

Kurland 3, Franklin S, Goldfinger D: Treatment of renal allograft rejection by

exchange plasmsdymphocytapheresis. Transfusion 20:337-340, 1980.

Lynggaard F, Ladefoged J, “3ans H: Intensive plasma exchange priof to renal

transplantation to prevent rejection. Plasma Ther 1:55-57, 1980.

Ota K, Tcma H, Takahashi K, et al: Plasma exchange for treatment of renal

allograft rejection. In Sieberth HG (edh “Plasma Exchange. Plasmapheresis -

plasmaseparation.” Stuttgart: F. K. Schattauer Verlag, 1980, pp 257-261.

Adams MB, Kauffman HM Jr, Hebert LA, Hussey CV, Duquesnoy RI, Tomasulo PA:

Plasmapheresis in the treatment of renal allograft rejectico. Proc Clin Did

Transplant Forum 9:252-255, 1979.

Cardella C3, Sutton DM, Uldall PR, et al: Renal allograft rejection and intensive

plasma exchange. Haemonetics Research Institute Advanced Component Seminar,

Bmton, 1979.

Naik RB, Ashlin R, Wilson C, Smith DS, Lee HA, Slapak M: The role of

plasmapheresis in renal transplantation. Clin Nephrol 2:245-250, 1979.

ARC Blood Services

Bibliography

TPB VI-2

Rifle G, Chalopin JM, Turc JM, Guigner F, Vialtel P, Dechelette E, Chenais F,

Cccdonnier D: Plasmapheresis in the treatment of renal allograft rej~tions.

Transplant Proc 11:20-26, 1979.

Terman DS, Garcia-Rinaldi R, M=almon R, Mattioli C, Cook G, Poser R:

!Modification of hyperacute renal xenograft rejection after extracorporeal immun~

adsorption of hetero-specific antibody. Int 3 Artif Organs 2:35-41, 1979.

Cardella CJ, Sutton DM, Falk 3A, Katz A, UldaU PR, deVeber GA: Effect of

intensive pl=ma exchange on renal transplant rejection and serum cytotoxic

antibody. Transplant Proc 10:617-619, 1978.

Vialtel P, Chenaise F, Dechelette E, Bayle F, Cordonnier D, Seigneurin JM:

Massive plasmapheresis in the treatment of acute graft rejection resistant to usual

treatment. Now Presse Med 7:2663, 1978.

Cardella CJ, Sutton DM, Falk JA, Katz A, Uldall PR, deVeber GA: Intensive

plasma exchange, complement dependent microcytotoxicity, and renal transplant

rejection. Proc Eur Dial Transplant ASSOC 14:328, 1977.

Cardella C3, Sutton D, Uldall PR, deVeber GA: Intensive pl=ma exchange and

renal-transplant rejection. Lancet 1:264, 1977.

Ymhioka H, McCalmon R, Putman C, Terman DS: Attenuation of hyperacute

xenograft rejection in unmodified host by ● xtracccporeal plasma perfusion. Transplantatim 23:72-76, 1977.

& Bone Marrow

Buckner CD, Williams B: Pheresis techniques in marrow transplantaticrt. In Mielke

CH Jr (edh “Apheresiw Development, Applications, and Collection Procedures.”

New Ycrk: Alan R. Liss, 1981, pp 81-89.

Buckner CD: Pheresis techniques in marrow transplantation. In “First AMual

Apheresis Symposium: Current Concepts and Future Trends.” Chicago: American

Red Cross Blood Services, 1979, pp 147-154.

Berkman EM, CapIan S, Kim CS: ABO-incompatible bone marrow transpl~tion:

Preparation by plasma exchange an in vitro antibody absorption. Transfusion

18:504-508, 1978.

Merkel FK, Bier M, Beavers CD, Merriman WG, Wilson C, Starzl TE: Modification

of xenograft response by selective plasmapheresis. Transplant Proc 3:534-537,

1971.

Bier M, Beavers CD, Merriman WG, Merkel FK, Eiseman B, Starzl TZ: Selective

plasmapheresis in dogs for delay of heterograft response. Trans Am SOC Artif

Intern Organs 16:325-333, 1970.
AMERICAN RED CROSS BLOOD SERVICES

Therapeutic Pheresis Bibliography No. Vll: Liver Diseases

A. Hepatitis, Hepatic Coma

Lbsgen H, Bnstner G, Schmidt FW: Removal of toxic metabolizes by plasma

exchange in patients with hepatic failure. In “New Membranes in Medical

Treatment.” 2nd Tutzing Symposium on Chemical Engineering in Medicine,

,Munich, 1981.

Lepd-e MJ, McKenna PJ, tMartinez BD, et al: Folminant hepatitis with coma

successfully treated by plasmapheresis and hyperimmune Australia-antibody-rich

plasma. Plasma Ther 1:49-56, 1979.

Gelfand MC, Winchester 3F, Knepshield 3H, Cohan S1, Schreiner GE: Reversal of

hepatic coma by charcoal perfusiom Clinical and biochemical observations. 3 Am

Sa Artif Intern Organs 1:37-43, 1978.

Kvasnicka J, Svejda 3, Rennerova 3, Rezac 3, Zalud P: Exchange plasmapheresis

and heparin in treatment of coma in viral hepatitis. Unitrni Lek 24:440-444, 1978.

Boland J, Broux R, Bury 3, Pirotte 3: La plasmapherese clans le traitement de

I’hepatite fulminate avec corm Rapport de 6 c=. Acta Clin Belg 31:173-187,

1976.

Gelfand MC, Knepshield 3H, Cohan SL, et al: Treatment of hepatic coma with

hemoperfusion through polyacrylamide hydrogel-coated charcoal. Kidney Int

10:S239, 1976.

3esipowicz IM, Jakubowska M, Karski 3, Osterowa K: Exchange transfusion with

plasmapheresis in the management of hepatic coma. Polish Med Sci History Bull

15:207-211, 1976.

Sanjo K, Fujimori Y, Yamazaki Z, et al: The effect of liver support system (plasma

perfusion detoxication) providing removal of plasma amino acids in patients with

fulminant hepatitis. Artif Orgars (Jpn) Suppl 5:231-234, 1976.

Buselmeier TJ, Merino GEj Rodrigo F, et ah Dialyzer-augmented whole blocd and

plasma exchange fcr patients with hepatic or hepatorenal failure. Crit Care Med

3:204, 1975.

Gazzard BG, Pfftmann BA, Weston iM3, Langley PG, Murray-Lyon IM, et al:

Charcoal haemoperfusion in the treatment of fulminant hepatic failure. Lancet

1:1301, 1974.

Gazzard BD, Weston MJ, Murray-Lyon IM, et al: Charcoal haemoperfusion in the

treatment of fulminant hepatic failure. Lancet 1:1301, 1974.

Buckner CD, Clift RA, Volwiler W, Donohue DM, Burnell JM, Saunders FC, Thomas

ED: Plasma exchange in patients with fulminant hepatic failure. Arch Intern iMed

132:487-492, 1973.

ARC Blood Services

Bibliography

TPB VII-2

Redeker AG, Yamahiro HS: Controlled trial of exchange transfusion therapy in

ftdminant hepatitis. Lancet 1:3-6, 1973.

Lepore MJ, McKenna PJ, Martinez DB, Stutman LJ, Bu’ianno CA, Ccmklin EF,

Robiletti JG: Fulminant hepatitis with coma successfully treated by plasmapheresis and hyperimmute Australia-antibody-rich plasma. Am J Gastroenterol

58:381-389, 1972.

.

Lef=e MJ, Stutman LJ, Bonanno CA, Conklin EF, Robilotti JG, McKmm PJ:

Plasmapheresis with plasma exchange in hepatic coma. Arch Intern LMed 120:900-

907, 1972.

Reynolds JDH, Wilber RD: Treatment of hepatic coma. J Kans Med Soc 72:54-57,

1971.

Rivera RA: Current status of exchange transfusion in fuJminartt hepatitis. Med

AM Distri@ of Columbia 41:277-280, 1972.

Abouna GM, Amemiya H, Fisher LLMcA, Still WJ, Porter KA, Costa G, Hume DM:

Hepatic support therapy by intermittent liver perfusion and exchange blood

transfusions. Transplant Proc 3:1589-1596, 1971.

Graw RG Jr, Buckner CD, Eisel R: Plasma ● xchange transfusion fm hepatic coma:

New technique. Transfusion 10:26-32, 1970.

Lepore MJ, Martel AJ: Plasmapheresis with plasma exchange in hepatic coma:

Methods and results in five patients with acute hepatic necrosis. Ann Intern Med

72:165-174, 1970.

Rivera RA, Seaughter RL, Boyce HW: Exchange transfusion in the treatment of

patients with acute hepatitis in coma Dig Dis 15:589-601, 1970.

Davidson CS, McDermott WV Jr, Trey C: Sustaining life during fulminant hepatic

failure. Ann Intern Med 71:415-416, 1969.

Demeulenaere L, Barbier F, Vermeire P: Plasmapheresis in hepatic coma. Lancet

2:152-153, 1969.

Reynolds TB: Exchange transfusion in fulminant hepatic failure. G~troenterology

56:170, 1969.

Cree IC, Berger SA: Plasmapheresis and positive-pressure ventilation in hepatic

coma with respiratory arrest. Lancet 2:976-977, 1968.

Exchange transfusion in fulminant hepatitis. Br Med J 1:270 (editorial), 1968.

Lederman RJ, Davis FB, Davis P3: Exchange transfusion as treatment of acute

hepatic failure due to antitherculosis &ugs. AM Intern [Meal 68:830-838, 1%8.

Sabin S, [Merritt 3A: Treatment of hepatic coma in cirrhosis by plasmapheresis and

plasma infusicm (plasma exchange). AM Intern [Meal 68:1-7, 1%8.

Burnell 3M, Dawborn 3K, Epstein RB, Butman RA, Leinbach MD, Thomas ED,

Volwiler W: Acute hepatic coma treated by cross-circulaticm or exchange

transfusion. N Engl J IMed 276:935-943, 1967.
ARC Blood Services

Bibliography

TPB VII-3

ARC Blood Services

Bibliography

TPB VII-4

Gelfand ML, Sussman L, Caimol BC, Florita C, Joson F: Successful treatment of

hepatic coma by exchange transfusions. JAMA 201:630-633, 1967.

Jones EA, Chin D, Clink HM, et al: Hepatic coma due to acute hepatic necrosis

treated by exchange blood transfusion. Lancet 2:169-172, 1%7.

Lepore M3, Martel All: Plasmapheresis in hepatic coma. Lancet 2:771-772, 1967.

Krek R, Flynn M: Treatment of hepatic coma with exchange transfusion and

peritoneal dialysis. 3AMA 199:430, 1967.

Berger RL, Liversage RM 3r, Chalmers TC, Graham JH, McGoldrick DM, Stohlman

F Jr: Exchange transfusion in the treatment of fulminating hepatitis. N Engl 3

tMed 247:497-499, 1966.

Berger RL, Stohlman F 3r: Evaluation of blood exchange in the treatment of

hepatic coma. Amer J Surg 112:412-418, 1966.

Eckhardt RD: Exchange transfusions for hepatic coma. N Engl 3 Med 274:1444,

1966.

Grey C, Bums DG, Saunders S3: Treatment of hepatic coma by exchange blood

transfusion. N Engl 3 Med 274:473-481, 1966.

Trey C, Burns DG, Saunders S3: Treatment of hepatic coma by exchange blood

transfusions. N Engl 3 Med 274:473-481, 1966.

Lee C, Tink A: Exchange transfusia in hepatic comsu Report of a case. Med 3

Aust 1:40-42, 1958.

B. Miscellaneous

Hughes RD, Williams R: Removal of protein-bound metabolizes in fulminant

nepatic failure. In Borberg H, Reuther P (edsh “Plasma Exchange Therapy.”

Stuttgart: Georg Thieme Verlag, 1981, pp 113-119.

Landini S, Coli U, Lucatello S, Bazzato G: Acute renal failure associated with

liver impairment treated by plasma-exchange. Proceedings of Symposium on Acute

Renal Failure. Tel Aviv, 1981, in press.

Lauterburg BH, Taswell HF, Pineda AA, Dickson ER, Bergstaler EA, Carlson GL:

Charcoal affinity column plasma perfusion for the treatment of intractable

pruritus of cholestasis. In Nemo G3, Taswell H (eds): “Proceedings of the WorkShop

on Therapeutic Plasmapheresis and Cytapheresis, April 1979.” Washington, DC:

U.S. Department of Health and Human Services, 1981, pp 269-276.

.

Levy VG, et al: Treatment of cholestasis by plasmapheresis. NOUV Presse Med

10:2588, 1981.

L6sgen H, Brunner G, Schmidt FW: Removal of toxic metabolizes by plasma

exchange in patients with hepatic failure. In “New Membranes in ,Medical

Treatment.” 2nd Tutzing Symposium on Chemical Engineering in ,Medicine,

,Munich, 1981.

Asanuma Y, et al: Clinical hepatic support by on-line plasma treatment with

multiple absorbents - evaluation of system performance. Trans Am Soc Artif

Intern Organs 26:400-405, 1980.

Bazzat G, Coli U, Landini S, LucateUo S: Plasma exchange and peritoneal dialysis:

Combined treatment in the management of severe Ieptospirosis. In Sieberth HG

(cd): “Plasma Exchange. Plasmapheresis - Plasm-eparation.” Stuttgart: F. K.

Schattauer Verlag, 1980, pp 347-351.

Brtrmer G, L8sgen H, Schmidt FW: Plasmapheresis treatment for support of the

failing liver and other forms of liver disease. In Sieberth HG (edh “Plasma

Exchange. Pl=mapheresis - Plasmaseparatica.” Stuttgart: F. K. Schattauer

Verlag, 1980, pp 329-333.

Carey WD, Noa~ Y, Ferguson DR, Asanuma Y, Smith 3W, Hermann RE, Malchesky

PS: Plasma perfusion in liver dise=e: Phase 1 study. In Sieberth HG (cd): “Plasma

Exchange. Plasmapheresis - Plasmaseparation.” Stuttgart: F.K. Schattauer

Verlag, 1980, pp 335-339.

Eriksson S, Lindgren S: Plasma exchange in primary biliary cirrhosis. N EfIgl J

Med 302:809, 1980.

Horiuchi T, Otsubo O, Takahashi 1, Yamada Y, Yamauchi 3, Inou T: Study of

plasma cross circulation in experimental hepatic failure. In Sieberth HG (cd):

“Plasma Exchange. Plasmapheresis - Plasmaseparation.” Stutigart: F. K .

Schattauer Verlag, 1980, pp 341-345.

Matloff DS, Kaplan [MM: D-penicillin-induced GoodPasture’s-like syndrome in

primary biliary cirrhosis: Successful treatment with plasmapheresis and immunosuppressives. Gastroenterology 78:1046- 1049, 1980.

.Milich DR, et al: Plasmapheresis of hepatitis B surface antigen carriers. Acta

Haematoi Pol 11:73-78, 1980.

Nos~ Y, tMalchesky PS, Asanuma Y, Zawicki 1: Plasma filtration detoxification on

hepatic patient= Its optimal operating conditions. In Gurland HJ, Heinze ~, Lee

HA (eds): “Plasmapheresis.” Berlim Springer Verlag, 1980 (in press).

Okamura 3, Kuroda H, Horikawa S, Shibata N, ,Monden M, Gotoh IM, Sikujara O,

Kosaki G, Sakurai ~M: Experiences on plasma exchange for treatment of intrahepatic cholestasis. In Sieberth HG (cd): “Plasma Exchange. Plasmapheresis -

Plasmaseparation.” Stuttgart: F. K. Schattauer Verlag 1980, pp 353-357.

Orlin 3B, Berkman ELM, .Matloff DS, Kaplan LMM: Primary biliary cirrhosis and cold

autoimm une hemolytic anemia: Effect of partial plasma exchange. Gastroenteroiogy 78:576-578, 1980.

Sheehy TW, Law DE, Wade BH: Exchange transfusion for sickle cell intrahepatic

cholestasis. Arch Intern Med 140:1364- 1366, 1980.
ARC Bled Services

Bibliography

TPB VI1-5

Milich DR, Vyas GN, Holland PV, et al: Preliminary observations on pl=mapheresis of chronic carriers of hepatitis B surface antigen. Blood 54:127a, 1979.

Pineda AA, Lauterburg BH, Taswell HF, Bwgstaler EA, Carlson GA, Dickson ER:

Charcoal affinity column plasma perfusicm for the treatment of intractable

pruritus of cholestasis. Transfusion 19:666, 1979.

Lauterburg BH, Pineda AA, Dickson ER, Baldas WP, Taswell HF: Plasmaperfusicm

for the treatment of intractable pruritis of cholestasis. Mayo Clin Proc

53:463-407, 1978.

Horisawa M, et al: Exchange transfusion in hepstorenaf syndrome with liver

disease. Arch Intern Med 136:1135, 1976.

Silva YJ, Parameswaran PG, 3ames P: Exchange transfusicm and major surgery in

acute hepatic failure. Swgery 80:343-349, 1976.

Buckner CD, Clift RA, VOlwiler W, et al: Plasma exchge in Patients with

fulminant hepatic failure. Arch Intern Med 132:487-49L 1973.

Redeker AG, Yamahiro HS: Controlled trial of exchange-transfusion therapy in

ftdminant hepatitis. Lancet 1:3-6, 1973.

Turnberg LA, Mahoney MP, Gleeson MH, Freeman CB, Gowenlock AFL Plasmapheresis and plasma exchange in the treatment of hyprlipaemia and xanthomatous

neuropathy in patients with primary biliary cirrhosis. Gut 13:976-981, 1972.

Marin GA, Montoya CA, Sierra J& et al: Evaluation of corticosteroid and

exchange-transfusion treatment of acute yellow-phosphorus intoxicaticm. N Engl 3

Med 284:125-128, 1971.

AMERICAN RED CROSS BLOOD SERVICES

Therapeutic Pheresis Bibliography No. VIII: Hemolytic Disease of the Newborn

Fraser ID, Bennett MO, Bothamley 3E: Antenatal plasma ● xchange in the

management of mothers with Rh antibodies. In Borberg H, Reuther P (eds~

“Plasma Exchange Therapy/’ Stuttgart: Georg Thieme Verlag, 1981, pp 224-226.

Graham-Pole 3, Willoughby M: Plasma exchange fw severe rhesus (Rh) disease. In

Nemo G3, Taswell H (eds): “Proceedings of the Workshop on Therapeutic

Plasmapheresis and Cytapheresis, April 1979.” Washington, De U.S. Department of

Hed~h and Human Services, 1981, pp 203-215.

Hauth JC, Brekken AL, Pollack W: Plasmapheresis w an adjunct to management of

Rh isoimmmization. Obstet Gynecol 57:132-135, 1981.

Robinson EAE: Unsuccessful use of absorbed autologous plasma in Rh-incompatible

pregnancy. N E@ J Med 305:1346, 1981.

Rock G: Plasma exchange in Rh disease: Past, present and future. In 7hird

Annuaf Symposium on Apheresis Current Concepts and Future Trends.n Skokie,

IL: American Society for Apheresis, 1981 (abatract).

Rock GA: Plasma exchange in the treatment of rhesus hemolytic disease. Plasma

Ther 2:21 1-225, 1981.

Rock G, Lafreniere 1, Chan L, McCombie N: Plasma exchange in the treatment of

hemolytic disease of the newborn. Transfusion 21:546-551, 1981.

Schwerdtfeger R, Malchus R, Hoff bauer H: Plaamapheresis and intrauterine

transfusions in Rh incompatible pregnancies. In Borberg H, Reuther P (edah

‘Plasma Exchange Therapy.” Stuttgart: Georg Thieme Verlag, 1981, pp 227-228.

Angela E, ● t al: Intensive plasma ● xchange in the management of severe Rh

disease. Br J Haematol 45:621-631, 1980.

Barclay GR, Greias MA, Urbaniak SJ: Adverse effect of plasma exchange on antiD production in rhesus immunisation owing to removal of inhibitory factors. Br

Med 3 1:1569-1571, 1980.

Harbord MG, et al: Antenatal plasma exchange therapy. Med J Aust 1:647-648,

1980.

Robirmn EAE, Tovey LAll Intensive plasma exchange in the management of

severe Rh disease. Br 3 Haernatol 45:621-631, 1980.

Teixeira DM, Abrash IMP, Smith CL, Sheets 31, Kateley JR, Makionado WE:

Treatment of severe rhesus disease by intensive plasmapheresi= A case report and

review of the literature. Plasma Ther 1:39-49, 1980.

Urbaniak S3, Barclay GR, Greiss MA: Adverse eff=t of plasma exchange on

maternal anti-D levels in HDN due to the removal of plasma ifiibitory factors.
ARC Blood Services

Bibliography

TPB VIII-2

ARC Blood Services

Bibliography

TPB VIII-3

Joint Meeting 18th Congress International Society of Hematology and 16th

Congress Internaticml Society of Blood Transfusion, August 1980, Montreal,

Canada (Abstract 1413).

Asanuma Y, Smith JW, Makhesky PS, Hermann RE, Carey WD, Ferguson DR, Nose

Y: Preclinical evaluation of membrane plasmapheresis with on-line bilirubin

removal. Artif Organs 3:279, 1979.

James V, Weston 3, Scott IV, et al: Intensive plaima exchange in rhesus

isoimmunization. Vox Sang 37:290-295, 1979.

Sussmann LN, Barias M, CoUi W: Intensive plasmapheresis during pregnancy and

spurious amniotic fluid bilirubin. Am 3 Obstet Gynecol 135:1 S6-157, 1979.

Tirnashenko LI, Timcahenko LV, Minchenko ZhN, Vovchenko VP: Use of plasmapheresis foc reduction of isoaensitization level in Rlwincompatible pregnancy. Vopr

Okhr Materin Det 24:61-64, 1979.

Weston JV, Scott IV, Doughty R, Tornlinson J, Whitfield M: Intensive plasma

exchange in Rhesus isoimmunization. Vox Sang 37:290, 1979.

Woyton J, Baranowski H, Kwoczynska K, Partyka T, Dzierzkowa W: Results of

treatment of Rh blood group incompatibility with plasmapheresis. Ginekol Pol

Suppl:62-64, 1979.

Fraser ID, Bothamley JE, Bennet Mb Alteraticm of amniotic fluid pigment values

and anti-D levels during plasmapheresis in severe rhesus haemolytic disease. Br 3

Haematol 39:175, 1978.

Herve P, Coffe C, Lapprand L, Peters A, Selva J, GiUet JY: Severe anti-D

all-immunization Failure of repeated antenatal plasmapheresis (a case report).

NOW Presae Med 7:1956-1957, 1978.

,McBride JA, CYHoaki P, Blajchman MA, et al: Rhesus alloimmunization following

intensive plasrnapheresis. Transfusion 1S:626-627, 1978.

Pepperell RT, Cooper IA: Intensive antenatal plasmapheresis in severe rhesus

isoimmunizatiort. Aust NZ J Obstet Gynaecol 18:121, 197&

Woyton J, Partyka T, Gajewska E, Kwoczynska K, et al: The use of plasma~,eresis

in pregnancy with antenatal prediction of a serious hemolytic disease due to Rh

immtmization. Arch Immmol Ther Exp (Warsz) 26:1139, 1978.

Fraser IB, BeMett MO, Bothamley 3E, et al: Intensive antenatal plasmapheresis in

severe rhesus isoimmunisation. Lancet 1:6, 1977.

Graham-Pole J, Barr W, Willoughby IMLN: Continuous-flow plasmapheresis in

management of severe rhe3us disease. Br ~Med J 1:1185-1188, 1977.

Iglesias J: Plasmapheresis in series in pregnant women severely sensitized to Rh

factor. Rev Chil Obstet Ginecol 42:1-12, 1977.

McGuiness EP3, Reen DJ: Plasma exchange in severe rhesus disease. Br Med J

1:1269, 1977.

Tilz GP, Weiss PA, Teubl 1, Lanzer G, Vollmann H: Successful plasma exchange in

rhesus incompatibility. Lancet 2:203, 1977.

Bowman 3M: Intensive antenatal plasmapheresis in severe rhesus iso-immmisation.

Lancet 1:421-422, 1976.

Fras~ ID, Bothamley JE, Bennett MO, Airth GR: Intensive antenatal plasmapheresis in severe rhesus isoimmunisation. Lancet 1:6-8, 1976.

Walker W: Management of Rh isoimmtmisaticn. Lancet 1:256-257, 1976.

Graham-Pole JR: Proceeding= Plasmapheresis in rhesus disease. Scott Med J

20:168-169, 1975.

Graham-Pole JR, Barr W, Willoughby MLN: Continuous-flow exchange-plasmapheresis in severe rhesus isoimmunisation. Lancet 1:1051, 1974.

Graham-Pole JR, Donald 1, Barr W, Willoughby MLN: Plasmapheresis in rhesus isimmunisation. Lancet 2:1459, 1974.

Pole JR, Barr W, Willoughby ML: Continuous-flow exchange-plasmapheresis in

severe rhesus isoimmunisation. Lancet 1:1051, 1974.

Pole JR, Donald 1, Barr W, Willoughby ML: Plasmapheresis in rhesus isoimmtmisation. Lancet 2:1459, 1974.

Fias 1, Dornbi E, Wenhardt E, Horwth I: Plasmapheresis in Rh isoimmunisation.

Lancet 1:1519-1520, 1973.

Kowacs L, KesfrU TL, Imre G: Plasmapheresis in Rh isoimmmisation. Lancet

1:1253, 1973.

Vasileva ZF, Kuznechikova VV, Anichkova S1, Laevskaia 5A, Susloparov LA:

Plasrnapheresis as a method of lowering the degree of Rh-sensitivity in pregnant

women. Akush Ginekol 49:62-64, 1973.

Crespo Cortina M, Arroyo A, Olivares Tinajero G, Manuel Septien J: Use of

plasmapheresis to control anti-Rh antibodies in isoimmunized mothers. Ginecol

Obstet Mex 31:485-490, 1972.

Maynier M, Cregut R, Maigret P, Poulain M: Development of anti-Rh antibody

titers after labor of immlmizecl women. Applicaticm to the immtme plasma sample

by plasmapheresis. J Gynecol Obstet Biol Reprod (Paris) 1:205-207, 1972.

Nublat M, Melis C, Boissieu G, Gaujoux J, Serment H: Repeated plasmapheresis in

severe rhesus isoimmunization. 3 Gynecol Obstet Biol Reprod (Paris) 5: Supp1 2,

205-207, 1972.

Isbister 3P, Ling A, Seeto KM: Development of Rh-specific maternaJ autoantibodies following intensive plasmapheresis for Rh immunization during pregnancy. Vox Sang 33:353-358, 1977.
ARC Blood Services

Bibliography

TPB VIII-4

Clarke CA, Elson CJ, Bradley J, Donohoe WTA, Lehane D, Hughes-Jones NC:

Intensive plasmapheresis as a therapeutic measure in rhesus-immtmised women.

Lancet 1:793-798, 1970.

Ivanov LV, Shuvaeva BA: Effect of plasmapheresis on rhesus-antibody titer. Probl

Gematol Pereliv Krovi 15:61-6A 1970.

Bowman JM, Peddle LJ, Anderson C: Plasmapheresis in severe Rh iso-immunization. VOX Sang 15:272-277, 1968.

Powell LC Jn Intensive plasmapheresis in the pregnant Rh-sensitized woman. Am

J Obstet Gynecol 101:153-170, 1968.

AMERICAN RED CROSS BLOOD SERVICES

Therapeutic Pheresis Bibliography No. IX: Cancer

Bansal SC, Bansal BR, Sjogren HO, Husberg B, Lindstrom C, Nylander G, Mark R:

Use of biological immunoabsorbents in the treatment of tumor host. In Nemo GJ,

Taswell H (eds): “Proceedings of the Workshop on Therapeutic Plasmapheresis and

Cytapheresis, April 1979.” Washington, DC: U.S. Department of Health and

Human Services, 1981, pp 281-299.

Edelson RL, Berger CL, Armstrong RB: Lymphapheresis in the treatment of the

leukemic phase of cutaneous T-cell lymphorna and pemphigus vulgaris. In Nemo

GO, ~aswell H (eds): “Proceedings of the Wmkshop on Therapeutic Plasma@eresis

and Cytapheresis, April 1979.” Washington, DC: U.S. Department of Health and

Human Services, 1981, pp 55-66.

Graf 3, Carpenter N, Medenica R, Miescher PA: Plasmapheresis in cancer

patients. In Bcrberg H, Reuther P (edsh “Plasma Exchange Therapy.” Stuttgart:

Georg Thieme Verlag, 1981, pp 229-232.

Harada T, et al: Regional arterial infusion of an anticancer drug combined with

direct hemoperfusion. Tohoku J Exp Med 133:423-429, 1981.

Hellstr6m KE, HeUstrUm I: Does perfusion with treated plasma cure cancer? N

Engl 3 Med 308:1215-1216, 1981.

Isr&”l L, Edelstein R, Samak R: Repeated plasma exchange in patients with

metastatic cancer. In Borberg H, Reuther P (edsk “Plasma Exchange Therapy.”

Stuttgart: Georg Thieme Verlag, 1981, pp 238-243.

Israel ~ Edelstein R, Sarnak R, et ab Clinical results of multiple plasmaphereses

in patients with advanced cancer. In Rosenfeld and Serrou (eds} Human Cancer

Immunology, vol. ~ North-Holland (in press).

Smit Sibinga CTlu Haematologi@ ~ortive therapy for cancer-chemotherapy,

and therapeutic plasmapheresis in a commwity blood bank by a ceJl separator unit.

In ‘Third AMUd Sympcaium on Apheresis: Current Concepts and Future Trends.”

Skokie, IL: American Society for Apheresis, 1981 (abstract).

Terman DS: ExtraCorporeal immtzmadsorbents for therapy of autoimmtme and

neoplastic disease. In Nemo G3, Taswell F (e&k Proceedings of the Work% hop on

Therapeutic Plasmapheresis and Cytapheresis, April 1979.’1 Washington, DC: U.S.

Department of Health and Human Services, 1981, pp 301-328.

Terman DS, Young 3B, Shearer WT, Ayus C, Lehane D, et al: Preliminary

observations of the effects on breast adenocarcinuna of plasma perfused over

immobilized protein A. N Engl J Med 305:1195-1200, 1981.

Beyer 3H, et al: First clinical experience with large volume plasma exchange in

m~ignmt tumor patients. ~weiz Med Wochenschr 110:1147-1149, 1980 (English

abstract).
ARC Blood Services

Bibliography

TPB IX-2

ARC Blood Services

Bibliography

TPB IX-3

Beyer 3-H, Klee M, Bartsch HH, Borghardt 3, et al: First experiences with

plasmapheresis in patients with neoplastic diseases. German Cancer Congress,

Munich, March 1980.

Isra&l L, Edelstein R, Mannoni P, et al: Plasmapheresis in patients with

di=eminated cancer. Plasma Ther 1:57-68, 1980.

Israel L, Sarnak R, Edelstein R: Multiple plasma exchange therapy fw metastatic

cancer. In Sieberth HG (cd): “Plasma Exchange. Pksmapheresis - P1asmaseparation:’ Stuttgart: F. K. Schattauer Verlag, 1980, pp 381-385.

Iwamoto H, Nakagawa S, Matsui N, Ycahiyarna N, Shinoda T, Shibamota T,

Takeucki J: An experience of plasma exchange by membrane separator for IgA

myeloma. In Sieberth HG (ed~ ‘Tlasma Exchange. Plasmapheresis - Plasmaseparation.” Stuttgart: F. K. Schattauer Verlag, 1980, pp 377-380.

Samak R, IsraiH L, Edelstein R: Influence of tumor burden, tumor removal,

immute stimulation, plsumapheresis on mortocyte mobilization in cancer patients.

In Escobar R, et al (edsh “lMacrophages and Lymphocytes,” part B. New York:

Plenum publishing Co., 1980, pp 411-423.

Shaw D, Trotter 3M, Colman KC: Plasma exchange to control sweats and pruritus

in malignant disease. Br Med 3 281:1459, 1980.

Zander AR, et al: Plasmapheresis as immunotherapeutic modality in the treatment

of the canine venereal tumor. Exp Hematol 8:1123-1128, 1980.

Isra&l I., Edelstein R: In vivo and in vitro studies on non-specific blocking factors

of host origin in cancer patients: Role of plasma exchange as an immunotherapeutic modality. Isr J Med Sci 14:105-130, 1978.

Isr*”l L, Edelstein R, McDonald 3, Weiss 3, Schein P: Immunological and plasma

protein changes in cancer patients following a single plasmapheresis. Biomedicine

28:292-297, 1978.

Zhukov 01, Pleshakov ~, Singaevski~SB: Hemodynamics in double plasmapheresis

in lung cancer. Vestn Khir 121:96-99, 1978.

Edelson RL: Efficacy of Ieukapheresis procedures in the management of cutaneous

T-cell Iymphoma-leukemic phase. Proceedings of the 4th Advanced Blood Components Seminar 4:1-7, 1977.

Hobbs JR, Byrom N, Elliott P, et al: Cell separators in cancer immunotherapy.

Exp Haematol 5:Suppl 95-103, 1977.

Isra&l L, Edelstein R, IMannoni P, Radot E, Greenspan EM: Plasmapheresis in

patients with disseminated cancer: Clinical results and correlation with change in

serum proteins. Cancer 40:3146-3154, 1977.

Hersey P, Isbister 3, Edwards A, Murray E, Adams E, Briggs J, Milton GW:

Antibody-dependent cell-mediated cytotoxicity against melanoma cells induced by

plasmapheresis. Lancet 1:825-828, 1976.

lsra~l L, Edelstein R, Mannoni P, Radot E: Plasmapheresis and immunological

control of cancer. Lancet 2:642-643, 1976.

IsraFl L, Mannoni P, Radot E, Greenspan E: Immune and tumor reacticns to plasma

exc@nge in advanced cancers. NOUV Presse Med 5:433, 1976.

Laroye G3: On the potential usefulness of exchange plasmapheresis in the

immunotherapy of cancer and of scxne chronic persistent infections. Med Hypotheses 2:214-218, 1976.

Whitehead RH, Teasdale C, Hughes LE: Plasmapheresis and immmological control

of cancer. Lancet 2:748, 1976.

Buckner CC, Clift RA, Thomas ED: Plasma exchange with the continuous flow

centrifuge. In Goldman 3M, Lowenthal RM (cd+ “Leukocytes: Separation

Collection and Transfusion.” London: Academic Press, 1975, pp 578-580.

Langved ~ Hyclen H, Wolf H, Kroeigaard N: Extracorporeal immunoadsorption of

circulating specific serum factors in cancer patien~. Br 3 Cancer 32:680 -692~

1975.

W aldman SR, Roth 3A, Kern DH, Pilch YH: Effects on cancer patients of

Ieukapheresis with the continuous-flow blood cell separator. 11. Immunologic

parameters in vitro. 3 Lab Clin Med 86:950-961, 1975.

Waldman SR, Roth 3A, Silverstein M, Velman LL, Pilch yH: Effec~ ~ cancer

patients of leukapheresis with the continuous-flow blood cell separator. L Hematoiogic and immunologic parameters in vivo. J Lab Ciin 86:938-949? 1975.

Browne O, Bell 3, Holland PDJ, Thornes PD: Plasmapheresis and immunostimuIation. Lancet 2:96, 1976.
AMERICAN RED CROSS BLOOD SERVICES

Therapeutic Pheresis Bibliography No. X: Skin Diseases

A. Pemphigus Vulgaris

Edelson RL, Berger CL, Armstrong RB: Lymphapheresis in the treatment of the

leukemic phase of cutaneous T-cell Iymphoma and pemphigus vulgaris. In Nemo

GJ, Taswell H (edsk “Proceedings of the Workshop on Therapeutic Plasmapheresis

and $ytapheresis, April 1979.” Washington, DC: U.S. Depanment of Health and

Human Services, 1981, pp 55-66.

Velte H, W rabetz-Wolke A, Eckert G, Marghescu S, Deicher H, Stangel W, Peter H,

Schedel I: Plasma ● xchange in the treatment of pemphigm Vulgaris In Borberg H,

Reuther P (eds} ‘Plasma Exchange Therapy/’ Stuttgart: Georg Thieme Verlag,

1981, pp 210-214.

Swanson DL, et al: Pemphigus vulgaris and plasma ● xchange: Clinical and

serologic studies. 3 Am Aced Dermatol 4:325-328, 1981.

Neppert J, Meissner K, Voigt H, Meigel W: Trials with therapeutic plasmapheresis

in pemphigua vulgaris. Z Hautkr 55:783-789, 1980.

Roujeau JC, Revuz J, Fabre M, Andre C, Akerman C, Mannoni P, Touraine R:

Plasma exchanges in pemphigus vulgaris. In Sieberth HG (edk ‘Plasma Exchange.

~ifllheresis - Plasmaseparatich.” Stuttgart: F. K. Schattauer Verlag, 1980, pp

.

Auerbach R, Bystryn 3(2 Plasmapheresis and immmos~pressive therapy. Effect

on levels of intercellular antibodies in pemphigus vulgaris. Arch Dermatol 115:728-

730, 1979.

Meurer M, Braun-Falco O: Plasma exchange in the treatment of pemphigus

vulgaris. Br 3 Dermatol 100:231-232, 1979.

Cotteri.11 3A, Barker D3, Millard LG: Plasma exchange in the treatment of

pemphigus vulgaris. Br J Derrnatol 98:243, 1978.

Ruocco V, Rossi A, Argenziano G, Aatarita C, Alviggi L, Farzati B, Papaleo G:

Pathogenicity of the intercellular antibodies of pemphigus and their periodic

removal from the circulaticm by plasmapheresis. Br J Dermatol 98:237-241, 1978.

& Erythrocyte Autosensitization

Hamblin TJ, Hart S, Mufti G3: Plasmapheresis and a placebo procedure in

autoerythrocyte sensitisation. Br Med J 283:1575-1576, 1981.

Lockwood CM, Pearson T: Use of plasma exchange in veatment of allergic

disease. Proceeding of Advanced Component Seminar. Haemonetics Research

Irutitute, Wayland, MA, 1977.

ARC Blood Services

Bibliography

TPB x-2

C. Miscellaneous

Anderson L, Ziter FA: Plasmapheresis via central catheter in dermatomycsitis: A

new method fcr selected pediatric patients. 3 Pediatr 98:240, 1981.

Bennington 31, et al: Patients with poiymycsitis and dermatomyositis who undergo

plasmapheresis therapy. Pathologic findings. Arch Neurol 38:553-560, 1981.

Mada K, Shhtzato T, Usuda M, Sezaki R, et al: Psoriasis treatment with

hemofiltraticm and plasma exchmge. In ‘7New Membranes in Medical Treatment.w

2nd Tutzing Sympcxsiurn on Chemical Engineering in Medicine, Munich, 1981.

Brewer E3 3r, Giannini EH, Rossen ED, et ah Plasma exchange therapy of a

chilrhood onset dermatomytxitis patient. Arttritis Rheurn 23:509-513, 1980.

M-er HW, Braine H, Pyeritz Rg Unman D, Murray C, Asbury AK: Therapeutic

trial of plasmapheresis in Refsum disease and in Fabry disease. Birth Def~ts

16t491-497, 1980.

Neumann E, Skdisz H, Bowszyc 3: Pbssrnapheresis in the treatment of bullous skin

diseases. PrzeglDerrnatol 67:487-49~ 1980.

Pyeritz R~ UUmen MD, M~er AB, BraiIw HG, Moser HW: Plasma exchange

removes glycosphingolipid in Fabry disease. Am J Med Genet 7:301-307, 1980.

Ycsmg DW, Thompson RA, Mackie Pl+ Plasmapheresis in hereditary angioneurotic

edema and systemic lupus erythematmus. Arch Intern Med 140:127-128, 1980.

Blaszcyk M, Ctwrzelaki T, D=zynski J, Kknowska ~ Beutner EH, lablonska S:

Plasmapheresis in the treatment of bullous skin dise~es. Przegl Dermatol 66:399-

404, 1979.

Dandona P, Marshall NJ, Bidsy SP, ● t al: Successful treatment of exophthalmos

and pretibial myxoedema with plasmapheresis. Br Med J 1:374-376, 1979.

Dav PS: Resolution of psori=is during plasmapheresis. Arch Dermatol 115:1171,

1979.

Howert DA, Kater L, de la Faille HB: Some applicaticms of plasmapheresis notably

in a patient with necrotizing ulcers. Br J Derrnatol 101:233-234, 1979.

Lewis RA, Slater N, Croft

responding to plasrnapheresis.

DN: Exophthalmoa and pretibial myxoedema not

Br Med J 1:390-391, 1979.
AMERICAN RED CROSS BLOOD SERVICES

Therapeutic Pheresis Bibliography No. X1: Lipid Disorders (Hyperlipidemia)

ARC Blood Services

Bibliography

TPB XI-2

Barr S1, et al: Plasma lipid and apoprotein levels following plasmapheresis in a

subject hornozygous for familial hypercholesterolemia. Experiential 37:1 14-115,

1981.

Borberg H, Greve V, Sawatski C, Oette K, Stoffel W: Specific continuous flow

immunoabscrption ex vivo in patients with familial hypercholesteri naemia. In

“New Membranes in Medical Treatment.” 2nd Tutzing Symposium on Chemical

Engineering in Medicine, Munich, 1981.

Kottt?e BA, Burgstaler EA, Taswell HF, Ellefson RD, Witte LD, Pineda AA:

Hypercholesterolemia treatment by heparin-agarose affinity column. In Nemo G3,

T=well H (edsh “Proceedings of the Workshop on Therapeutic Plasmaphereais and

Cytapheresis, April 1979.” Washington, DC: U.S. Department of Health and

Human Services, 1981, pp 341-346.

Schriewer H, As$man G: Aspects of familial hypercholesterolemia with regard to

plasma exchange. In Bccberg H, Reuther P (eds~ “P1ssma Exchange Therapy.”

Stuttgart: Georg Thieme Verlag, 1981, pp 104-109.

Stein EA, et al: Repetitive intermittent flow plasma exchange in patients with

severe hypercholesterolemi~ Atherosclerosis 38:149-164, 1981.

Stoffel W, Bcrberg H, Greve V: Application of specific ● xtracorporeaJ removal of

low density lipoprotein in familial hypercholesterolaemi~ Lancet 2:1005-1007,

1981.

Thompson GR: Long-term plasma exchange in severe familial hypercholesterolemia. In Nemo GJ, Taswell H (eda} ‘Proceedings of the W cddwp on

Therapeutic Plasmapheresis and Cytapheresis, April 1979.n Washington, DC: U.S.

Department of Health and Human Services, 1981, pp 235-246.

Thompson GR: Plasma exchange for hypercholesterolaemia Lancet 1:1246-1248,

1981.

Graisely B, Cloaree M, Salmon S, Polonovski 3, et al: ~tracorporeal pl=ma

therapy for homozygous familiar hypercholesterolaemi~ Lancet 2:1 147, 1980.

King ME, Breslow 31, Lees RS: Plasma-exchange therapy of homozygous familial

hypercholesterolemia N Engl J Med 302:1457-1459, 1980.

Stoffel W, Demant Th, Sieberth HG, Bcfberg H, G16ckner WM: Selective removal

of Apo B containing serum lipoproteins from blood plasma. In Sieberth HG (cd):

“Plasma Exchange. Plasmapheresis - Plasmsseparation$’ Stuttgart: F. K.

Schattauer Verlag, 1980, pp 127-132.

Thompson GR: Plasma exchange for hypercholesterolemi= A therapeutic mode

and investigative tool. Plasma Ther 1:5-15, 1980.

Thompson GR, ,Myant NB, Kilpatrick D, Oakley CM, Raphael M3, Steiner RE:

Assessment of long-term plasma exchange for familial hypercholesterolaemia. Br

Heart J 43:668-680, 1980.

W itzturn IL, W illiarns JC, Ostlund R, Sherman L, Siccard G, Schonf eld G:

Successful phsmapheresis in a 4-year-old child with homozygous familial hyperCholesterolemi& J Pediatr 97:615-618, 1980.

Soutar AK, Myant MB, Thompson GR: Metabolism of apolipoprotein+-containing

Iipoproteim in familial hypercholesterolaemia Effects of plasma exchange.

Atheroaderosis 32:315-325, 1979.

Apstein CS, Zilversmit DB, Lees RS, George PK: Effect of intensive pl=mapheresis on the plasma cholesterol concentration with familial hyperchole~

terolemia Atherosclerosis 31:105-115, 1978.

Berger GMB, Miller JL, Bonnici F, Jaffe HS, Dubovsky DW: Continuous flow

plasma exchange in the treatment of homozygous familial hypercholesterolemi~

Am J Med 65:243-251, 1978.

Berger GMB, Miller JL, Bonnici F, Joffe HS, Dubovsky DW: Plasma exchange in

the treatment of homozygous familial hypercholesterolaerni= Criteria f cc patient

selection. S Afr Med J 53:194, 1978.

Betteridge D3, Bakowski M, Taylor KG, Reckless JPD, de Silva SR, Galton DJ:

Treatment of severe diaiutic hypertriglyceridaernia by plasma exchange. Lancet

1:1368, 1978.

SimonS LA, Gibson JC, Isbister 3P, Biggs 3C: The effects of plasma exchange on

cholesterol metabolism. Atherosclerosis 31:195-204, 1978.

Thompson GR, Kilpatrick D, Oakley C, Steiner R, Myant N: Reversal of

cholesterol accumulation in familial hypercholestefolemia by long-term plasma

exchange. Circdatim Suppl 2:171, 1978.

Thompson GR, Kilpatrick D, Raphael M, Oakley C, Myant NB: Use of plasma

exchange to induce regression of atheroma in familial hypercholesterolaem(a. Eur

J Clin Invest 7:233, 1977.

Berger GMB, Miller JL, Bcrmici F, Jaffa HS, Dubovsky DW: Continuous flow

plasma exchange in treatment of homozygous familial hypercholesterolemi~ Am J

Med 65:243-251, 1976.

L,upien PJ, Mcmrjori S, Arrad J: A new approach to the management of familial

hypercholesterolaemia Lancet 1:1261-1265, 1976.

Thompson GR, Myant NB: Low density lipoprotein turnover in familial hypercholesterolaemia after plasma exchange. Athercaclerosis 23:371-377, 1976.
ARC Blood Services

Bibliography

TPB Xl-3

Thompson GR, Lowenthal R, Myant NB: Plasma exchange in the management of

homozygous familial hypercholestrolaemia. Lancet 1:1208-1211, 1975.

Apstein CS, Gecrge PK, Zilversrnit DB, Feldman HA, Lees RS: Cholesterol

reducticm with intensive plasmapheresis. Clin Res 22:459A, 1974.

Pittermann E, H8cker P, Lechner K, Stacher A: Plasmaphereses with the

continuous flow blood cell separator in the treatment of macroglobulinaemia,

multiple myelom~ hemophilia and hyperlipidaemia. In Goldman 3M, Lowenthal

RM Ads): “Leucocyte* Separatia Collection and Transfusion.” London:

Academic PreS, 1974, pp 561-567.

Turnberg LA, Mahoney MP, Gleeson MH, Freeman CB, Gowenlock AH: Plasmapheresis and plasma exchange in the treatment of hyperlipaem~a and xanthomatous

neuropathy in patients with primary biliary cirrhosis. Gut 13:976-981, 1972.

Gennes 31 de, Touraine R, Maunand B, Truffert J, Laudat P: Homozygous cutaneotendinous fcrms of hypercholesteremic xanthomatosis in an exemplary familial

case. Trial of plasmapheresis ans heroic treatment. Bull Mem Soc Med Hop (Paris)

118:1377-1402, 1%7.

AMERICAN RED CROSS BLOOD SERVICES

Therapeutic Pheresis Bibliography No. XII: Immu’tological Disorders

A. Immwmdeficiency

Branda RF, McCullough 33: Plasmapheresis in the treatment of immme disease.

In Nemo GJ, Taswell H (edsh “Proceedings of the Workshop on Therapeutic

Plasmapheresis and Cytapheresis, April 1979.” Washington, DC: U.S. Department

of Health and Human Services, 1981, pp 125-133.

WegmUller E: The therapeutic significance of plasmapheresis in immunologic

disease. Schweiz Med Wochenscher 111:443-449, 1981.

Cal~”rese LH, Clough 30, Krakauer RS, Hoeltge GA: Plasmapheresis therapy of

immunologic disease. Report of Nne cases and review of the literature. Cleve

Clin Q 47:53-72, 1980.

Samtleben W, et al: Membrane plasma separation for treatment of immtsmIogically mediated diseases. Trans Am Soc Artif Intern Orgam 26:12-16, 1980.

Birdsall HH, Brewer EJ, Rcasen RD, Moake JL: Clinical improvement associated

with hypocomplementemia following plasrnapheresis. In DSU PC (cd): “Plasmapheresis and the Immmobiology of Myasthenia Gravis2’ Boston: Houghton Mifflin,

1979, pp 191-198.

G1-man AB: Immtme responses: The raticmle for plasmapheresis. Plasma Ther

1:13-18, 1979.

Lbckwood CM, W odledge S, NidolaS A, Cotton LC, Peters DK: Reversal of

impaired splenic function by plasma ● xchange. N Engl J Med 300:524-530, 1979

Pinching AJ: Recent advances in immmological therapy: Plasm-exchange and

immunc6uppression. Br 3 Anaesth 51:21-28, 1979.

Winkelstein A, Volkin RL, Starz TW, ● t al: The effects of plasma exchange on

immunologic factors. Clin Res 27:691A, 1979.

Gilcher RO: Plasma exchange in immtme and autoimmtme diseases. Haemonetics

Research Institute, 1978.

Isbister 3P, Biggs JC, Penny R: Experience with large volume plasmapheresis in

malignant paraproteinaemia and immune disorders. Aust NZ J Med 8:154-164,

1978.

Keller AJ, Urbaniak S3: Intensive plasma exchange on the cell separator: Effects

on serum immunoglobulins and complement components. Br 3 Haematol

38:531-540, 1978.

Lakwood CM, Rees AJ, Pinching AJ, Pussell B, Sweeny P, Uff J, Peters DK:

Plasma exchange and immunosuppression in the treatment of fulminating immune

complex cresc+entic nephritis. Lancet 1:63-67, 1977.
ARC Blood Services

Bibliography

TPB XII-2

ARC Blood Services

Bibliography

TPB XII-3

Rossen RD, Hersh E&i, Sharp JT, et al: Effect of plasma exchange on circulating

immt.me complexes and antibody f ormatim in patients tieated with cyclophosphamide arid prednisone. Am J Mecl 63:674-682, 1977.

Browne O, Bell J, Holland PDJ, Themes RD: Plasmapheresis and immunostimdation. Lancet 2:96, 1976.

Plasma@eresis and immwms~pression. Lancet 1:1 113-1114, 1976.

Brands RF, Moldow CF, McCullough 33, Jacob HS: Plasma exchange in the

treatment of immtme disease. Transfusicm 15:570-576, 1975.

Friedman BA, Schak MA, Modal JL, et W Short-term and long-term effects of

plasrnapheresis on serum proteim and immtmoglobulins. Transfusion 15:467-472,

1975.

Branda R, Moldow C, McCullough 3, Jacob H: Plasma exchange in the treatment

of immune disease. Clin Res 21:831, 1973.

Bystryn JC, et al: Regulation of antibody famation by serum antibody. II.

Removal of specific antibody by means of exchange transfusion. J Exp Med

132:1279, 1970.

Bach J-F: The immmological treatment of autoimmute and immme complex

disease= An overview. In Sieberth HG (edh “Plasma Exchange. Plasmapheresis -

Plasmaseparatiom” Stuttgart: F. K. !khattauer Verlag, 1980, pp 17-19.

k Immme Complex Diseases

Clough JD, Calabrese LH: Theoretical aspects of immune complex removal by

plasrnapheresis. Plasma Ther 2:73-81, 1981.

LM6d A, et al: Plasmapheresis in patients with Ieukaemi% multiple myeloma and

immune complex diseases. Haernatologia (Budap) 14:49-56, 1981.

Pussell BA, Lockwood CM, Bartolotti SR, Peters DK: Plasma exchange in immune

complex disease and GoodPasture’s syndrcme. In Nemo G3, TasweIl H (eds):

“Proceedings of the Workshop on Therapeutic Plasmapheresis and Cytapl)$resis,

April 1979.’1 Washington, DC: US. Department of Health and Human Services,

1981, pp 147-160.

Valbonesi M, GarelJi S. Mosconi L, Mcatani F, Camerone G: Plasma exchange and

combined immunosuppressive therapy in management of severe renal darnage due

to imrnme complex disease. Plasma Ther 2:139-142, 1981.

Bach J-F: The immmological treatment of autoimmune and immune complex

diseases: An overview. In Sieberth HG (cd): “Plasma Exchange. Plasmapheresis -

Phsmaseparation.” Stuttgart: F. K. Schattauer Verlag, 1980, pp 17-19.

Clough 3D, Calabrese LH, Verbic MA, Mansfield LR, Frank SA, Getzy D: Effect of

plasmapheresis on circulating immuie complex (IC) levels in patients with IC

dise=es. Fed Proc 39:681, 1980.

Lustenberger N, Neumann KH, Muller H-3, Elrlich HH, Stolte H: In vitro

characterization of plasma exchange membrane and in vivo application in rat

immme complex glomerulopathy. h Sieberth HG (cd): “Plasma Exchange.

Plasrnapheresis - Plasm aseparation.” Stuttgart: F. K. Schauttauer Verlag, 1980, pp

225-Z30.

M&l A, FUst G, Harskyi V, Natonek K, Paos A, Szabo 3, Hollan SIU Plasmapheresis in patients with Ieukaemia, multiple myeloma and immune complex

diseases. Acta Haematol Pol 11:165-171, 1980.

Simon TL, Goldman R, Tung TSK: Relationship between circulating immune

complexes and pl=mapheresis. Transfusion 19:667, 1979.

Gilcher RO. Plasma exchange in immune and autoimmune diseimes. Haemonetics

Research Institute, 1978.

Immtme complexes in health and disease. Lancet 1:580 (editorial), 1977.

Hamblin T3: Proceedings: The therapeutic use of plasmapheresis in an immune

complex disease. J Clin Pathol 29:83, 1976.

.

Calabrese LH, Sa@er DN, Verbic MA, et al: Plasma exchange in immune complex

mediated disease. Clin Res 28:138A, 1980.
AMERICAN RED CROSS BLOOD SERVICES

Therapeutic Pheresis Bibliography No. XIII: Miscellaneous Diseases

A. Thyroid Storm

Brehm G: Plasma exchange in thyreotoxicosis. In Borberg H, Reuther P (edsk

“Plasma Exchange Therapy.” Stuttgarc Gecfg Thieme Verlag, 1981, pp 121-125.

Haire W, Newcomer 3, Hartman C: Plasmapheresis in the management thyroid

storm. Plasma Ther 2:3-5, 1981.

Dan@na P, Nathan AW, Marshall NJ, Bidey S, Havard CWH: Plasmapheresis as

treatment for acute fulminant endocrine exophthalmos. In Sieberth HG (edk

“Plasma Exchange. Plasmapheresis - Plasmaseparaticm” Stuttgart: F. K.

Schattauer Verlag, 1980, pp 321.

Siegenbeck van Heukelom LH, der Kinderen PJ, Vingerholds ACM: Plasmapheresis

in L-thyroxine intoxication. Plasma Ther 1:33-37, 1980.

van Heukelorn LHS, der Kinderen PJ, Vingerlmeds ACM: Plasmapheresis in Lthyroxine intoxication. Plasma Ther 1:33-37, 1980.

Herrmann J, Rudorff KH, Gockenjan G, ● t al: Charcoal haemoperfusim in thyroid

storm. Lancet 1:248, 1977.

Hcrn K, Brehm G, Habermann J, Pickardt CR, Saiba PC: Successful treatment of

thyroid storm by continuous plasmapheresis with a blood-cell separatm. Klin

Wochenschr 54:983-986, 1976.

Tsirch LS, Drews J, Liedtke R, Schemmel K: Treatment of thyroid storm with

plasmapheresis. Med Klin 70:807-811, 1975.

Herrmann J, Hilger P, Rusde HJ, Kruskernper HL: Plasmapheresis in the

treatment of thyrotoxic crisis. Dtsch Med Wochenschr 99:888-892, 1974.

Ashkar FS, Katims RB, Smoak WM, Gilson AJ: Thyroid storm: Treatment with

blood exchange and plasrnapheresis. 3AMA 214:1275-1279, 1970.

& Pulmonary Edema

Lucian S, Nicolae M: Plasmapheresis in nte pulmonary edema. N Engf J Med

283:1289-1290, 1970.

C. Hypertension

Kris M, Whit DA: Treatment of eclampsia by plasma exchange. Plasma Ther

2:143- 147, 1981.

ARC Blood Services

Bibliography

TPB XIII-2

d$Apice AJF, et al: Treatment of severe pre-eclampsia by plasma exchange. Aust

NZ J Obstet Gynaecol 20:231-235, 1980.

Whitworth 3A, d’Apice AJF, Kincaid-Smith P, Shulkes AA, Skirmer SL: Antihypertensive effect of plasma exchange. Lancet 1:1205, 1978.

D. Poisoning

Gelfand MC, Winchester JF: Hemoperfusicm and toxin adsorptia in the treatment

of poisonings. In Nemo GJ, Taswell H (edsh “Proceedings of the Wcckshop on

Therapeutic Plasmapheresis and Cytapheresis, April 1979.” Washington, DC: U.S.

Department of Health and Human Services, 1981, pp 249-263.

Stevens DC, Kleiman MB, Lietman PS, Schreiner RL: Exchange transfusion in

acute chlorarnphenicol toxicity. J Pediatr 99:651-653, 1981.

Davison AM, Masci&Taylor BH, Robimon ~, Barnard DL: The use of plasma

● xchange, transfusion and haemodialysis in the management of sodium chlorate

intoxicatim. In Sieberth HG (ed~ “Plasma Exchange. Plasmapheresis - PlasmaSeparation.’ $ StuttgarC F. K. Schattauer Verlag, 1980, pp 373-374.

Am= Ph, Barret L, Chenais F, Debru JL, Faure J: Digitoxin intoxicatia treated

by plasma ● xchange. In Sieberth HG (edk TIasma Exchange. Plaamapheresis -

Plasrnaseparation.w Stuttgart: F. K. Schattauer Verlag, 1980, pp 369-371.

Kessler D~ Smith AL, Woo&um DE: Ctdorarnphenicol toxicity in a neonate

treated with exchange transfusitm. J Pediatr %:140, 1980.

Rommes JH, Imhof JW, Kreek PI Successful plasma ● xchange in thyrotoxic crisis.

In Sieberth HG (ed~ ‘Plasma Exchange. Plasmapheresis - Piasmaseparation.”

Stuttgart: F. K. Schattauer Verlag, 1980, pp 361-363.

Arimi G, Ciccarelli P, Ghergo GF, Reverberi R: Therapeutic treatment of 3 cases

of acute Amanita phalloides poisoning. Minerva Anestesiol 45:335-344, 1979.

Mastrangelo F, et ah Hernodialysis and hemoperfusion in the treatment of

paraquat or diquat poisming. Minerva Hefrol 26:399-403, 1979 (English abstract).

Berlyne GM: Plasrnapheresis, aluminum, and dialysis dementia Lancet 2:1155-

1156, 1978. ‘

Elliott HL, MacDougaU AI, Fell GS, Gardiner PHE: Piasmapheresis, aluminum, and

dialysis dementia. Lancet 2:1255, 1978.

Dearnley DP, Lindstrom MFR: Plasmapheresis fcr paraquat poisoning. Lancet

1:16~ 1978.

Elliott HL, McDougall AI, Fell GS, Gardiner PHE: Plasmapheresis in the treatment

of dialysis encephalopathy. Lancet 2:940-941, 1978.

Miller J, Sanders E, Webb D: Plasmapheresis fcf paraquat poisoning. Lancet

1:875-876, 1978.
Lembeck F, Beubler E, Lepuschutz HT, Stolze A:

o! toxic substances with marked plasma protein

Wochenschr 89:257-260, 1977.

Luzhnikov EA, Yaroslavsky AA, Molodenkov MN,

sukov VF: Plasma perfusion through charcoal

Lancet 1:38-39, 1977.

ARC Blood Services

Bibliography

TPB XIII-3

Plasmapheresis for elimination

binding properties. Wien Klin

Shurkalin BK, Enseer NG, Barin methylparathion poisoning.

Mercurial F, Sirchia G: Plasma exchange for mushroom poisoning. Transfusion

17:644-646, 1977.

Winchester JF, Gelfand MC, Knepshield 3H, et al: Dialysis and hemoperfuion of

poisons and drugs - update. Trans Am Soc Artif Intern Organs 23:762-842, 1977.

Mercurial F, Sirchia G: Plasma exchange for mustmom poisoning. In Proceedings

of Advanced Component Seminar, Vol. 4. Haemonetics Research Institute,

Wayland, MA, 1976.

Okonek S: Haemoperfusia with coated activated charcoal for treating acute

poisoning by remedies, plant protestants, and fungi. Wochenschr Klin Praxix

71:112, 1976.

Lo@hin IM, Kmoarov BD, Luzhnikow EA, Shimanko U, Molodenkov MN: Treatment of acute barbiturate poisoning by the methcxf of hemosorption. Sov Med 11:3,

1975.

Vale 3A, Rees AJ, Widdop B, Goulding R: Use of charcoal haemoperfusion in the

management of severely poisoned patiem. Br Med 3 1:5, 1975.

Winchester IF, Edwards RO, Tilstone W3, W oodclock BG: Activated charcoal

hemoperfusion and experimental acetarninophen pOiSOI’Iing. Toxicol Appl

Pharmacol 31:120, 1975.

~ Asthma

Gartmann 3: Plasmapheresis in severe asthma. Lancet 1:903-904, 1978.

Gartmann 3, Grob P, Frey M: Plasmapheresis in severe asthma. Lancet 2:40, 1978.

Muers MF, Dawkins KD: Plasmapheresis in severe asthma. Lancet 2:260, 1978.

F. Crohn’s Disease

Harnblin T, Holdstock G, Fisher A, Loehry C: Plasma exchange in Crohn’s disease.

In Sieberth HG (edh “plasma Exchange. Plasmapheresis - Plasmaseparatiom”

Stuttgart: F. K. Schattauer Verlag, 1980, pp 309-313.

Holdstock GE, Fisher 3A, Hamblin TJ, Loehry C: Plasmaphere$is in Crohn’s

disease. Digestion 19:197-201, 1979.

ARC Blood Services

Bibliography

TPB XIII-4

Holdstock G, Fisher A, LoelYy C, Hamblin T3: Trial of plasmapheresis in patients

with Crohn’s disease. Gut 19:974-975, 1978.

G. Miscellaneous

Simon TL: Therapeutic pl=ma exchange: A request fcr information. Pl=ma Q

4:8, 1982.

Yarrish RL, Janas 3S, Nosanchuk JS, Steigbigel RT, Nusbacher J: Transfusion- ~quired falciparum malaria Treatment with ● xchange transfusion following

delayed diagmsis. Arch Intern tMed 142:187-188, 1982.

Blumberg N, Katz AJ: Therapeutic phsrnapheresis and cytapheresis. A review.

Corm Med 45:85-90, 1981.

Bulova S: Pl=mapheresis as a therapeutic modality. In “Apheresis: Application,

Collection, and Research Procedures Seminar.” Bethesda, MD: National Naval

Medical Center and Haemonetics Research Institute, December 1981.

Cahill KM, Benach JL Reich LH, Bilrnes E, Zins 3H, Siegel FP, Hochweis S: Red

cell exchange: Treatment of babesicais in a splenectomized patient. Transfusion

21:193-198, 1981.

Cm’gut R: Theoretical model of epuration by plasma exchange. Rev Fr Transfus

[mmunohematoi 23:365-371, 1981.

Dau PC: Plasmapheresis in idiopathic inflammatory myopathy. Experience with 35

patients. Arch Neurol 38:544-553 1981.

Del Tavero A, et al: Clinical use of pl=mapheresis. Clin Ter %:93-99, 1981.

Freireich EJ: Future trends in apheresis. In ,Mielke CH Jr (edh “Apheresis:

Development, Applications, and Collection Procedure$.” New York Alan R. Liss,

1981, pp 155-162.

Handley SL, Vogel RA: Therapeutic apheresis. New Yorlc L.F. Rothschild,

Unterberg, Towbin, 1981 (status report).

Hill N: Therapeutic studies on Ieukapheresis and plasmapheresis. In MielketEH Jr

(edk “ApheresiS Development, Applications, and Collection Procedures.” New

Ycclc Alan R. Liss, 1981, pp 147-154.

Kellogg RM, Hester 3P: Plasma exchange by continuous flow Centrifugation. In

Borberg H, Reuther P (eds): “Pl=ma Exchange Therapy.” Stuttg%t: Georg Ttieme

Verlag, 1981, pp 5-10.

Klein H: Clinical erythrocytapheresis. [n “Apheresis: Application, Collection, and

Research procedures Seminar.” Bethesda, MD: National Naval ,Medical Center and

Haemonetics Research Imtitute, December 1981.

Klein HG: Therapeutic cytapheresis. In “Third Annual

Current Concepts and Future Trends.” Skokie, IL:

Apheresis, 1981 (abstract).

Symposium on Apheresis:

American Society for
ARC Blood Services

Bibliography

TPB XIII-5

Kris M, Whit DA: Treatment of eclampsia by plasma ● xchange. Plasma Ther

2:143-147, 1981.

Landini S, Coli U, Lucatello S, Bazzato G: Plasma exchange in severe 1eptospirosis. Lancet 2:1 119-1120, 1981.

Ltndsgaard-tlansen P, Riedwyl H, Deubelbeiss K: Computer simulation of therapeutic plasma exchange. In Borberg H, Reuther P (eds): ‘Tlasma Exchange

Therapy.” Stuttgart: Georg Thieme Verlag, 1981, pp 53-59.

McGtlllough 3, Chopek M: Therapeutic plasma exchange. Lab Med 12:745-753,

1981.

Mielke CH 3r, Mielke MR: Technical and therapeutic applications of plasma

exchange. In Mielke CH Jr (cd): “Apheresiw Development, Applications, and

CoUectiort Proceciures2’ New York: Alan R. Lias, 1981, pp 123-145.

New blood washing therapy: Catching on big despite lack of controlled studies.

Med World News 22:47, 1981.

Nusbacher 3: Therapeutic cytapheresis and plssma exchange. In Petz LD, Swisher

SM (cd} 7he Clinical Practice of Blood Transfusion.” New York: Chuchill

Livingston, 1981, pp 719-734.

Perveev Vk Direct exchange blood transfusions and therapeutic phsmapheresis in

the overall treatment of severely burned patients. Vism Khir 126:124-128, 1981.

Pineda AA, Taawell HF, Moore SB: Therapeutic plasmapheresis and cytapheresis.

In Nemo G3, Taswell H (edsh “Proceedings of the Workshop on Therapeutic

Plasmapheresis and Cytapheresis, April 1979.” Washington, DC: U.S. Department

of Health and Human Services, 1981, ~ 1-23.

Plasmapheresis: Turning old techniques into new therapy. Washington, DC: GWU

~Medical Center 4:1, 1981.

Rock G: A forum for information: Plasma therapy. Plasma Ther 2:51-52, 1981.

Samet 3M, Simon TL: Idiopathic pulmonary fibros”u treated with plasma exchange.

Pla$ma Ther 2:135-137, 1981.

Schmidt PJ: Therapeutic plasma exchange. Arch Intern Med 141: 1661-1662,

1981.

Shapiro M: Medical-1egal considerations of apheresis. In ‘Apheresis: Application,

Collection, and Research Procedures Seminar.” Bethesda, MD: National Naval

Medical Center and Haemonetics Research Institute, December 1981.

Singsen BH: Plasmapheresis: A pediatric perspective. J Pediatr 98:232-235, 1981.

Solcxnon JM: Apheresis and health care: Current policies and long term

consequences. In “Apheresis: Application, Collection and Research Procedures

Seminar.” Bethesda, MD: National Naval Medical Center and Haemonetics

Research Institute, December 1981.

ARC Blood Services

Bibliography

TPB XIII-6

Taft EG, Baldwin ST: Plasma exchange transfusion. Semin Thromb Hernostas

7:15-21, 1981.

Verrier Jones J: Plasrnapheresis: Current research and success. Heart Lung

9:671-674, 1981.

Wenz B, Barland P: Therapeutic intensive plasmapheresis. Semin Hematol

18:147-162, 1981.

Wright DG, et al: Lymphocytapheresis. Prog Clin Biol Res 58:217-224, 1981.

Wright DG, ● t al: Lymphocyte depletion and immunosuppresaion with repeated

leukapheresis by continuous flow centrifugatitm. Blood 48:451-458, 1981.

Wysenbeek AJ, Smith JW, Krakauer RS: Plasmapheresis II: Review of clinical

experience. Plasma Ther 2:61-71, 1981.

Blumberg N, Katz AJ: Psrtial plasma exchange: Diseases in which it is of

reported efficacy. In Berkman EM, Umlas J (edsb ‘Therapeutic Hernapheresis.”

Washington, DC: American Associatial of Blood Banks, 1980, pp 79-95.

d’Apice AJF, et ah Treatment of severe pre-eclampsia by plasma exchange. Auit

NZ J Obstet Gynaecol 20:231-235, 1980.

Das PC: Phsma exchange prograrnme f m patient in a regional blood transfusion

service. In Smit Sibinga CT, Das PC (edsk “Symposium on Donor Management and

seminar of Pheresis Programmed.” Proceedings of 4th Annual Symposium and

Seminar on Blood Transfusion. Groningeru Drukkerij H. Schut, 1980, pp 137-146.

Gilctmr RO Therapeutic plasmapheresis and plasma exchange. In Sherwood WC,

Cohen A (eds~ transfusion Therapy. The Fetus, Infant, and Child.’” New York:

Masson Publishing USA, Inc., 1980, pp 201-209.

Gratwotd A, et al: Experience with intensive plasma exchange. Schweiz !Med

Wahendu 110:1449-1451, 1980 (English abstract).

Guidelines for therapeutic apheresis. Braintree, MA: Haemonetics Research

Institute, 1980.

Hughes GR: Plasma ● xchange (plasmapheresis). Agents Actions (Suppl) 7?62-65,

1980.

Hughes GRV, Ryan PFJ: Plasma exchange conference report. AM Rheum Dis

39:95-96, 1980.

Pinching AJ: Recent advances in immunological therapy: Plasma-exchange and

immunosuppression. Br J Anaesth 1:21-28, 1980.

Plasma exchange. Lancet 2:241-242 (editorial), 1980.

Schmitt E, Falkenhagen D, Preussner S, Tessenow W, Holtz M, Klinkrnann H:

Plasma separation (PS) and plasmapheresis (PP) - a comparative study. In Sieberth

HG (cd): “Plasma Exchange. Plasmapheresis - Plasmaseparation.” Stuttgart: F.

K. Schattauer Verlag, 1980, pp 99-103.
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ARC Blood Services

Bibliography

TPB XIV-2

ARC Blood Services

Bibliography

TPB XIV-3

o

CD

cd

I

. .

0

tW

Aufeuvre 3P, ,Morin-Hertel F, Cohen-Solal M, Lefloch A, Baudelot 3: Hazards of

plasma exchange. A nation-wide study of 3431 exchanges in 592 patients. In

Sieberth HG (cd): “plasma Exchange. Plasrnapheresis - PlasmaSeparation.”

Stuttgart: F. K. Schattauer Verla& 1980, pp 149-157.

Beyer 3-H, Klees M, K6stering H, Nagel GA: Coagulation studies before, during

and after repeated plasma exchanges with a 5% human albumin/saline solution in

normal donors. In Sieberth HG (cd): “Plasma Exchange. Plasmapheresis -

Plasmaseparation.” Stuttgart: F. K. Schattauer Verlag, 1980, pp 87-92.

Chopek M, McCullough 3: Protein and biochemical changes during plasma

exchange. In Berkman EM, Umlas J (eds): ‘71terapeutic Hemapheresis.”

Washington, DC: American Assoaation of Blood Banks, 1980, pp 13-52.

Evans RT, MacDcmld R, Robinson A: Suxamettmnium apnoea associated with

plasrnaphoresis. Anesthesia 35:198-201, 1980.

Fabre M, Andreu G, Mannoni P: Sane biological modifications and clinical hazards

observed during plasma exchanges. In Sieberth HG (cd): “Plasma Exchange.

Plasm apheresis - Plasmaseparation.” Stuttgart: F. K. Schattauer Verlag, 1980, pp

143-148.

Gelabert A, Ruig L, Maragall S, LMonteagudo 3, Castillo R: Coagulative alterations

during massive plasmapheresis. In Sieberth HG (edh “Plasma Exchange. Plasmapheresis - Plasmaseparation.” Stuttgart: F. K. Schattauer Verlag, 1980, pp 71-75.

Lumley J: Prolmgation of suxamethonium following pIasma exchange. Br J

Anaesth 52:1149-1150, 1980.

Malchesky PS, et al: Complement removal by sorbents in membrane plasmapheresis with on-line plasma treatment. Trans Am SoC Artif Intern Organs 26:541-

545, 1980.

L~ilich DR, et al: Plasmapheresis of hepatitis B surface antigen carriers. Acta

Haematol Pol 11:73-78, 1980.

Muse EE, Hohnadel DC, Genco P, et al: Decreased ionized calcium during

therapeutic plasma exchange, pheresis and plateletpheresis. Johns Hopkins ~Med 3

146:260-263, 1980.

Orlin JB, et al: Partial plasma exchange using albumin replacement: Removal and

recovery of normal plasma constituents. Blood 56:1055- 1059, 1980.

Peters U, Risler T, Grabensee B: Digitoxin elimimtion by plasma exchange. In

Sieberth HG (cd): “Plasma Exchange. Plasmapheresis - Plasm aseparatiOn.”

Stuttgart: F. K. Schattauer Verlag, 1980, pp 365-368.

Schooneman F, Janet C, Streiff F: Hemolysis following cytapheresis. 2 cases.

iNouv Presse Med 9:540, 1980.

Urbaniak S3, Barclay GR, Greiss MA: Adverse effect of plasma exchange on

maternal anti-D levels in HDN due to the removal of plasma inhibitory factors.

Joint ,Meeting 18th Congress International Society of Hematology and 16th

Congress Internatimal Society of Blood Transfusion, August 1980, Montreal,

Canada (Abstract 1413).

Watson DK, Penny AF, Marshall RW, et al: Citrate induced hypocalcemia during

cell separation. Br 3 Haematol 44:503-507, 1980.

Flaufh MA, Cuneo RA, Appelbaum FR, Deisseroth AB, Engel WK, Gralnick HR:

The hemostatic imbalance of plasma-exchange transfusion. Blood 54:694-702,

1979.

Keller AJ, Chirnside A, Urbaniak S3: Coagulation abnormalities produced by

plasma exchange on the cell separator with special reference to fibrinogen and

platelet levels. Br 3 Haematol 42:593-603, 1979.

Kilpatrick D, Fleming 3, Clyne C, Thompson CR: Reduction of blood viscosity

following plasma exchange. Atherosclerosis 32:301-306, 1979.

Paterson 3L, Walsh ES, Hall GM: Progressive depletion of plasma cholinesterase

during daily plasma exchange. Br Med J 2:580, 1979.

Shafrir E, Brenner T: Lipoprotein lipid and protein synthesis in experimental

nephrosis and plasm apheresis. 1: Studies in rate in vivo. Lipids 14:695-702, 1979.

Simon TL: Changes in hernostasis during plasma exchange. Blood 54:129a, 1979.

Sul- Y, Bu=el A, Maisonneuve P, Poupeney M, Sitty’ X, Gajdos P: Potential

danger of thrombosis after plasma exchange in the treatment of patients with

immme disease. Transfusim 19:588-593, 1979.

Winkelstein A, Volkin RL, Starz TW, et al: The ● ffects of plasma ● xchange on

immunologic factors. Clin Res 27:691A, 1979.

Avanzi G: The apheresi= plasmapheresis, plateletpheresis, Ieukapheresis. Physiopathology of the donor. Pathologic 70:467-480, 1978.

Drescher WP, Shih N, Hess K, et al: Massive extracorporeal blood clotting during

discontinuous flow leukapheresis. Transfusion 18:89-90, 1978.

Gorodetskv~ VM: Reactions obaerved in blood donors and patients during cytapheresis on the blood cell separator. Ter Arkh 50:129-131, 1978.

Keller A3, Urbaniak S3: Intensive plasma ● xchange on the cell separator: Effects

on serum immunoglobulins and complement components. Br 3 Haematol 38:531-

540, 1978.

Mme JR: Influence of plasmapheresis on total and T-lymphocyte count. Blut

36:175-178, 1978.

Wood G3, Hall GM: Plasmapheresis and plasma cholinesterase. Br 3 Anaesth

50:945-949, 1978.
ARC Blood Services

Bibliography

TPB XIV-4

Isbister JP, Ling A, Seeto KM: Development of Rh-specific maternal autc+

antibodies following intensive plasmapheresis f- Rh immutizatim during preg-

-“ Vox sang 33:353-358, 1977.

Ltmdsgaard-Hanaen P: Intensive plasmapheresis as a risk factor for arterisclerotic cardiovascular disease? Vox Sang 33:1-4, 1977.

Pinching AJ, Rees AJ: Plasmapheresis and plasmacholinesterase. Lancet 2:134-

135, 1977.

Wood GJ: Plasmapheresis and plasm~linesterase. Lancet 1:1305-1306, 1977.

Browne 0, Bell J, Holland PO, Thornes RD: Plasmapheresis and immunostimuIation. Lancet 2:96, 1976.

Buskard NA, Vqhese A Wills MR: Correction of hypocalcaemic symptoms *ring

plasma exchange. Lancet 2:344-345, 1976.

Hersey P, Isbister J, Edwards A, Murray & Adams E, Biggs J, Milton GW:

Antibody-dependent, cell-mediated cytotoxicity against melanom a cells induced by

@aSMaphefeSiS. Lancet 1S25-827, 1976.

Howard 3E, Perkim HA: Lysis of donor RBC tiring plateletpheresis with a blood

processor. 3AMA 236:289-290, 1976.

Isbister JR, Biggs 30 Reacticns to rapid infusion of stable plasma protein solution

tiing large volume plasma exchange. Anaeath Intensive Care 4:105, 1976.

Plasmapheresis and irnmumw.qpression. Lancet 1:1113-1114 (editorial), 1976.

Strauss RA, Kling TF, Levinsohn MW, et ah Facilitation of ● xchange transfusions

with Suibner shunts in Reye’s syndrome. Am J Surg 131:772, 1976.

White JM, White YS, Buskard N, GiUies IDS: Increasing whole blood oxygen

affinity during rapid exchange transfusion: A potential hazard. Transfusion

16:232 1976.

Bayer WL, Farrales FB, Summers T, Belcher C: Coagulatica studies after pkma

exchange with plasma protein fraction and lactated Ringeds solution. [n Goldman

JM, Lowenthal RM (edsh “leucocyt- Separation, Collection and Transfusion.”

Londonx Academic Press, 1975, pp 551-560.

Friedman BA, Schork MA, Mocnial 3L, et al: Short-term and long-term ● ffects of

plaamapheresis on serum proteins and immunoglobulins. Transfusion 15:467-472,

1975.

Oon CJ, Hobbs 3R: Medical problems in donors on treatment using the continuous

flow blood separator. In Goldman IM, Lowenthal RM (eds): ‘%eucocytes:

Separation, Collecticm and Transfusion.” London: Academic Press: 1975, pp 576-

577.

Shanbrom E, Lmdak R, Walford RL : Long-term pl=mapheresis: Effects on

specific plasmaproteins. Transfusion 12:162-167, 1972.

ARC Blood Services

Bibliography

TPB XIV-5

Salvaggio 3, Arquemboug P, Bickers 3, Bice D: The effect of prolonged

plasmapheresis on immtmogloklirn, other serum proteim, delayed hypersensitivity

and phytohemagglutinin-induced lymphocyte transformation. Int Arch Allergy Appl

Immmol 41:883-894, 1971.

Murphy GP, Williams PD, Brede HD, Mirand EA, Groenewald 3H, Weber HW, Grace

JT Jr: The effect of lymphocyte depletion by continuous flow centrifugation in

canine renal allotransplants. 3 Surg Oncol Z257-270, 1970.

Ar&io F, Loire R, Roche L: Quick death from myocardial infarct durin

plasmapheresh Clinical and anatomic study. Med Leg Dmtm Corpor (Parisf

2:278-281, 1969.

Pacitti (2 Metabolic ● ffects caused by blood protein restoraticm after plasmapheresis. Arch Fisiol 67:215-223, 1969.

Pacitti C, Mondino M: Nitrogen balance in rats exposed to plasmapheresis. Arch

Fisiol 67:205-214, 1969.

Gutnik RB, Zinevich AK: The electrolyte content of donor blood in frequently

repeated pkrnapheresis. Vrach Delo 2:150-151, 1968.
ARC Blood Services

Bibliography

TPB XIII-7

ARC Blood Services

Bibliography

TPB xIII-8

Schurek HG, von de Heyde C, Velte H, Deicher H, Marghescu S, Stolte H:

Different applicaticms of plasma exchange and optimal adaption of exchange

procedure. In Sieberth HG (edk “Plasma Exchange. Plasmapheresis - Plasmaseparation.” Stuttgart: F. K. Schattauer Verlag, 1980, pp 93-98.

Shiokawa Y, et al: Plasmapheresis in treatment of rheumatic fever. 3pn Circ 3

44:797-)300, 1980.

van

?

WieI A, et al: Plasma exchange in herpes gestationis. Br Med J

281: 041-1042, 1980.

Waldenstr8m JG: Plasmapheresis - bloodletting revived and refined. Acta Med

Scand 208:1-4, 1980.

Amemiya Y, Baba M, Itoh T, Ntmokawa H, Kohzu H, Shindo T, Morita K, Amaki 1:

Therapeutic pheresis. Rimho Ketsueki 20:1191-1197, 1979.

Isbister 3P: Plasma exchange: a selective form of blood-letting. Med J Aust

2:167-173, 1979.

James MP, Kingston P3: Plasmapheresis slows destructive bodies (newsk Am Fam

Physician 20:191-192, 1979.

Katz A3, Blurnberg N, King C: Meeting therapeutic pheresis needs in the region. In ,~ir~t Annu~ Apheresis SYmPo$ium: Current Concepts and Future Trends:’

Published Proceedings. Chicago: American Red Cross Blood Services, 1979.

Lewis RA, Slater N, Croft DN: Exophthalmoa and pretibial myxoedema not

responding to plasmapheresis. Br Med J 1:390-391, 1979.

Lockwood CM: Plasma-exchange: An overview. Plasma Ther 1:1-12, 1979.

Lockwood CM? Wcrlkdge S, Nicholas A, Cotton LC, Peters OK: Reversal of

impaired splemc function by plasma exchange. N Engl 3 Med 300:524-530, 1979.

Ltmdsgaard-Hansen P, Deubelbeiss K: Computer simulation studies of therapeutic

plasmapheresis. ISBT Symposium, Warsaw, 1979, Book of Abstracts, p 23.

Muggeo ,M, Flier 3S, Abrams RA, Harrison LC, Deisseroth AB, Kahn CR: Treatment by plasma exchange of a patient with autoantibodies to the insulin receptor.

N En@ 3 Med 300:477-480, 1979.

Newsom-Davi$ 3, Ward CD, Wilson SG, Pinching A3, Vincent A: Pla$ma@eresis:

Short- and long-term benefits. In Dau PC (edh “Plasmapheresis and the

Immunobiology of Myasthenia Gravis.” Boston: Houghton Mifflin, 1979, pp

199-208.

Nca~ Y, Malchesky PS: Therapeutic application of pl=maphere$is. Plasma Q

1:102- 103, 1979.

Pineda AA, Timwell HF, Moore SB: Therapeutic plasma and cpaphere$is.

Transfusion 19:666, 1979.

Raich PC, Traver MI: Therapeutic plasrnapheresis. Wis Med J 78:37, 1979.

Roncoroni A3, Martino OH: Therapeutic use of exchange transfusion in malaria.

Am J Trop Med Hyg 28:440, 1979.

Roasi PL: Therapeutic value of the cell separator. Review and case reports.

Minerva Med 70:1289-1298, 1979.

Betteridge DJ, Bakowski M, Taylor KG, Reckless JP, de Silva SR, Galton DJ:

Treatment of severe diabetic hypertriglyceridaemia by plasma exchange. Lancet

1:1368, 1978.

Obeid D, Cotton P: Plasmapheresis. Br Med J 1:1486-1487, 1978.

Pinching AJ: Plasma exchange. Br J Heap Med 20:552-558, 1978.

Pl=maphere$is. Br Med J 1:1011-1012, 1978.

Laningham JET: Partial plasma exchange, an adjunct in therapy to complex

clinical problems. Transfusion 17:547-554, 1977.

Pineda AA, Brzica SM Jr, Taswell HF: Continuous- and semicontinuou-flow blood

centrifugation systems: Therapeutic applications, with plasma-, platelet-,

Iympha-, and eosinapheresis. Transfusion 17:407-416, 1977. -

Verrier Jones J: Plasmapheresis: Great economy in the use of horses. N Engl J

Med 297:1173- 1175, 1977.

Buskard NA, Varghese A Wills MR: Correction of hypocalcaemic symptoms during

plasma exchange. Lancet 2:344-345, 1976.

Tilz GP, Teubl I, Kopplhuber CH, Vollman H, Lanzer G: Therapeutische Plasmaphese: Eineneue Form der symptomatischen Therapie. ,Med Klin 71:1952-1957,

1976.

Lagreco G, Sprovieri L: Phsmapheresis on children of less than twenty kilograms.

Haemonetics Proceedings of the Advanced Component Seminar, Natick, IMA, 1975.

Lockwood M, Pearson T: Use of phsma exchange in treatment of allergic d~>eases.

Haemonetics Research Institute, 1975, pp 1-8.

McCullough J: Therapeutic plasma exchange. Advanced Pheresis Seminar.

Boston: Haernonetics Research Institute, 1975.

Oon CJ, tiobb$ JR: Clinical application of the continuous flow blood separator

machine. Clin Exp [mmunol 20:1-16, 1975.

McCullough J, Forttmy IE, Kennedy B], Edson JR, Branda RF, Jacob HS: Rapid

pi-a exchange with the continuous flow centrifuge. Transfusion 13:94-99, 1973.

Agolini G, Giunta L, Nicoiini R: Plasmapheresis as a basis for new therapeutic

possibilities in transfusion. Fracastoro 61:647-652, 1968.
ARC Blood Services AMERXCAN RED CROSS BLOOD SERVICES

Bibliography

TPB XIII-9 Therapeutic Pheresis Bibliogra~y No. XXV: Clinical Reactions, Comp!icatims

Speiser P: Plasrnapheresis. Wien Klin Wochensctr 79:689-694 1967. Appelgate R, et al: Removal of tobramycin during plasma exchange therapy. Ann

Intern Md 94:820-821, 1981.

Abel 33, Rowntree LG, Tuner BB: Plasma removal with return of corpuscles

(Plasmapheresis). J Pharmacol Exp Ther 5:625-641, 1914. Chirnside A, Urbaniak SJ, Prowse CV, Keller A3: Coagulation abnormalities

following plasma ● xchange on the cell separator. II. Effects on f actors I, II, V, VII,

WI, IX, X and antithrnbin W Br 3 Haematol 48:627-634, 1981.

Gutnik RB, Iaralova PV, Muravova LP, Kovalkina LA, Khazan LD: State of the

cardiovascular system in donors wwlergoing multiple, frequently repeated plasmapheresis. Probl Gernatol Pereliv Krovi 26:27-29, 1981.

Hester 3P, KeUo& RM, McCredie KB, Freireich E3: Cross cellular contamination

in plateletpherems, leukapheresis and plasma exchange. In Mielke CH Jr (edh

“Apheresis: Development, Applications, and Collection Procedures.” New Yorlc

Alan R. Lisa, 1981, pp 109-121.

Levy J: Safety and standards f= therapeutic apheresis. In 7hird AMUSl

Symposium on Apheresis Current Concepts and Future Trends.” Skokie, IL: Am

Soc Apheresis, 1981 (abstract).

McLeod BC, Viemes A, Sassetti F3: Complement activation cktring membrane

plasmapheresis. Blood 58 (Suppl Ik 18* 1981.

Monaghan WP: Reactions, monitoring and complicatims. In “Apheresis Application, Collection, and Research Proce@es Seminar.n

Bethesda, MD: National

Naval Medical Center and Haemonetics Research Ir’stitute, December 1981.

Seiler FR, K=ges H, Geursen R, Sedlacek HH: Possibilities, problems and hazards

with blood plasma sdxtitutim therapy. In Borberg H, Reuther P (edsh ‘Plasma

Exchange ?he=py.” Stuttg- G-g Thieme Verlag, 1981, pp 37-52

Shapiro M: Medical-legal consideraticms of apheresis. In “Apheresis: Applicatiq

Collection, and Research Procedures Seminar.” Bethesda, MD: National Naval

Medical Center and Haemonetics Research Imtitute, December 1981.

Sharp DE: Drug kinetics following plasmapheresis. In “ApheresiS Application,

Collection and Research Procedures serninsr.” Bethesda, MD: Naticnal Naval

Medical Center and Haemonetics Research Institute, December 1981.

Sutton DMC, Cardella CJ, Uldall PR, deVeber GA: Complicatims of intensive

plasma ● xchange. Plasma Ther 2:19-23, 1981.

Wing EJ, Brms F3, Fraiey DS, Segel DP, Adler S: l%smaphereais, infection and

renal disease. JAMA 246:1545, 1981.

Wright DG, et al: Lymphocyte depletia and immums~pression with repeated

leukapheresis by continuous flow cenTrifugation. Blood 48:451-458, 1981.
AMERICAN RED CROSS BLOOD SERVICES

Therapeutic Pheresis Bibliography No. XV: Technical Aspects

Ah J, Adjizian 3C, Droulle Ch, Toupance O, Le Roux G, et al: Cryoprecipitatedepleted plasma as a replacement fluid. Plasma Ther 2:243-246, 1981.

Anderson L, Ziter FA: Plasmapheresis via central catheter in dermatomyositis: A

new method for selected pediatric patients. J Pediatr 98:240, 1981.

Cchen PG: Circulatory access for extracorporeal blood modification. Plasma Ther

2:235-238, 1981.

Gre<; TP: Gentamicin elimination during exchange transfusion. J Pediatr

98:507-508, 1981.

Kalinin NN: Principles and methods of using apparatus for plasmocytapheresis with

donors and patients. Probl Gematol Pereliv Krovi 26:11-16, 1981.

Lyday 3G: Formulas to simplify partial red cell exchange. Plasma Therapy

2:1 11-115, 1981.

Mielke CH Jr, Mielke MR: Technical and therapeutic applicatiwts of plasma

exchange. In Mielke CH 3r (edh ‘OApheresk Development, Applkatiomj and

Collection Procedures.” New York Alan R. Liss, 1981, pp 123-145.

Nos~ Y: Technical aspects of therapeutic separation of plasma macromolecules by

membrane filtratim and cryogelation. In wThird Ann~ pkreSk symposium:

Current Concepts and Future Trends.” Skokie, IL: American Society of Apheresis,

1981 (abstract).

Passlick J, ● t al: Puncttre of the internisl jugular vein ss an access for

extracorporeal circulation in hemodialysis, hemoperfusion and plasma separation.

Med Welt 32:1143-1145, 1981 (In German).

Prince AS, Kliegman R, Phaneuf D, Neu HC: The ● ff ect of exchange transfusion

on the blood levels of ampicillin and gentamicin in neonates. Infection 9:1-5, 1981.

Stellon AJ, et al: Polygeline compared with plasma protein fraction as the sole

replacement fluid in plasma exchange. Br Med 3 (Clin Res) 282:696-697, 1981.

Taft EG: Choice of replacement solutions for plasma ● xchange. In ‘Third Amual

Apheresis Symposium: Current Concepts and Future Trends.” Skokie, IL: American

Society fcr Apheresis, 1981 (abstract).

Biacklock HA, et al: Therapeutic plasmapheresis by continuous flow centrifugation. NZ Med 3 92:145-148, 1980.

Chimel H: Technologische Aspekte zur Membranplasmapherese. Bialys*Arzt&

Wcrkshop, Bernried, 1980.

Goudemand M, Toussain-Brevan B, 3uvet 3P: Utilisation de I’albumine @uee l-s

des plasrnaphereses therapeutiques. Communication au symposium sur les plasmaphereses therapeutiques, Cologne, 1980.

ARC Blood Services

Bibliography

TPB XV-2

Kliegman RM, Bertino JS, Fanarof AA, Gavan TL, Speck WT: Pharmokinetics Of

gentamicin during exchange transfusions in neonates. J Pediatr %:927, 1980.

Lundsgaard-Hartsen P, et al: Computer simulation studies of therapeutic plasmapheresis. Acta Haematol Po1 11:117-120, 1980.

McLeod BC: Automated plssmapheresis through a single central vein. Plasma

Ther 1:45-49, 1980.

Orlin JB, Berkman EM : Partial plasma ● xchange using albumin replacement:

Removal and recovery of nccrnal plasma constituents. Blood 56:1055-1059, 1980.

Chopek M, McCuUough 33: Scrne hematologic and biochemical effects of plasma

exchange. Transfusion 19:651, 1979.

Epstein M, Puguay D, Smith A: Effect of exchange transfusion on serum

arninoglycoside concentrations. Pediatr Res 13:368, 1979.

McLeod BC2 Technical =pects of therapeutic plasmapheresis. Pl=ma Ther

1:43-51, 1979*

Menke AM, Dau ~ Technical notes on pl=mapheres.is. In Dau PC (edh

‘T%+smapheresis and the Immunobiology of Myasthenk Gravis.” Bostom Houghton

Miffliw 1979, pp 351-358.

Taft EG, SuUivan SA, Beckef HA, Hammer CE: Plasma ● xchange transfusion:

Kinetics, dose and markem. Transfusion 19:651, 1979.

Wzwd WJ: A relative value unit fcr pheresis prorkcts. Transfusion 19:622, 1979.

Zitko M, Reuter H, Borberg H, Mishler JM: The utilisation of a new strength

citrate anticoagulant during centrifugal plateletpheresis. III. Assessment of in

vitro platelet metabolism. Vox Sang 36:347-352, 1979.

,Menke A, Dau PC: Technical aspects of plasmapheresis. Muscle Nerve 1:342,

1978.

Moulinier 3, Vegon G, Conte PH, Fizet D, Lauroua P: Applicaticms therapeutiques

des echanges pkrnatiques a l’aide de separateurs a flux discontinue. XVll C>ngress

of Inter Soc Hematol, 1978, p 330.

Rcwsgger H, Zach M, Gleispach H, Beitzke A: Digoxin elimimtion by exchange

transfusion. Eur J Pediatr 127:217-222, 1978.

Strauss RA, Kling TF, Levinsohn MW, et al: Facilitation of exchange transfusions

with Scribner shunts in Reye]s syndrome. Am 3 Surg 131:772, 1978.

Winchester IF: Haemmtatic changes induced by adsorbent haemoperfusion. In

Kenedi RM, Courtney IM, Gaylor JDS, Gilchrist T (eds): ‘Artificial %-.”

London: Macmillan, 1977, pp 280-290.
ARC Blood Services

Bibliography

TPB XV-3

Szymanski LO, Patti K, Kilrnan A: Efficacy of Latham blood processor to perform

plateletpheresis. Transfusion 13:405, 1973.

Colart DJ, Watson D, Howard MR: Effect of exchange transfusion in plasma

digoxin levels. Arch Dis Child 47:814-815, 1972.

Marsaglia G, Thomas ED: Mathematical consideration of cross circulation and

exclypge transfusion. Transfusion 11:216, 1971.

Cohen MA, Oberman HA: Safety and long term effects of plasmapheresis.

Transfusion 10:58-66, 1970.

Smalik S: Therapeutic effect of plasma obtained by long-term massive plasmapheresis (preliminary report). Vnitr Lek 16:1022- 1029, 1970.

AMERICAN RED CROSS BLOOD SERVICES

Therapeutic Pheresis Bibliography No. XVk Alternative Methods

Anderson L, Ziter FA: Plasmapheresis via central catheter in dermatomyasitis: A

new method for selected pediatric patients. J Pediatr 98:240, 1981.

Asanuma Y, Malchesky PS, Blumenstein M, Zawicki I, Smith 3W, $ayashima K, Kyo

A, Suzuki M, Shimgawa S, Krakauer RS, Calabrese L, Nose Y: Continuous

cryofiltration for rheumatoid artlritis. Artif Organs (accepted), 1981.

Besa EC, Ray PK, Swami VK, Idiculla A, Rhoads JE Jr, Bassett 3G, Joseph RR,

Coo~r DR: Specific immumadsorption of lgG antibody in a patient with chronic

Iymphocytic leukemia and autoimmune hemolytic anemia A new form of therapy

for the acute critical stage. Am J Med 71:1035-1040, 1981.

Buff aloe GW, Dau P: Development and clinical evaluation of a parallel plate

membrane pl=ma exchange system. In “Third Annual Apheresis Symposium:

Current Concepts and Future Trends.” Skokie, IL: American Society of Apheresis,

1981 (abstract).

Csstino F, Friedman 11, Wiltbank TB, Danie.ls JR, Grapka B, Solomon in BA:

Plasma separation by membrane filtration. In Bwberg H, Reuther P (eds} ‘Tlasma

Exchange Therapy.” Stut&~t: Georg Thieme Verlag, 1981, pp 11-19.

Gurland H3, Sarntleben W, Schmidt B: Plasmaperfusion. In Borberg H, Reuther P

(edsh ‘Plasma Exchange Therapy:’ Stuttgart: Georg Thieme Verlag, 1981, pp

26-29.

Hellstr?3m KE, HeUstr6m k Does perfushm with treated plasma cure cancer? N

Engl J Med 308:1215-1216, 1981.

Kanamono T, Iwata H, Yarnanaka N, Ohta K, Maeda K: Plasma separation using

various kinds of hern~filters in rheumatoid arthritis. In “New Membranes in

Medical Treatment:’ 2nd Tutzing Symposium cm Chemical Engineering in Medicine, Munich, 1981.

Ldsgen H, Bnsmer G, Schmidt FW: Removal of toxic metabolizes by plasma

exchange in patients with hepatic failure. In “New Membranes in Medical

Treatment,” 2nd TutZing Symposium on Chemical Engineering in Medicine, Mmich,

1981.

McLeod BC, Viernes A, Sassetti FJ: Complement activation during membrane

plasrnapheresis. Blood 58 (Suppl l):183a, 1981.

Maeda K, Shinzato T, Usuda M, Sezaki R, et al: Psoriasis treatment with

hernofiltratiqn and plasma exchange. In “New Membranes in Medical Treatment.”

2nd Tutzing Sympcaium on Chemical Engineering in Medicine, Mtmich, 1981.

Passlick 3, et al: Puncture of the internal jugular vein as an access for

extracorporeal circulation in hemodialysis, hemoperfusion and plasma separation.

Med Welt 32:1143-1145, 1981 (In German).

I

I
ARC Blood Services

Bibliography

TPB XVI-2

Sieberth HG, G16ckner WM: Separation of cells from plasma in man using hollowfiber membranes of large pore size. 1n Bofberg H, Reuther P (eds): “Plasma

Exchange Therapy.” Stuttgart: Georg Thieme Verlag, 1981, pp 20-25.

Stoffel W, Borberg H, Greve V: Application of specific extracorporeal removal of

low density lipoprotein in familial hypercholesterolaemia. Lancet 2:1005- 1007,

1981.

Terman DS, Ycung JB, Shearer WT, Ayus C, Lehane D, et al: Preliminary

observations of the effects on breast adenocarcinoma of plasma perfused over

immobilized protein A. N Et@ J Med 305:1195-1200, 1981.

Agishi T, et ak Double filtration plasrnapheresis. Trans Am Soc Artif Intern

Organs 26:406-411, 1980.

Asaba H, Bergstr6m 3, Bendz R, LUfquist B, et al: Plasma exchange with a

membrane plasma filter for treatment of glomeruionephritis. In Sieberth HG (cd):

“Plasma Exchange. Plzmmpheresis - Plasmaseparation.” Stuttgart: F.K.

Schattauer Verlag, 1980, pp 207-211.

Asaba H, et ah Clinical trial of plasma ● xchange with a membrane filter in

treatment of crescentic glomeruionephritis. Clin Nephrol 14:60-65, 1980.

Asanuma Y, ● t ai: Clinical hepatic support by on-line plasma treatment with

multiple absorbents - evaluation of system perfffmance. Trans Am Soc Artif

Intern Organa 26:400-405, 1980.

Das PC, Smit Sibinga CT: Replacement fluid in plasma exchange. Lancet 2:644,

1980.

Grob PJ, Gmllr 3, von Telten A, Frey-Wettstein M, Hartmann S, Gartmann 3:

Plasma exchange and non-specific immune parameters. Comparison of two

methods. In Sieberth HG (edh “Plasma Exchange. Plasmapheresis -PlaSm~

separation.” Stuttgart: F. K. Schattauer Verlag, 1980, Pp 113-119.

Horiuchi T, Otsubo O, Takahashi I, Yamada Y, Yamauchi J, Inou T: Study of

plasma cross circulation in experimental hepatic failure. In Sieberth HG (cd):

“Plasma Exchange. Plasmapheresis - Plasm=eparation:’ Stuttgart: F. K.

Schattauer Verlag, 1980, PP 341-345.

Malchesky PS, Asanuma Y, Smith J, Zawicki I, Ncae Y: Membrane plasma&eresis

with on-line plasma treatment. In Sideman S, Chang TMS (dsh ‘Yiemow’fuaom

Kidney and Liver Supports and Detoxification.” Washington, DC: Hemisphere

Publishing Corporation, 1980 (in press).

Malchesky PS, et al: Complement removal by sorbents in membrane plasmapheresis with omline plasma treatment. Trans Am Soc Artif Intern Organs

26:541-545, 1980.

Otsubo O, et al: Handy type haemofilt.ration - phi.$ma exchange apparatus. PrOC

Eur Dial Transplant Assoc 17:357-361, 1980.

ARC Blood Services

Bibliography

TPB XVI-3

Samtleben W, et al: Membrane plasma separation for treatment of immunlogically mediated diseases. Trans Am Soc Artif Intern Organs 26:12-16, 1980.

Inoue N, Yamazaki Z, Sakai T, Kanai K, et al: A new method for plasmapheresis

using cellulcae acetate hollow fibers as a plasma separator. Artif Organs 3:18,

1979.

Lauterburg BH, Dickson ER, Pineda AA, Carlson GL, Taswell HF: Removal of bile

acids and bilirubin by plasmaperfusion of USP charcoal-coated glass beads. 3 Lab

C1irrK4ed 94:585, 1979.

Sieberth HG, G16ckner W, Hirsch HH, 130rberg H, Mahieu P: Plasmaseparation by

membranes in man. LSAIO, 1979, in press.

Terman DS, Buff aloe G, Mattioli C, Cook G, TiUquist R, Sullivan M, Ajus 3~

Extracccporeaf immunoadscrption: Initial experience in human systemic lupus

erythematosus. Lancet 1:824-826, 1979.

Gelfand MC: Charcoal hemoperfusicm: Georgetown University Hcapital experience.” In Chang TMS (edh “Artificial Kidney, Artificial Liver, and Artificial

Cells.” New York Plenum Press, 1978, PP 117-123.

GIUckner WM, Sieberth HG: Plasmafiltration, a new method of plasma exchange.

Proceedings of the European Society for Artificial Organs, Vol. 5, 1978, p 214.

.

Solomon BA, Castino F, Lysaght M3, Colton CK, Friedman Ll: Continuous flOW

membrane filtraticm of plasma from whole blood. Trans Am Soc Artif Intern

Organs 24:21, 1978.

Gelf and MC, Winchester JF, Knepshield 3H, Hartson KM, Cohan SL, S?rauch BS,

Geoly KL, Kennedy AC, Schreiner GE: Treatment of severe dug overdcsage with

charcoal hemoperf usion. Trans Am Sa Anif Intern Organs 25:599, 1977.

Hill 3B, Palaia FLj Hores CR: The design of a charcoal hemoperfusion system. In

Kenedi R, Courtney JM, Gaylcr JDS, GilChrist T (edsk “Artificial OrganS.”

Londom Macmillan, 1977, pp 123-132.

Winchester 3F, Apiliga MT, Kennedy AC: Short term evaluation of charcoal

hemoperfusion combined with dialysis in uremia patients. Kidney Int 10: S315~

1977.

Gazzard BG, Weston MJ, Murray-Lyon IM, et al: Experience at King’s College

Hospital with charcoal haemowrfusioru Overall resul~ in 37 patients. In Williams

R, Murray-Lyon IM (eds): “Artificial Liver Support.” London: Pitrnan, 1976, P ~.

Gelfand MC, Knepshield JH, Cohan SL, et al: Treatment of hepatic coma with

hemoperfusion through polyacrylamide hydrogel-coated charcoal. Kidney Int

10: S239, 1976.

Nos~ Y, Malchesky PS, Castino F, Koshino I, Scheucher K,

hemoperfusion systems for renal/hePatic suPPorto Kidney Int

Nokoff R: Improved

10:S244, 1976.
ARC Blood Services

Bibliography

TPB XVI-4

R~enbaum JL, Kramer MS, Raja R: Resin hemoperfusion for acute dug

intoxication. Arch Intern Med 136:263, 1976.

Sanjo K, Fujimori Y, Yamazaki Z, et ah The effect of liver support system (plasma

perfusion detoxicatiat) providing removal of plasma amino acids in patients with

fuhninant hepatitis. Artif Organs (3pn) Suppl 5:231-234, 1976.

ThyseIl H, Linkholrn T, Heinegard D, Henrikson H, Johnson E, Nylen U, Svensson T,

Bergkvist G, Gullberg CA: A haemoperfusion column using cellophane coated

charcoal. Proc E- Soc Anif Organs 2:231, 1976.

Gazzard BG, Portmann BA, Weston M3, Langley PG, Murray-Lyon IM, et al:

Charcoal haemoperfusion in the treatment of fulminant hepatic failure. Lancet

1:1301, 1974.

Gazzard BD, Weston MJ, Muray-Lyon IM, ● t ah Charcoal haemoperfusion in the

treatment of fulminant hepatic failure. Lancet 1:1301, 1974.

Medd RK, Widdop B, Braithwaite RA, Rees A3, Goulding R: Comparison of

haemoperfusion and haemodialysis on the therapy of b= bittrate intoxication in

*%$. Arch ToxiCOi 31:163, 1973.

Rosenbaum 3L, Winsten S, Kramer MS, Moms 3, Raja R: Resin hemoperfusi~ in

the treatment of &ug intoxication. Trana Am Soc Artif Intern Organs 16:134,

1970.

Hagstam KE, ~sson LE. Thysell 1+ Experimental studies on charcoal hemoperfusion in Phenob=bital intoxication and uremia. Acta Med Scand 180:593, 1966.

Yatzidis H: A convenient haemoperfusion mifxo-apparatus over charcoal for the

treatment of endogenoua and exogenous intoxications. Its use as an artificial

kidney. Proc Eur Dial Transplant Assoc lt83, 1964.

AMERICAN RED CROSS BLOOD SERVICES

Therapeutic Pheresis Bibliography No. XVII: Texts, Symposia

Nusbacher 3: Therapeutic hemapheresis. Clin Lab Med 2(1), March 1982.

‘Apheresis: Application, Cohection and Researd Proceckmes seminar.” Csponsored by National Naval Medical Center and Haemonetics Research Irstitute,

Bethesda, MD, December 1981.

Borberg H, Reuther P (edsk ‘Plasma Exchange Therapy.n Stuttgart: Georg Thieme

Verlag, 1981.

/

Hennessen W (edk “Albumi~ Plasma Substitutes and Plasmapheresis.W Basel:

Karger, 1981.

Hennessen W (ed~ “Internatimal Sympoaium on Standar dizatia of Albumi~ Plasma

Substitutes and Plasmapheresis.” Basel: S. Karger, 1981.

Mielke CH 3 (edk “Apheresis Development, Applicatims, and Collection Pr~

cedures.n New York Alan R. Liss, Inc, 1981.

Nemo G3, TaswelJ H (edsh ‘Proceed“rigs of the Workshop on Therapeutic Plasmpheresis and Cytapheresis, April 1979.W Bethes@ Mh U.S. Department of Health

and Hwnan Services, 1981 (NIH Publication No. 82-1665).

Rubin &Stenzel KH, Sullivan 3S (edsk %linical and Experimental Dialysis and

ApheresisJ’ New Yorlo Marcel Dekker, Inc, 1981. .

‘Third Annual Apheresis Symposium: Current Concep?s and Future Trends.n

Published abstracts. Skokie, IL: American Society of Apheresis, 1981.

Berbnan EM, Umlas J (edsk Therapeutic Hemapheresis. A Technical Workshop.W

Washington, DC: American Associatia of Blood Banks, 1980.

Borberg H, Reuther P (e&h Tlasma Exchange Thempy.” Proceedings of

Internatiwtal Society on Plasma Exchange Therapy, Wiesbaden, 1980. New York

Thieme-Stratton, Inc, 1980.

Hamblin T3: “Plasmapheresis and Plasma Exchange.” St. Albans, VT: Eden

Medical Research, Inc, 1980.

“Second Annual Apheresis Sympmium: Cwent Concepts and Futue Trends.W

Published Proceedings. Skokie, IL: American Society for Apheresis, 1980.

Sherwood WC, Cohen A (edsh Vransfusicm Therapy. The Fetus, Infant, and Child.n

New York Masson Publishing USA, Inc., 1980.

Sieberth HG (edh “Plasma Exchange. Plasmapheresis - Plasmaseperation.n

Stuttgart: F.K. Schattauer Verlag, 1980.

Dau & (edh ~?pl=m~=esis ~ the Immtnobi~ogy of Myasthenia Gravis.W

Bostom Houghton Mifflin, 1979.
ARC Blood Services

Bibliography

TPB XVII-2

“First Annual Apheresis Symposium: Current Concepts and Future Tren@.”

Published Proceedings. Chicagot American Red Cross Blood Services, 1979.

%eukapheresia and Donor Safety W orkshop.n June 4, 1979. Bethesda, MD: Bureau

of Bidogics.

“Pheresis A Vital Blood Service.n Workshop for American Red Cross Pheresis

Staff. Washington, DC: American Red Cross Blood Services, 1979.

Gddrmn 3M, Lowenthal RM (edsh ‘Leukocytes Separation Collection and

Transfusion.” Londom Academic Press, 1975.

AMERICAN RED CROSS

BLOOD SERVICES

Therapeutic Phereais Bibliography

Sqplement No. 2

hmlary 1983
AMERICAN RED CROSS BLOOD SERVICES

Supplement 2

Therapeutic Pheresis Bibliography No. 1: Neuroiogiatl Disorders

A. Myasthenia Gravis

Another antibody in myasthenia gravis sera? JAMA 247:1237, 1982 (editorial)

3acobsen H, Thorlaci S, Aarli 3A: Plasmapheresis in myasthenia gravis - clinical

resu~ and changes in serum-proteins. Acta Neurol Scand 65:128-129, 1982

Lenzhofer B, Mamoli B, Graninger W, 2eitlhofer 3: Reduction of anti-acetylchoiine receptor antibodies by plasmapheresis in myasthenia gravis. In ‘international Symposium on Plasmapheresis: Therapeutic Applications and New Techniques.” Cleveland: Int Soc Artif Organs, 1982, p 21

Mizuno Y, Humphrey 3, ~sch HM, Gelfand EW: Carbamylcholine modulation of Erosette formation - effect of plasrnapheresis in myasthenia-gravis. Clin Exp

Immunol 49:209-216, 1982

Nielsen VK, et al: Rapid improvement of myasthenia gravis after plasma ● xchange.

Ann NeUrOl 11:160-169, 1982

Pascuzzi RM, Coslett HE, Johns TR: Treatment of myasthenia gravis: Extension of

data on prednisone and adjunctive thyrnectomy, antimetabolit~ and plasmapheresis. AM hkurol 12:109, 1982

Valbonesi M, Garelli ~ Zerbi D, Forlani G, Cornelio F, Pelucchetti ~ Plasma

exchange combined with cytotoxic drugs and lyrnphocytapheresis for myasthenia

gravis. VOX sang 143:142-146, 1982

Vincent A: Role of plasma exchange in myasthenia gravis and the Eaton-Janbert

syndrome. Boston: Haemonetics Advanced Component Sernina r, Boston: 1982

(abstract)

Arahata K, Sato T, Narabayashi H: Evaluation of plasma exchange in management

of myasthenia gravis. “IUnsho Shinkeigaku 21:597-606, 1981 (English abstract)

Dau PC: Response to plasmapheresis and immmos~pressive drug therapy in sixty

myasthenia patients. Ann NY Acad Sci 377:700-708, 1981

Gajdos P, et al: Plasma ● xchange in myasthenia gravis and polyradiculonephritis.

Rev Fr Transfus Immunohematol 24:657-659, 1981 (In French)

Keesey J, ● t al: Plasma exchange alone as therapy for myasthenia gravis. Ann NY

Acad W 377:729-743, 1981

Milkr RG: Plasmapheresis in myasthenia gravis. Ann Neurol 10:396-397, 1981

ARC Blood Services

Bibliography Supplement 2

TPB I-2

Motomura S, Konishi T, Tsukie T, Ohta M, Matsubara F, Nishitani H, Yasuda M,

Kotani R: Treatment of myasthenia gravis with intermittent plasmapheresis and

on the new double filtration method of plasmapheresis. In Oda T (cd): ~erapeutic Plasrnapheresis.” Stuttgart: F. K. Schattauer Verlag, 1981, pp 215-219

Nishitani H, et al: Plasma exchange in the treatment of myasthenia gravis.

Nippon Rinsho 39:3302-3309, 1981 (In Japanese) f

Olarte MR, et ah Effect of plasmapheresis in myasthenia gravis 1978-1980. Ann

NY Acad Sci 377:725-728, 1981 ~

e

Pasternak 3F, Hageman 3, Adams MA, Philip AGS, Gardner TH: Exchange &

transfusion in neonatal myasthenia. J Pediatr 99:644-646, 1981

●

Perlo VP, et al: Effect of plasmapheresis in myasthenia gravia. Ann NY Acad Sci ?

377:709-724, 1981 g

Reuther P, Wiebecke D, BUske A, Martens HG: Die Plaamaaustausch-Behandlung

bei Myasthenia gravis und anderen neuropsychiatrischen Erkrankungen. In Gurland

HJ, Heirue V, Lee HA (eds): therapeutic Plasma Exchange.” New York: Springer

Verlag, 1981, pp 55-73 (In German)

Riley TL, Monaghan WP: Plasmapheresis in myasthenia gravis: Decline in

antireceptor antibody without clinical improvement. Case report. Miiit Med

146:724-725, 1981

Rodnitzky RL, Bosch E% Plasmapheresis as a guide for azathiopritw therapy in g

prednisone-resistant myasthenia gravis. Muacie Nerve 4:529-530, 1981

$!

Sato T, Arahata K, Nishimiya H, Morimoto K, Amo M, Narabayashi H, Yuasa S: ~

Treatment of myasthenh gravis by plasma exchange and corticosteroids: Levels of ?“

antibody to =etylcholine receptor and clinical states. In Oda T (cd): ‘Theral=tic

Plasmapheresis.” Stuttgart: F. K. Schattauer Verlag, 1981, pp 221-225 i

Dau PC, Poole M: Plasmapheresis in myasthenia gravis. NHK 9:139, 1980

~

Goulon M, et ah Determination of anti-etylcholine receptor antibodies in ?

myasthenia gravia and its treatment by plasma exchange and immunos~pressants.

C R Soc Biol (Paris) 174:467, 1980 (In French) $

~.

Lisak RP, Schotland DL: Piasmapheresis in the treatment of myasthenia gravis.

Trans Am Neurol Assoc 103:292, 1980 *

Bender AN, Genkins G: Phsmapheresis in myasthenia gravis: Controlled study.

Lancet 2:629, 1979 T

G“

Arahata K, Imai H, Yokoi Y, Ishi H, Yuasa S, Marabayashi H: Plasma exchange in

myasthenia gravis. Minkei Naika 9:477, 1978 (In Japanese) I

Arrigo A, Ascari E, Ippoliti G, Piccolo G, Pinelli P, Rubert G: The effect of

plssmapheresis on myasthenic blocking of neuromuscular transmission: A follow-up

electromyographic investigation. Muscle Nerve 1:341, 1978

Dau PC, Lindstrom JM, Cassel CK, Clark EC: Plasmapheresis in myasthenia gravis

and polymyowtis. Muscle Nerve 1:341, 1978
ARC Blood Services

Bibliography Supplement 2

TPB I-3

Denys EH, Dau PC, Lindstrom JM: Neuromuscular transmission before and after

plasmapheresis in myasthenia gravis and the myasthenia syndrome. Muscle Nerve

1:341, 1978

Lisak RP, Abramsky O, Schotiand SL: Plasmapheresis in the treatment of

myasthenia gravis: Preliminary studies in 21 patients. Muscle Nerve 1:341, 1978

Pinching A3, Peters DK, Newsom-Davis 3: Plasma exchange in the investigation

and treatment of myasthenia gravis. Boston: Haemonetics Advanced Component

Seminar, 1977

B. Multiple Sclerosis

Hauser S: Plasmapheresis, Iymphocytapheresis and immunosuppressive therapy in

mtdtiple sclerosis. Boston: Haemonetics Advanced Com~nent Seminar, 1982

(abstract)

Hauser SL, Dawson D, Beal MF, Lehrich JR, Kevy SV, Ropper RD, Mills 3A:

Controlled randomized trial of high-dose cyclophosphamide, plasmapheresis, and

ACTH in progressive multiple-sclerosis. Neurology 32:78, 1982

H&ker P, Summer K: Plasma ● xchange and Iymphocytapheresis in multiple

sclerosis. Boston: Haemonetics Advanced Component Seminar, 1982 (abstract)

Khatri BO, McQuiUe MA Plasmapheresis (PP) in chronic progressive multiplesclerosis (CPMS) - a pilot study. hkurology 32:148, 1982

Plasmapheresis with immunosuppressives may help MS patient. Intern Med News

15:14, 1982

Stefoski D, Schauf C~ McLeod BC, Haywood CP, Davis FA: Plasmapheresis

decreases neuroelectric blocking activity in multiple sclerosis. Neurology 32:904-

907, 1982

Tindall RSA, Waika JE, Ehle AL, Near L, Rollins J, Becker D: Plasmapheresis in

multiple sclerosis - prospective trial of pheresis and immunosuppression versus

immunos~pression alone. Neurology 32:739-743, 1982

Uchida A, Maida EM, Lenzhofe R, Micksche M: Natural killer cell-activity in

patients with multiple sclerosis - interferon and plasmapheresis. Immunobiology

160: 392-402, 1982.

Vaibmesi M, Garelli S, Mosconi L, Zerbi D, Forlani G: Plasma exchange in the

management of patients with multiple sclerosis: Preliminary observations. Vox

Sang 41:68-73, 1981

C. Refsum’s Disease

Braine HG, Pyeritz RE, Folstein MF, Moser HB, UUman MD: A prospective doubleblind study of plasma exchange therapy for the acroparesthesia of Fabryk disease.

Transfusion 21:686-689, 1981

Blauhut B, Lenz H, Bergman H: PIUma exchange in Refsumts disease. In Rainer H

(cd): “Cell Separation and Cryobiology.” Stuttgart: F. K. Schattauer Verlag, 1978,

p 332

ARC Blood Services

Bibliography Supplement 2

TPB I-4

D. GuiIlain-Barr~ Syndrome

Fimini G, Bigi G, Paracchini ML, Marinig C, Gibelli A: Immunological monitoring

of a patient with GuiUain Barr~ syndrome successfully treated with plasma

exchange. Vox Sang 42:304-307, 1982

Osterman PO, Fagius 3, Safwenbe 3, Danerstm A, Wallin K, Nordesjo LO:

Treatment of the GuiUain-Barr~ syndrome by plasmapheresis. Arch Neurol 39:148-

154, 1982

Brettle RP: Successful plasmapheresis in the Miller Fisher syndrome. Br Med 3

282:1627, 1981

de lager AE, et al: Plasma exchange in five patients with acute Guillain-Barrif

syndrome. Int J Artif Organs 4:230-233, 1981

de Jager AE, The TH, Sibinga CThS, Dau PC: Plasma exchange in Guillain-Barr~

syndrome. Br Med J 282:794, 1981

Hughes RA: Plasma exchange of ~ute polyradiculoneuritis (Guillain-Bar~ syndrome). Int J Artif Organs 4:275-276, 1981 “

Squara P, et al: Recurrence of Guillain-Barr~ syndrome treated by plasma

exchange. Parallel courses of clinical symptoms and circulating immune complexes. Nouv Presse Mad 10:3854-3855, 1981 (In French)

Thomas L, et al: Plasma exchange treatment of Guillain-Barr~ syndrome. The

need for a controlled study. Nouv Resse Med 10:2911, 1981

Valbonesi M, Garelli S, Moaconi L, Zerbi D, Celano 1: Plasma exchange aS a

therapy for GuiUain-Barr~ syndrome with immme complexes. Vox Sang 41:74-78,

1981

Zerbi D, ● t al: Plasmapheresis in the treatment of four cases of Guillain-Barr6

syndrome (acute form). Ital J Neurol Sci 2:331-336, 1981

Dureux 3B, Gerard A, Roche G, Lehey$ B, Canton Ph, Schonemsm F, 3annot C,

Streiff F: Treatment of Guillain-Barre syndrome by plasma ● xchange. Nouv

Presse Med 9:3696, 1980

Garelli S: Confirmation of the utility of plasma-exchange in the treatment of

severe Guiliain-Barr~ syndrome. Riv Emoter Irnmunoematol 27:187-194, 191)0

IL Miscellaneous: Polyneuropathy, Motor Neuron Disease,

Amyotrophic Lateral Sclerosis

Connor RK, Ziter FA, Anstall HB: Childhood chronic relapsing polyneuropathy:

Dramatic improvement following plasmapheresis. 3 Clin Apheresis 1:46-49, 1982

Dau PC, et al: Experience with plasmapheresis in 153 necrologic patients. Int J

Artif Organs 5:37-46, 1982
Lin 3, Rowe V, Abdou

immune parameters in

32:154-155A, 1982

ARC Blood Services

Bibliography Supplement 2

TPB I-5

NI: Effect of plasrnapheresis on specific and nonspecific

chronic inflammatory polyradiculoneuropathy. Neurology

Lovaste MG, Bonimsegi C, Girardi P, Ferrari G: Plasmapheresis in acute idiopathic

polyradiculoneuritis - report of 3 cases._Ital J Neurol Sci 3:129-132, 1982

Norris FH, Denys EH, Mielke CH: Plaamapheresis (plasma-exchange) in necrologic

disorders. ClirI Nuropharrnacol 5:93-114, 1982

Poplard A, Emile 3, Bernat Ch, Alcalay D, Vincent F: Plasma exchange in

Parkinson% disease: A new therapeutic approach with successful results. Boston:

Ham%netics Advanced Component Seminar, 1982 (abstract)

van Nunen SA, Gateby PA, Pollard 3D, Deacon M, Clancy RL: Specificity of

plasmapheresis in the treatment of chronic relapsing polyneuropathy. Aust NZ J

Mad 12:81-84, 1982

Gross MLP, Thomas PK: The treatment of tionic relapsing and chronic

progressive idiopathic inflammatory polyneuro

Sci 52:69-78, 1981

pathy by plasma exchange. 3 Neurol

Mass ~ Busch HP, w der Heul Q Plasma infusion and plasma exchange in

chronic idiopathic polyneuropathy. N Engl J Mad 395:344, 1981

Newton fU Plasma me in acute post-infectious demyelinatian. Dev Mad

Child Neurol 23:538-543, 1981

hwyer c, Aitdsorl 3, Sutton J, Bemett w: Treatment of theophylline neurotoxicity with resin hemoperfusion. Ann Intern Mad 88:516-517, 1978

Norris FH Jr, Denys EH, Mielke CN p~re* ~ amyotrophic latef~

sclerosk Muscle Nerve 1:343 1978

AMERICAN RED CROSS BLOOD SERVICES

Supplement 2

Therapeutic Pheresis Bibliography No. II: Blood Diseases

A. Hemophilia

Erskine 3G: Plasma exchange in patients with inhibitors to factor VIIICL Plasma

Ther-Transfus Technol 3:123-130, 1982

Francesco M, Korniger C, ?lwder & Niessne r H, Hocker P, Lechner K: Plasmapheresis - its value in the management of patients with antibodies to Factor VIII.

Haemostasis 11:79-86, 1982

Salmassi S, Uangovan & Kasprisin DG Treatment of hemophilia A with factor VIII

inhibitor by plasma exchange transfusion. Plasma Ther Transfus Technol 3:131-

136, 1982

Erakine JG, Wrnett AK, Walker ID, Davidson 3F: Plasma exchange in nonhaemo-

_ with ~itors to factor vm~ ~ Mad 3 n2z758-759, 1981

Kawagoe H, et al: Plasma exchange in Weber-Christian disease and ● case with

anti-factor VIII antibody. Rinsho Ketsueki 22:1616-1620, 1981 (h hpanese)

Kawagoe H, Matwbchi T, Shhohara Y: Plasma exchange therapy for WkberChristian% d- and anti-factor VIII antibody disease In ode T (edk 7herafMUtiC p~r~.” s~~: F. K. ~~ Ver”&; 1981, pp 113-118

Mugishima H, et al: HB virus induced fulminan

successful management with p

t hepatith in hemophilia B:

ksmapheresia and hemoperfusion. Rinsho Ketsueki

22:1628-1631, 1981 (In Upanese)

Skombe GW, Newland AC, Colvin MP, Colvin BT: ~role of intensive plasma

exchange in the prevention and management of haemomhage in patients with

inhibitors to factor VIII. Br 3 Haematol 47:577-585, 1981

Fridrich L, Piller G, Niessner H, Hkker Pj Rainer HS Lechner K: Plasma exchange

in hemophiliacs with antibodies to factor VUL In Rainer H (ad): %ekseparation

and cryobiology.” Stuttgart: F. K. Schattauer Verlag, 1978, p 174

Piller G, H6cker H, Ludwig & Niessner H: PMnapheresk Its role in the

qement of inhibitor patients. Workshop in Inhibitors of Factor VIII and IX.

Wlen Facultas-Ver&g, 1977, p 57

& Autoirnmme Hemolytic Anemia

Krakauer R, Smith 3, W yaenbeek & Malchesky P, Nose Y: New technologies for

plasma ● xchange in autoimmune disease. In %ternatiortd Symposium on Plasma-
ARC Blood Services

Bibliography Supplement 2

TPB II-2

ARC Blood Services

Bibliography Supplement 2

TPB 11-3

pheresia: Therapeutic Applications and New Techniques.” Cleveland: Int Soc Artif

Organs, 1982, p 17

Lawe JE: Successful exdmnge transfusion of an infant for AIHA developing late in

mother% pregnancy. Transfusion 22:66-68, 1982

Monch H, Lynen R, Beyer J-H, MueUer-Eckhardt C: Plasma exchange in a case of

autoirnmune hemolytic anemia with temporary Evan% syndrome. In Beyer J-H,

Borberg H, Fuchs Ch, Nagel GA (eds): ‘Plasmapheresis in immunology and

Oncology.” Baseh S Karger, 1982, pp 232-237

Lopukhin IuM, Chuchalin AC, Shurkalin BK, Evseev NG, Gorchakow VD: Hemosorption in the therapy of autoimmune diseases. Sov Med 10:49-53, 1981 (English

abstract)

Ofuji T, Kurata N: Plasma exchange and thoracic duct drainage in autoimmune

diseases. Nippon Rinsho 39:1841-1846, 1981 (In Japanese)

C. Aplastic Anemia

Mangan KF, Shadduck RK, Winkelstein A : Plasmapheresis and anti-thy mocyte

globulin treatment of chronic refractory pure red-cell aplasia - correlation of

clinical results with in vitro erythroid culture studies. Clin Rea 31 X323A, 1982

Iabister 3P, Ralston M, Hayes JM, Wright R: Fulminan t lupus pneumonitis with

acute renal failure and RBC aplaah Successful management with plasmapheresis

and immunosuppression. Arch Intern Mad 141:1081-1083, 1981

Marinone G, et ah Bone marrow erythrobhstic recovery after plasmapheresis in

acquired pure red cell anemia. Case report. Haematologica (Pavia) 66:796-802,

1981

M essner HA, Fauser AA, Curtis 3E, Dotten D: Control of antibody-mediated pure

red cell aplasia by plasmapheresis. N Engl 3 Mad 304:1334-1338, 1981

Sakalova A, Gazova S, Hrubisko M, Pokorna G, Mayer J: Follow+ of certain

immunologic indicators in the treatment of plasmacytoma with cyclophosphamide

in combination with plasmapheresis. Neoplasma 22:63-67, 1975

D. Immune Thrombocytopenic Purpura

Blanchette V, Hogan V, Rock G: Plasma exchange in immune thrombocytopenic

purpura (ITP). In ‘International Symposium on Plasmapheresis: Therapeutic

Applications and MW Techniques.” Cleveland: Int Soc Artif Organs, 1982, p 5

International Medical Service: Plasmapheresis improves outcome in thromboC’Ytoplc purpura. (Summary of ACP No. Califmnia Regional Meeting repcrt by

Dr. David Cooney). Intern Med News 15:9, 1982

Kelton JG, McBride 3, Wilson W, Gauldie 3: The pretreatment identification of

those patients with idiopathic thrombocytopenic purpura who respond to plasmapheresis. Clin Res 30:320A, 1982

Beyer 3-H, Schuff-Werner P, M8nch H, Klee M, Kaboth U, Kt?stering H, Nagel GA:

Plasma exchange in 3 patients with idiopathic thrombocytopenic purpura (ITP). In

Nydegger UE (cd): “lmmt.mohemotherapy. A Guide to Immtmoglobulin Prophylaxis

and Therapy.*’ London: Academic Press, 1981, pp 405-408

Buskard NA: Plasma exchange for the treatment of immtme thrombocytopenia. In

Nydegger UE (cd): “lmmunohemotherapy. A Guide to Immunoglobulin Prophylaxis

and ~rapy.” London: Academic Press, 1981, pp 395-404

Saigo K, et al: Plasma exchange in idiopathic thrombocytopenic purpura. Rinsho

Ketsueki 22:1624-1627, 1981 (In Japanese)

Buskard NA: Plasma exchange for the treatment of immune ttuombocytopenia.

Proceedings of International Society of Hematology, Abstract 138, 1980

Branda RF, Tate DY, McCuUough 33, et al: Plasma exchange in the treatment of

fulminant idiopathic (autoimmune) thrombocytopenic purpura (ITP). Blood 50A:

235, 1977

Zittoun R, Bergeret S, Thierry S, Piliier C, Radeau-Coquin E, Bussel A, BilskiPaaquier G: Value of plasma exchange in the management of acute immunoallergic

tlrombocytopenic Purpura Nouv Reese Med 10483-688, 1981 (English abstract)

1% Tlrombotic Ttrombocytopenic Purpuras

Hemolytic Uremic Syndrome

Bambauer R, 3 utzler GA, Hartmann H, Stolz D, Schmengler K, Kohler M, Wahlen

W: Hemolytic uremic syndrome, successfully treated by plasma exchange. In

‘International Symposium on Plasmapheresis: Ttxwapeutic Applications and New

Techniques.n Cleveland: Int Soc Artif Organs, 198L p 2

Breckenridge RL 3 r, SoIberg LA, Pineda AA, Petitt RM, Dharkar DD: Treatment

of thrombotic thrombocytopenic purpura with plasma exchange, antiplatelet

agents, corticosteroiG and plasma infusion: Mayo Clinic experience. J Clin

Apheresis 1:6-13, 1982

FeMoff CM: Plasmapheresis in recurrent hemolytic uremic syndrome in a child.

Int J Pediatr Nurs 3:118, 1982

Kalmin ND, Himot Eb Plasmapheresis in a child with the hemolytic-uremic

syndrome. Transfusio& 1982 (acuspted)

Kwaan HG Tlrombotic tlrombocytopenic purpura. 3 AMA 247:31 19-3120, 1982

Liu E, Rebenstein M: Phenytoin removal by plasmapheresis in thrombotic

thrombocytopenic purpura. Clin Pharmacol 31:762-765, 1982
ARC Blood Services

Bibliography Supplement 2

TPB II-4

Parries B, Dtbe VE, Simon NM, Miller H3 : Adult hemolytic uremic syndrome

successfully treated with plasma exchange. Plasma Ther Transfus Technol 3:57-61,

1982

Pini M, et al: Normal protacyclirdike activity and response to plasma exchange in

thrombotic thrombocytopenic ~pura: Report of 2 cases. Acta Haematol (Base:+

67:198-205, 1982

Rothberg H, Pachter I, Koamin M, Stevens DB: Ttrombotic thrombocytownic

PI-WFWSU Recovery after pl=mapkresis, corticosteroids, splenectomy, and antiplatelet agents. Am 3 Hematol 12:281-287, 1982

Spencer CD, Crane FM, Kumar JR, Alving BM: Treatment of postpartum

hemolytic uremic syndrome with plasma exchange. JAMA 247:2808-2809, 1982

Beattie T3, Murphy AV, Willoughby Mu MaChin S, Defreyn G: Plasmapheresis in

the haemolytic-uraemic syndrome in chikken. Br Med J 282:1667-1668, 1981

Berkessy S, et al: Successful treatment of thrombotic thrombocyto nic purpura

with plasma transfusion. Orv Hetil 122:1387-1390, 1981 (In Hutgarian r

Pedersen RS, et ah Hemolytic uremic syndrome. Treatment by plasma exchange.

Ugeskr Laeger 143:2800-2802, 1981 (English abatract)

Rossi EC, del Greco F: The adapth of hemodialysis to facilitate rapid ● xchange

transfusion in patients with thrombotic ttrombocytopenic purpura (TTP). Semin

Thromb Hemostas 7:22-24, 1981

Shinoda A, Kitada H, Suzuki S, Klrihara S, Saito Y, Yuri T, Ishikawa k Accessible

plasma exchange using membrane filter - a successfully treated case of TTP with

repeated plasma exchanges. Artif Organs 5:248-253, 1981

F. Sickle Cell Disease

Legout J, Aufeuvre 3P, Casteran R, CUX M, Morin-Hertel F, Baudelot T: Sickle

cell anemia and surgery. Value of the cell separator in preparation for the

operation. Rev Fr Transfus Immmohematol 24:229-232, 1981 (In French)

Kleinman S, Thompson-Breton R, Rifkind S, GoMfinger D: Exchange red blood cell

pheresis in the management of complications of sickle cell anemia Plasma Ther

Transfus Technol 1:27, 1980

Morrison 3C, Whybrew WD, Bucovaz ET: Use of partial exchange transf usiom

preoperatively in patients with sickle cell hemoglobinopathies. Am J Obstet

Gynecoi 132:59-63, 1978

ARC Blood Services

Bibliography Supplement 2

TPB II-5

G. Leukemia, Myeloproliferative

Syndrome, ~“zary Syndrome

Ford 3 M, CuUen MH, Roberts MM, Brown LM, Oliver RTD, Lister TA: Prophylactic granulocyte transfusions. Results of a randomized controlled trial in patients

with acute myelogenous leukemia. Transfusion 22:311-316, 1982

Hester J P, McCredie KB, Freireich ~: Response to chronic leukapheresis

procedures and survival of chronic myelogenous leukemia patients. Transfusion

22:305-307, 1982

Mielf& CH, Dobbs CE, Winkkr DF, Yam LT: Therapeutic leukapheresis in hairy

all leukemia Arch Intern Med 142:700-70~ 1982

Worsley A, Cuttner 3, Gordon R, Reilly M, Ambinder EP, Conjalka M: Therapeutic

Ieukapheresis in a patient with hairy cell leukemia presenting with a white cell

cmmt greater than 500,000/’. Transfusion 22:308-310, 1982

Imamura N, et ah Cytapheresis therapy of adult T-cell leukemia ‘A case report.

Rinsho Kets@d 22:885-890, 1981 (English abstract)

Quaglino D, De Pasquale A, Montagnani G: Unusual response to leukapheresis in a

case of myelofibrosis with elevated peripheral cdl cmmt. Haematologica 66:327-

334, 1981

Pineda M, Winkelman RK: Leukapheresis in the treatment of S&ary syndrome. J

Am Aced Dermatol 5:544-549, 1981

Polianskaia AM, Khorashko ND, Baidurin SA, Kalinin NN, Kasatkina VV: Mechanisms of the therapeutic action of leukapheresis in Ie&emias. Probl Gematol

Pereliv Krovi 26:6-10, 1981 (In Rtian)

Semen G: Ultrastructural study of B-lmdies in Ieukapheresed cds of patients with

acute leukemia Ondogy 38:20&209, 1981

Cuttner 3, Holland 3F, Ambinder E, et al: Randomized studY of leukapheresis (L)

in acute myelocytic leukemi& Proc Am Soc Clin Oncol 21:443, 1980

Eisenstaedt RS, Berkman EM: Rapid cytoreduction in acute leukemisu Management of cerebral Ieukostasis by cell pheresis. Transfusion 18:113-1 15, 1978

H. Thrombocytosis

Gonzales L, cargella F, Ancochea L, Casals F, ViUalta J, Ingelmo M,

Blue toe syndrome in a patient with essential thrombocythemk

response to plateletpheresis. Med Clin 79:133-136, 1982 (In S~kh)

Gorina AB:

Favorable

Wiebecke D, Gmzer U, Kondler R, Pfrang C, Wilke H3: Cytapheresis in

combination with azathioprine for the management of ttrombocpsis in myeloproliferative diseases. Blut 45:188, 1982

Fabris F, et al: Improvement of platelet aggregation abnormalities in thrombocytosis after thrombocytopheresis. Folia Haematol (Leipz) 108:853-86~ 1981

●

!3.

!!
ARC Blood Services

Bibliography Supplement 2

TPB 11-6

AMERICAN RED CROSS BLOOD SERVICES

Supplement 2

Puig L, et al: Indication for plateletpheresis in the treatment of essential

thrombocythemia. Sangre (Bare) 26:517-518, 1981 (In Spanish)

Therapeutic Pheresis Bibliography No. 111: Malignant Paraproteinemias

A. Hyperviscosity Syndrome

L Miscellaneous

Blumenstein M, Samtleben W, Randerson DH, Habersetzer R, Gurland H3: Membrane plasma filtration for treatment of plasma cell disease. In “International

Symposium on Plasmapheresis: Therapeutic Applicaticm and New Techniques.”

Cleveland: Int Soc Artif Organs, 1982, p 6

Deubelbeiss KA: TIwwapeutische Zytapherese aus der Sicht des Hamatologen und

Onkologen. Therapeutische Umschau/Revue Therapeutique 39:512-514, 198 2

(English abstract)

Dialer P, Day R, Burman N, Blekkenh G, Esdes L: Treatment of hemodialysisrelated porphyria cutanea-tarda with plasma-exchange. Am J Med 72:989-993,

1982

Pimstone NR, Gandhi SN, Mukerji SK: Effect of plasmapheresis on porphyrin

kinetics in an atypical case of congenital erythropoietic porphyria (CEP). Clin Res

30: A327, 1982

Szymanski IO, Snyder LM: Treatment of Iife-threatening anemia with plasmapheresis in a patient with paroxysmal nocturnal hemoglobulinuria. Plasma Ther

Transfus Technol 3:51-56, 1982

Wenz B, et al: Partial immmologic reconstitution of a patient with acquired

agammaglobulinemim A transient phenomenon accompanying therapeutic plasmapheresis. Blood 59:233-235, 1982

Yoahida Y, Yoshida H, Ohkubo T, Kamamoto T, Sawada H, Hiraoka A, Yamagishi

M, Urchino H: Plasmapheresis in the treatment of hemopoietic diseases. ICU &

CCU 6:21, 1982 (In Japanese)

Anderson E, Skw F, Hippe E: A case of cold haemoglobulinuria with later

sarcoidosis: Treatment with plasmapheresis and immunosuppression. Scand 3

Haematol 24:47-50, 1981

Erskine 3G, Burnett AK, Walker ID, Davidson IF: Plasma exchange in nonhaemophiliacs with inhibitors to factor VIIIC. Br Med3 282:758-759, 1981

Isbister J P, Ralston M, Hayes J M, Wright R: Fulminant lupus pneumonitis with

acute renal failure and RBC aplasia. Successful management with plasmapheresis

and immtamsuppression. Arch Intern Med 141:1081-1083, 1981

Kawagoe H, et al: Plasma exchange in Weber-Christian disease and a case with

anti-factor VIII antibody. Rinsho Ketsueki 22:1616-1620, 1981 (In 1 apanese)

Beck 3R, QUiM BM, Meier FA, Rawnsley HM: Hyperviscosity syndrome in paraprot “nemia. Managed by plasma exchange; monitored by serum tests. Transfusion

22:5 -53, 1982 ?

Fazzini G, AIbanese B, Manescal P, Lombardi C, Pasquini G, Bartoli V: Biochemical and haemoreheological findings during treatment of plasma-cell dyscrasias by

plasmapheresis or plasma exchange. Clin Hemorh 1:565-573, 1981

Isbister 3 P: Plasma exchange in the management of hyperviscosity syndrome. Bibl

Haematologica 47:228-241, 1981

Somer T, et al: Clinical and theological studies in a patient with hypervismsity

syndrome due to Waldenstrt5mts macroglobulinernia. Bibl Haematologica 47:242-

246, 1981

Blaha M, et ah Case report of hypervi.wmsity syndrome treatment with plasma

exchange using the “Amincon separator. Vnitr Lek 26:786-791, 1980 (In Czechoslovakian)

Anamiya Y, Baba M, Hisamitsu 3, Ito T, Amaki T: Application of an apparatus for

plasmapheresis (Haemonetics Model 30) in hyperviscosity syndrome. Rinsho

Ketsueki 19:1436, 1978 (In Japanese)

B. Macroglobulinemia

Euler H-H, Beress R, GUIZOW K, Kleine L, Laessing C, Burck HC, LUffler H:

Clinical evaluation of different plasmapheresis techniques in IgM-paraproteinemias. In ‘International Sympcasium on Plasmapheresis: Therapeutic Applications

and New Techniques.” Cleveland: Int Soc Artif Organs, 1982 p 10

Kawai T, Yamagishi Y, Narita Y, Yuda M, Chiba A: Some pertinent. factors

involving blood viscometry. In Oda T (cd): “Therapeutic Plasmapheresis.” Stuttgart: F. K. Schattauer Verlag, 1981, pp 41-46

Somer T, et al: Clinical and theological studies in a patient with hyperviscosity

syndrome due to WaldenstrBmls macroglobulinemia. Bibl Haematologica 47:242-

246, 1981

Brehm G, Dorn W, Fateh-Moghadam A, Lydtin H: Plasmapherese beim

WaMenstr6m mit dem IBM-Blutzell separator. Congr Dtsch Oster Ges HamatoIogie, 1975 (In Grman)

Pillar G, HUcker H, Ludwig E, Niessner H: Plasmapheresis. Its role in the

management of inhibitor patients. Workshop in Inhibitors of Factor VIII and IX.

Wien Facuitas-Verlag, 1977, p 57
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Bibliography Supplement 2

TPB III-2

C. Multiple Myeloma

Pourrat J P, Dueymes 3 M, Conte 33, Pourrat O, Alcalay D, Touchard G, Patte D:

Plasma exchange in myeloma renal failure. In “International Symposium on

Plasmapheresis: Therapeutic Applicatiaw and New Techniques.” Cleveland: Int

Soc Artif Organs, 1982, pp 32-33

Iwamoto H, Nakagawa S, Matsui N, Yoahiyama N, Shinoda T, Shibamoto T ,

Takeuchi ~: An experien~ of plasma exchange by membrane separator for IgA

myelonm In Sieberth HG (ed)s ‘Plasma Exchange. Plasmapheresis -

plasmaseparation.” Stuttgart: F. K. Schattauer Verlag, 1980, pp 377-380

Ray PK, Idiadla A, Rhoads JE Jr, Besa E, Bassett J G, Cooper DR: Immuoadsorption of I@ molecules from the plasma of multiple myeloma and autoimmune

hemolytic anemia patients. Plasma Ther Transfus Technd 1:11, 1980

D. Cryoglobuli~mia

Viguier E, Quaranta JF, Ortonne J P, Cassuto J P, Duplay H, Dujardin P: Effect of

plasma exchange in the course of uyogiobulinemiast Study of 6 cases. In

%ttemational Symposium on Plasmapheresis: Tkapeutic Applications and New

Techniques. W Cleveland: Int Soc Artif Organs, 198~ p 47

Geltner D, Kohn RW, Gorevic P, Franklin E(2 The effect of combination therapy

(steroids, immunosuppressive and plasmapheresis) on 5 mixed cryoglobulinemia

patients with renal, necrologic and vascxdar involvement. Arttritis Rheum

24:1121-1127, 1981

McKenzie RG, et ah Glomerukmephritis secondary to mixed polyclmal cryoglo~-

Iinernb Response to immnosuppression and plasmapheresis. Aust NZ J Med

11:529-533, 1981

Reik L Jr, Kern JH: Cryogloblimmia with encephalopathy: Successful treatment

by plasma exchange. Ann Neurol 10:488-490, 1981

Houwert DA, et al: Effect of plasmapheresis (PP), corticosteroids and cyclophospbrnide in essential mixed polyclonal cryoglobulinemia associated with glomerulonephritis. Proc EW Dial Transplant Assoc 17:650, 1980

L’Abbate AL Paciucci A, Bartolomeo F, Misefari V, Mobile F, Cerrai T, Maggiori

Q Selective removal of plasma cryogbbulins in cryoglobulinemia. Proc Eur Dial

Transplant Assoc 14:486, 1977

E. MiSCekU)&)US

Valboneai M, Gareili S, Montaini F, Cefis M, Rossi U: Management of immtmemediated and Parapromiwmic diseases by membrane plasma separation and

-cade filtration. Vox Sang 43:91-101, 1982

ARC Blood Services

Bibliography Supplement 2

TPB III-3

Iwamoto H, Matsui N, Nakagawa S, Takeuchi 3: An experien~ of plasma exchange

in malignant paraproteinemia. In Oda T (edh ‘Therapeutic Plasmapheresis.”

Stuttgart: F. K. Schattauer Verlag, 1981, pp 107-112

Blank H3, Brinkmann OH, 3 unge+iulsing G: Plasmapheresis: An ● ffective

procedure for paraproteinemia coma. Dtsch Med Wschr 105:1396, 1980 (In German)

Camerone G, et ah Use of plasma exchange in treating kidney failure from

paraproteinemic diseases. Riv Emoter Immwmematol 27:168-174, 1980( In Italian)

lako J, Schopper 3: Plasma exchange in paraproteinemi~ In Rainer H (edk ‘Cellseparation and Cryobiology.n Stuttgart: F. K. Schattauer Verlag, 1978, p 148
AMERICAN RED CROSS BLOOD SERVICES

Supplement 2

ARC Blood Services

Bibliography Supplement 2

TPB IV-2

Therapeutic Pheresis Bibliography No. IV: Renal Diseases

A. GoodPasture’s Syndrome

EuIer H-H, Kleine L, GutSchmidt H3, Herrlinger 3 ~ Effect of early plasmapher~is and high-dose cyclophosphamick therapy in Goodpasture’s syndrome. In

Beyer H+, Borberg H, Fuchs Ch, Nagel GA (eds): ‘Plasmapheresis in Immunology

and Oncology.w Basek S. Karger, 1982, pp 238-246

Euler H-H, Kleine L, Gutschrnidt H3, Herrlinger 3 D GoodPasture’s syndrome:

Rapid remission after early plasmapheresis and high-dose cyclophosphamide

therapy. Klin Wochensdu 60:635-636, 1982 (English summary)

Arnold P, Dicker P: Experiences in often repeated plasma separation by membrane

in a ame of Goodpasture’s syndrome. Nieren-u. Hochdruckkrankht 9:136, 1980

Goudable C, Segonds A, Eschapasse Y, Ton That H, Durand D, Gassia 3P, Suc 3M:

Plasma separation in a Goodpasttre’s syndrome associated with angeitis. Nieren-u.

Hochdruckkrankht 9:14% 1980

Kamanabroo D, Intorp H W, Loew H, MWer K: Plasma exchange in combination

with cytotoxic drugs and corticosteroids in the treatment of Goodpasture’s

syndrome. Nieren-w Hoch&uckkrankht %144, 1980

Oldenbroek C, Bakker P, Krediet RT, Arisz L: Plasma filtration in the treatment

of Goodpasture’s disease. Nieren+ Hochdruckkrankht 9:147, 1980

GIUckner WM$ Kindler 3, Vlaho M, Maerker-Alzer G, Mahieu P, Sieberth HG: Antikorper-Eliminiertmg mittels Plasmafiltration uber Hohlfasermembranen am Beispiel des Goodpasture-Syndroms. Verh Dtsch Ges Inn Med 85:971, 1979 (In German)

Hensel A, Herrath DV, Schaefer K, St3woter-Lankowsky R: Goodpasture-Syndrom:

erfolgreiche Behandkmg durch Plasmapherese Kombiniert mit immunosuppressiver

Therapie. Diegnostik Intensivtherapie 4:136, 1979 (In German)

Pussell BA: Plasma exchange in immune complex diseases and GoodPasture’s

syndrome. Workskp on Therapeutic Plasma and Cytapheresis, Mayo Clinic, April

1979

Ericlson St. B, Kurtz SB, Donadio JV Jr, Honey KE, Velosa J, Wilson CB, Pineda

AA: Treatment of Goodpasture’s syndrome by plasmapheresis and immunoauppression. Kirhey Int 11:640, 1978

Gltkkner WM, Sieberth HG: Plasmafiltration in der Behandhmg des GoodpastureSyndroms. Z Immun Forsch 18:155, 1978 (In German)

Kamanabroo D, Intorp H W, MUller K, Loew H: Plasma exchange in the treatment

of Goodpasture’s syndrome. In Rainer H (ad): ‘Cell Separation and cryobiology.”

Stuttgart: F. K. Schattauer Verlag, 1978, p 114

Lockwood CM, Rees Al, Russell B, Wilson CB, Peters DK: Plasmapheresis, cytoxic

drugs, and corticosteroids in the management of GoodPasture’s syndrome. Muscle

Nerve 1:339, 1978

Sieberth HG, Borberg H, Kinder J, Mahieu P, SeeIing J: Plasmaphoresebehandlung

des Goodpasture-syndrom. In Watschinger B (cd): %econd Donau-Symposium fur

Nephrologie, Budapest, 1977

& Glomerulonephritis

Batomini V, et al: Effect of plasma exchange and thoracic ~ct drainage on

immmological status in giomerulonephritk Proc Eur Dial Transplant Assoc

18:736-742, 1981

Gltkkner WM, Dienst C, Kinder J, Sieberth HGr Plasma exchange in rapidly

progressive glomerulonephritis. Dtsch Mad Wochenschr 106:1616-1620, 198 1

(English abstract)

Kauffmann RH, et ah Plasmapheresis in rapidly progressive Henoch-Schoenlein

glomerulonephritis and the effect on arculating IgA immune complexes. Clin

Nephrol 16z155-160, 1981

Kuperi M, et ah Plasma exchanges in ttw treatment of rapidly progressive

glomeruionephritis associated with chronic dental infection. Acta Med Scand

21 OZ511-514, 1981

McKenzie RG, et al: Glomerulonephritis secondary to mixed polyclonal cryoglobuIinernim Response to immunosuppression and plasmapheresis. Aust NZ 1 Med

11z529-533, 1981

Peters DK, Lockwood CM: Plasma exchange in anti-GBM disease. In Gurland HJ,

Heinze V, Lee HA (eds): therapeutic Plasma Exchange.W New Yoda Springer

Verlag, 1981, pp 139-147

Rifle G, et ah Treatment of idiopathic acute crescentic glomerulonephritis by

immunosuppression and plasma+ xchanges. A prospective randomized study. Proc

Eur Dial Transplant Assoc 18:493-502, 1981 ,.

Sieberth HG, GIUckner WM, Borberg H, Kindler J, Vlaho M, Dienst C, Mitrenga D,

Vaith P: Plasmaseparation in der Behandlung von rapid progressive Glomerulonephritiden. In Gurland HG, Heinze V, Lee HA (eds): ‘Therapeutic Plasma

Exchange.” New York: Springer Verlag, 1981, pp 149-164 (In German)

Houwefl DA, et al: Effect of plasmapheresis (PP), corticosteroids and cyclophoaphamide in essential mixed polyclonal cryoglob@nernia associated with gJom*

rulonephritis. Proc Eur Dial Transplant Assoc 17:650, 1980
ARC Blood Services

Bibliography Supplement 2

TPB IV-3

Lockwood CM, Rees A2, Pussell B, Peters DK: Experience in the use of plasma

exchange in the management of pote-ntially fulminating glomerulonephritis. In

Rainer H (cd): ‘CelI Separation and Cryobiology. n Stuttgart: F. K. Schattauer

Verlag, 1978, p 134

McKenzie EE, Clarkson AR, Taylor H, Seymour AE, Woodroffe A3, Chan YL:

Plasma exchange therapy in glomerular diseases. Aust NZ J Med 8:225, 1978

Banks RA, May S, Wellington

Recovery after plasmapheresis.

C. Miscdhmeous

T: Acute renal-failure in dense deposit disease:

Br Med J 284:187, 1982

Clark WF, Williams W, Cattran DC, Chodirler WB, Koval 33, Lindsay RM, Linton

AL: Controlled trial of chronic plasma exchange therapy in SLE nephritis. Boston:

Iiaemonetics Advanced Component Seminar, 1982 (abstract)

Hene RJ, Valenti RM, Kater L: Plasmapheresis in nephritis of the HenochSchoniein purpura and primary 1gA nephropathy. Eur 3 Clin Invest 12:16, 1982

Iwanaga T, et al: Plasma exchange in intractable nephrotic syndrome and active

systemic erythematosus. Rinsho Ketsueki 22:1620-1623, 1982 (In 3 apanese)

Lopot F, et & Haemofiltration - a new method of treatment for chronic renal

failure. Cas Lek Cesk 121:210-213, 1982 (English abstract)

MontoJiu J, Bergada E, Arrizaba P, Revert L: Acute renal-failure in dense deposit

disease - recovery after plasmapheresis. Br Med3 294:940, 1982

Pourrat 3P, Dueymes J M, Conte 13, Pourrat O, Alcalay D, Touchard G, Patte B

Plasma ● xchange in mydoma renal failure. In %ternationai Symposium on

Plasmapheresis: Therapeutic Applications and New Techniques.” Cleveland: Int

Soc Artif Organs, 1982, pP 32-33

Sharon L Roberts 3 L, Fennell 3S, Schwartz MM, Lewis El: plasmapher=i$ in lupus

nephritis. Plasma Ther Transfus Technol 3:163-169, 1982

Bazzato G, et al: Plasmapheresis in the treatment of chronic secondary nephropathy of various etiologies. Minerva Nefrol 28:235-241, 1981 (English abstract)

Itoh K, Narumi F, Ono M, Kawaguchi H: Plasmapheresis in the treatment of severe

renal diseases in children. In Oda T (edh ‘Therapeutic Plasmapheresis.W Stuttgart:

F. K. Schattauer Verlag, 1981, pp 201-206

Kuroda M, Akiyama T, Miyazaki R, Tofuku Y, Takeda R: Plasma exchange in the

treatment of various renal diseases. In Oda T (edh ‘Therapeutic Plasmapheresis.”

Stuttgart: F. K. Schattauer Verlag, 1981, pp 191-200

Landini S, Coli U, Lucatello S, F racasso A, Morachiello P, Toffoleto P, Bazzato G:

Plasma-exchange and dialysis. Combined treatment in acute renal insufficiency

secondary to severe hepatopathies. Minerva Nefrol 28:179-186, 1981 (English

abstract)

ARC Blood Services

Bibliography Supplement 2

TPB IV-4

Morse E& pisciotto PT: Therapeutic plasmapheresis in patients with renai disease.

Ann Clin Lab Sci 11:361-366, 1981

Sici&d A: Plasma ● xchange in kidney disease. Pol Arch Med Wewn 65:67-77, 1981

(In Polish)

Stefoni S, et al: Con%ined hernodialysis-hemoperfusion treatment reduces the

time of substitutive therapy in chronic uremi~ hw3 Artif Organs 4:186-191, 1981

Camerone G, et al: Use of plasma exchange in treating kidney failure from

Paraproteinernic diseases. Riv Emoter Immunoematol 27:168-174, 1980 (In Italian)

Swailwon CP, Urbaniak SJ, Robson 1S : Plasma exchange in the successful

treatment of drug-induced renal failure. Nieren-u. Hochdruckkrankht 9:150, 1980

Vilches AR, et ah Plasmapheresis and its use in nephritis. Medicine (B Aires)

40:196-20~ 1980

Apolstoloff E, Blauarmel O, Kramm I-U, Meffert H: ~rapieeffekt ~d Antikor

per verhalten nach Plasmaphorese bei Lupus erythematodes visceralis mit LupusNephritis. Dtsch Gemndh Wesen 34:64, 1979 (In German)

Clark WF, Lindsay RM, Chodriker WB, Cattran DC, Linton AL: Elective plasmaphereaia in SLE nephritis: Pilot for a controlled prospective study. Am Soc

Nephrcd, 1979, p 928

Lockwood CM, Puasell B, Wilson CB: Plasma exchange in nephritis. Adv Nephrol

8:383, 1979

Pinching Al, et al: Plasma exchange in nephritis. 3 R Soc Mad 72:97-108, 1979

Uldall RP, Dyck RF, Woods F, Merchant N, Martin GS, Cardel.la Q, Sutton D, de

Veber GA: Subclavian cannula for temporary vascular access for haemodialysis or

plasmapheresis. Dial Transplant 9:963, 1979
AMERICAN RED CROSS BLOOD SERVICES

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Supplement 2

Therapeutic Pheresis Bibliography No. V: Connective Tissue Disorders

A. Systemic Lupus Erythematosus

Clark WF, Williams W, Cattran DC, Chodirker WB, Koval Xl, Lindsay RM, Linton

AL: Controlled trial of chronic plasma exchange therapy in SLE nephritis. Boston:

Haeoaonetics Advanced Compcnent Seminar, 1982 (abstract)

Eden&! C, Herrlitz H, Lindholm L, Mulec H, Westberg G: Plasmapheresis in

systemic lupus erythematosus. In “International Sympc6ium on Plasmapheresis:

Therapeutic Applications and New Techniques.” Cleveland: Int Soc Artif Organs,

1982, p 9

Gwtby P: Plasmapheresis to be tried in systemic lupus. 3AMA 2~7:1688, 1982

Hamblin T3, et al: Severe deafness in systemic IU

r

● rythematosus: Its

immediate relief by plasma exchange. Br Med 3 [’n R 284:1374, 1982

Iwanaga T, et al: Plasma exchange in intractable nephrotic syndrome and active

systemic erythematoaus. Rirtsho Ketsueki 22:1620-1623, 1982 (In lapane=)

Lewis E3: Plaamapheresis for the treatment of severe lupus nephritis. - uncontrokd observations. Am 1 Kichey 2;182-187, 1982

Plasmapheresis to be tried in systemic lupus. J AMA 247:1688, 1982 (editorial)

Sharon Z, Roberts J L, Fennel J S, Schwartz MM, Lewis U: Plasmapheresis in lupus

nephritis. Plasma Ther Transfus Technol 3:163-169, 1982

Tsokos GC, Balow JE, Huston DP, Wei N, Decker 3 L: Effect of plasmapheresis on

lymphocyte-T and lymphocyte-B functiom in patients with systemic lupus erythematosus - a double-blind study. Clin Exp Immunol 48:449-457, 1982

Wallace Dl, Goldfinger D, Bluestone R, Klinenberg JR: Plaamapheresis in lupus

nephritis with nephrotic syndrome: A long-term followup. J Clin Apheresis

1:42-45, 1982

Amano I, Inagaki U, Tsuzuki K, Yamamoto T, Sugiyama T, Ide M, Kanoh H:

Experiences with plasma exchange for treatment of paraquat intoxication, SLE,

and acute liver failure. Artif Organs 10:563, 1981

Evans DT, Giles M, Home D3, @Apice M, Riglar A, Toh BH: Cerebral lupus

● rythematosus responding to plasmapheresis. Postgrad Med 3 57:247-251$ 1981

Hambtrger MI, Gerardi EN, Fields TR, Bennett RS: Reticuloendothelisd system Fc

receptor function and phismapheresis in systemic lupus erythematosus: A preliminary report. Artif Organs 5:264-268, 1981

ARC Blood Services

Bibliography Supplement 2

TPB V-2

Kater L, et al: Effect of plaamapheresis in active systemic lupus erythematosus.

Neth J Med 24:209-216, 1981

Matsumoto Y, Masaoka A, Kotoh Y: plasma-exchange-regimes in the treatment of

autoimmune disorder= Systemic lupus erythematosus and pemphigus. In Oda T

(eclh “Therapeutic Plasmapheresis.” Stuttgart: F. K. Schattauer Verlag, 1981, pp

209-214

Millman RP, et al: Systemic lupus erythematosus complicated by acute pulmonary

hemorrhage: Recovery following plasmapheresis and cytotoxic therapy. J

Rheumatol 8:1021-1023, 1981

Nasonova VA, et al: Hemoperfusion through activated charcoaI in the compiex

treatment of systemic lupus erythematosus. Ter Arkh 53:107-112, 1981 (In

Russian)

Verrier Jones J, Robinson MF, Parciany RK, Layfer LF, McLeod B: Therapeutic

plasmapheresis in systemic lupus erythematmus. Effect on immune complexes and

antibodies. Arthritis Rheum 24:1113-1120, 1981

Apolstoloff E, Blauarmel 0, Kramm HJ, Meffert H: Therapieeffekt und Antikorperverhalten nach Plasmaphorese bei Lupus erythematodes vis~ralis mit LupusNephritis. Dtxh Gesundh Wesen 34:64, 1979 (In German)

Clark W, Lindsay RM, Chodriker WB, Cattran DC, Linton AL: Elective plasmapheresia in SLE nphritk Pilot for a controlled prospective study. Am Soc

Nephrol, 1979, p 928

Verrkr 301WS 3, Cumming RH, Bucknall RC, Asplin CM, Fraser ID, Bothamiey J,

Davis P, Hamblin T3: A therapeutic role for plasmapheresis in the management of

acute systemic lupus erythematosus. Bmton: Haemonetics Advanced Component

Seminar, 1976

B. Polyarteritis Nodosa - Wegener’s Granuloma

Suchy B-R, Schley R, Nogai K, Bennhold J, Pribilla W: Plasma exchange in a case

of Wegener’s gramdomatosis. In Beyer J-H, Borberg H, Fuchs Ch, Nagel GA (eds):

“Plasmapheresis in Immtmology and Oncology.n Basal: S. Karger, 1982, pp 247-250

C. Rheumatoid Arthritis

Cooling, then culling blood complexes combats arthritis. 3AMA 248:632, 1982

Hamburger MI: A critical review of therapeutic apheresis in the treatment of

severe rheumatoid artkitis. Boston: Haemonetics Advanced Component seminar,

1982, abstract

Heyse SP, Renault PR, Perry S: Naticmal Center for Health Care Technology

assessment of therapeutic apheresis for rheumatoid arthritis, 1981. 3 Clin

Apheresis 1:50-54, 1982
ARC Blood Services

Bibliography Supplemen

TPB V-3

Krakauer RS, Aaanuma Y, Zawicki I, Caiabrese L, Malchesky PS, Nae’ Y :

Circulat-ing immuns complexes in rheumatoid arthritis: Selective removal by

cryogelation with membrane filtration. Arch Intern Med 142:395-397, 1982

van Wanghe P, Deqmker 3: Effect of intravenous cyclophosphamide as an adjuvant

to therapeutic plasma exchange in rheumatoid arttritis. Plasma Ther Transfus

Technol 3:171-176, 1982

Wallace IXl, Goldfinger D, Brachman M, Klinenberg J: A double-blind controlled

study of lymphoplasmapheresis (LP) in rheumatoid arthritis (RA). Bostoru Haemoneti~ Advanced Component Seminar, 1982 (abatract)

Waila~ D, Goldfinger D, Lowe C, Nichols S, Weiner J, Brachman M, IQlrlenberg

3 R: A double-blind, controlled study of Iymphoplasmapheresis versus sham

apheresis in rheumatoid arthritis. N Engl 3 Mad 306:1006-1410, 1982

Asada H, Kobayashi S, Niwa T, Sezaki R, Kano K, Kawanishi A, Yokoyama M, Kishi

T, Kawaguchi S, Maeda K: Plasma exchange in the treatment of psoriasis pustulosa

and malignant rheumatoid artlritis. In Oda T (edh %rapeutic Plasmapheresia.w

Stuttgart: F. K. Schattauer Verhg, 1981, pp 145-151

Azuma N, Nobuto T, Suzdci M, Asanuma Y, Malchesky PS, Shirno K, Takahashi M,

Suzuta T, N-” Y: Clinical effect of plasmapheresis with continuous ayofiltration

for three cases of rheumatoid arttritis. In ode T (edk %rapeutic Plasmapheresis.m Stuttgart: F. K. Schattauer Verlag, 1981, pp 159-163

Denman AM Removal of lymphocytes in rhewpatoid art)ritis. Br Mad 3 283:1492,

1981

Dequeker J, Naessens M, Martens J, Pieters R: The effect of plasma exchange on

synovitis in rheumatoid arthritis. Scand 3 Rheumatol 10:273-279, 1981

Dequeker 3, Walravens M, Leys A, Pieters R: Arteritis associated with hyperviscosity-like syndrome in rheumatoid arthritis, treated by intermittent plasmaexchange for 2.5 years. Rbumatol Rehabil 20:203-207, 1981

Hamburger MI, Gerardi EH, Fields TS, Bernstein ML, Bennett RS: Lymphoplasmapheresis and reticuloendotM.ial system (RES) Fc receptor faction in

rheumatoid arthritis (RA). Arthritis Rbum 24: S98, 1981

Karsh 3: Plasmapheresis or lymphapheresia in rheumatoid arttritis. In Gurland HJ,

Heirue V, Lee HA (edsb %rapeutic Plasma Exchange.w New Yorlc Springer

Ver@, 1981, PP”lll-123

Russell AS, Davis P, Percy 3S: Plasma ● xchange in rheumatoid arttritis? 3

Rheumatol 8:364-366, 1981

Sam DG, Bacon PA, Bothamley J E, AlhM C, Elson Q, Wellington TB: Plasma

exchange in rheumatoid vasculitis. J Rheumatol 8:433-439, 1981

Shimo K, Suzuta T, Suz~i M, Noae Y: Basic and clinical studies on amtinuous

cryofiltration: A new treatment for rheumatoid arthritis. Rheumachi 21:61, 1981

ARC Blood Services

t2 Bibliography Supplement 2

TPB V-4

Shiozawa K, Yamagata J, Shiokawa Y, Yuasa S, Hashimoto H: Plasma ● xchange

for rheumatoid arthritis. In Oda T (ed)z “Therapeutic Plasmapheresis.H Stuttgart:

F. K. Schattaww Verlag, 1981, pp 166-168

Takahashi K, Ogita T, Miyamoto Y, Takaishi T, Saito K, Yoehizawa H, Horiuchi Y:

Effect of plasmapheresis as a new therapy for rheumatoid arthriti~ In Oda T (cd):

“Therapeutic Plasmapheresisom Stuttgart: F. K. Schattauer Verlag, 1981, pp

169-173

Wallace IN, Goldfinger D, Klinenberg JR: Cwrent status of therapeutic pheresia

in rheumatoid artkitis. Artif Organs 5:297-298, 1981

Yano T, Naiki K, Kato R, Kazui H, Terasawa T, Tsuchioka H: Plasma exchange in

a case of malignant rheumatoid arthritis with ulcers of legs and feet. In Oda T

(edk “Therapeutic Plasmapheresis. “ Stuttgart: F. K. Schattaww Verlag, 1981, pp

153-157

K~sh 3, Wright DC, Klippel JH, Deisaeroth AB, Decker J L Lymphocyte removal

by continwus flow cell separation in rheumatoid arthritis. Arthritis Rheum 22:626,

1979

Wallace D3, Gatti R, Goldfinger D, Klinenberg JR: Promising results reported in

trial of plasmapheresia in rheumatoid arthritis treatment. Rheum News Int, vol 7,

1979

D. Raynaud% Syndrome

OReilly M: Raynaud-Syndrom-lJ&era heilen nach Plasmapherese. Medical Tribune

Kongressbericht, May 1978 (In German)

E. Misdhneous

Bjelle A, et al: Plasma exchange in two patients with rheumatoid vasculitis. Scand

J Rheumatol 11:58-6~ 1982

Camerone G, et ah Plasma exchange treatment in a patient with severe

Schoenlein-Henod pqmr~ Minerva Mad 73:1185-1187, 1982 (English abstwsct)

~re FA, Spiva DA, Langley 3W: Plasmapheresis/lymphocytapheresis for the

treatment of dermatomyositis and poiymyositis. Boston: Haemonetics Advanced

Component Seminar, 1982 (abstract)

Gipstein RM, Adarns DA, Grabie MT, Peter J B: Response of lupus nephritis to

plasmapheresis without demonstration of circulating immune-complexes. Am 3

Med Sci 283:37-41, 1982

Hamblin T, Clark Cl: Plasma exchange in polymyositis and Sjogren’s syndrome.

Boston: Haemonetics Advanced Component Seminar, 1982 (abstract)
ARC Blood Services

Bibliography Supplement 2

TPB V-5

Mandel D, Calabrese L, Clough J: Plasma exchange therapy of immme complex

mediated vasctitis. In ‘international Symposium on Plasmapheresis: Therapeutic

Applications and New Techni~s.W Cleveland: Int Soc Artif Organs, 1982, p 28

Wysenbeek A3, Calabrese LH, Mandel DR, Clough 3 D: Limited plasmapheresis in

fuiminant leukocytoclastic vasculitis. 3 Rheumatol 9:315-318, 1982

Bennington 3 L, Dau PC: Patients with polymyositis and derrnatomyositis who

ndergo plasmapheresis therapy. Pathologic findings. Arch Neurol 38:553-560,

1981

Brubaker DB, Winkelstein A: Plasma exchange in rheumatoid vascuiitis. Vox Sang

41:295-301, 1981

Dau PC, Kahleh MB, Sagebiel RW: Plasmapheresis and immmosuppressive drug

therapy in scleroderma Arthritis Rheum 24:1128-1136, 1981

Dmitriev AA, ● t al: Experience using hemoaorption therapy in allergic cutaneous

vasculitis. Vestn Dermatol Venerol 9:19-22, 1981 (English abstract)

Eliasson S, Flmence 3, Reppun T: Idiopathic inflammatory myopathy and plasmapheresis. Muscle Nerve 4:446-447, 1981

Kawagoe H, et al: Plasma exchange in Weber-Ctwistim disease and a case with

anti-factor VIII antibody. Rinsho Ketsueki 22:1616-1620, 1981 (In la-)

Pieters R, Dequeker J: Infectious complications with plasma-exchange in connective tissue diseases. Abstract 643, 15th International Congress of Rheumatology, Paris, 3tme 1981

Smtt DGI, Bacon PA, Bothamley JE, Allen C, Elaon C3, Wellington TB: Plasma

exchange in rheumatoid vaaculitis. 1 Rheumatol 8:433-439, 1981

Cohen 3, Lockwood CM, Calnan CD: Plasma+xChange in treatment of leucocytoChStiC vascul.itis. 3 R Soc Med 73:457-460, 1980

Valbonesi M, GareUi S, Mcaconi L, Camerone G, Bedarida ~, Di Guardo G: Plasma

exchange in the management of a patient with diffuse necrotizing cutaneous

VaSditiS. VOX Sang 39:241-245, 1980

3affe IA: Comparison of the effect of plasmapheresis and penicillamine on the

level of circulating rheumatoid factor. AM Rheum Dis 22:71-76, 1963

AMERICAN RED CROSS BLOOD SERVICES

Supplement 2

Therapeutic Pheresis Bibliography No. VL Transplantation

A. Renal

Alle< N, Dyer P, Harris K, Smith 3, Lee HA, Slapak M: Effects of plasma exchange

on immunoglobulins, complement, and immune complexes in renal transplant

recipients. Plasma Ther Transfus Technol 3:157-162, 1982

Cardella a : Does plasma exchange have a role in renal transplant rejection?

Plasma Ther Transfus Technol 3:153-156, 1982

3 oekes AM, Amir-Ansari B: Plasmapheresis in transplant rejections. In %temational Symposium on Therapeutic Plasmapheresis: Therapeutic Applications and

New Techniques.” Cleveland: Int Soc Artif Organs, 1982, p 15

KAeinman S, Nichols M, Strauss F, Goldfinger D: Use of iymphoplasmapheresis or

phssmapheresis in the management of acute renal allograft rejection. 1 Clin

Apheresis 1:14-17, 1982

McCurdy PR, Darr FW: Treatment of steroid resistant renal allograft rejection

with plasmalymphapheresis. Boston: Haemonetics Advanced Component Seminar,

1982 (abstract)

McCurdy PR, Darr F W, Helfri~ GB, Philips T, Pechan BW, Alijani M, Papadopolous

ZL, Glfand M: Treatment of steroid resistant renal allograft rejection with

plasmalymphapheresis. In %ternatirmal Symposium on Plasmapheresis: Therapeutic Applications and New Techniques.” Cleveland: Int Soc AI%if Organs, 1982,

pp 29-30

Slapak M, Naik RB, Lee HA: The effect of plasma exchange on crossing the major

blood group barrier in renal transplantation: Clinical and experimental observations. Boston: H~monetics Advanced Component Seminar, 1982 (abstract)

Allen NH, Slapak M, Lee HA: Plasma exchange in renal allograft rejection. In

Gurland I-U, Heinze V, Lee HA (eds): “Therapeutic Plasma Exchange.” New York

Springer Verlag, 1981, pp 175-190

Cardella C3, Sutton DMC, Katz A, Uldall PR, Harding M, Cook CT, deVeber GA:

Plasma exchange in renal transplantation. In Zurukzoglu W, Papadimitrious M,

Pyrapasopoub M, Sion M, Zamboulis C (eds): ‘Proceedings, 8th International

Congress of Nephrology.W Stuttgart: S. Karger, University Studio, 1981, pp 681-685

Kirubakaran MC, Disney APS, Norman 1, Pugsley 03, Mathew TH: A controlled

trial of plasmapheresis in the treatment of renal allograft rejection. Transplantation 32:164-165, 1981
ARC Blood Services

Bibliography Supplement 2

TPB VI-2

Ltmdgren G, Asaba H, Bergstrom J, Groth CG, Magnusson G, Moller E, Strindberg

J, Wehle B: Fulminating anti-A autoimmune hemolysis with anuria in a renal

transplant recipient: A therapeutic role of plasma exchange. Clin Nephrol 16:211-

214, 1981

Power D, Nicholls A, Muirhead N, MacLeod AM, Engeset J, Catto GRD, Edward N:

Plasma exchange in acute renal allograft rejection: Is controlled trial really

necessary? Transplantation 32:162-163, 1981

Burrows L, Schanzer H, Hairnov M, Jhaver K, Deutsch V, Ambinder E: Reversal of

rejection and subsidence of immunoglobulinuria by intensive plasmapheresis. Proc

Eur Dial Transplant Assoc 17:491-495, 1980

Disney A, Taylor H, Norman J, Fazzalari R, Pubsley D, Mathew T: Plasmapheresis

in renal transplantation. Aust Soc Nephrol 8:227, 1978

Merkel FK, Bier M, Beavers CD, Merriman WG, Stand TE: Delay of the

heterograft reaction by selective plasmapheresis. Surg Forum 21:261-263, 1970

B. Bone Marrow

Bensinger Wh Plasma exchange and immmoadsorption for removal of antibodies

prior to ABO incompatible bone marrow transplant. Artif Organa 5:254-258, 1981

Buckner CD, et al: Pheresis ~iquas in marrow transplantation. Prog Clin Biol

Rea 65:81-89, 1981

Gonzalez Lopez MA, Montoro 3A, MartiIwz J, Sanz MA, Perez Castellanos T, Soler

MA, Marty ML: Massive plasmapheresis in the conditioning for ABO-incompatible

bme-rnarrow transplant. Sangre (Bare) 26:497-503, 1981 (English abstract)

Harada M, et al: Plasmapheresis in familial hypertilesterolemia and bone marrow

transplantatim from an ABO incompatible donor. Rinsho Ketsueki 22:1632-1635,

1981 (English abstract)

Higby DJ, et ah Reversal of possible marrow graft rejection with plasma exchange

therapy. J Med 12:455-461, 1981

Clift RA, Sanders JE, Thomas ED, Williams B, Buckner CD: Granulocyte

transfusions for the prevention of infection in patients receiving bone marrow

tRilMp&ntS. N Engl J Med 298:1052-1057, 1978

AMERICAN RED CROSS BLOOD SERVICES

Supplement 2

Therapeutic Pheresis Bibliography No. VII: Liver Disease

A. Hepatitis, Hepatic Coma

Landni S, Coli U, Lucatello S, Fracasao A : Morachiello P, Rightto F, Bazzato G:

The ● ffect of plasma-exchange (PE) on bpatic coma in Ieptospirosis and fulminant

hepatitis. In ~nternational Symposium on Plasmapheresis: T~rapeutic Appfi~-

tions and New Techniques.n Cleveland: Int Soc Artif Organs, 1984 p 18

lnoue N: Treatment of fulminant hepatitis - preventicm of com~lications and

plasma exchange therapy. Kango Gijutiu 27:25-33, 1981 (h Japanese

Kono Y, Tsuchihashi N, Shimizu C: Management and nursing of a patient with

fulminant hepatitis receiving plasma exchange. Kango Gijutsu 27:51-56 1981 (In

3apanese)

Mugishima H, et ah HB virus induced fulminant hepatitis in hemophilia B:

Successful management with plasmapheresia and hemoperfusion. Rinsho Ketsuaki

22:1628-1631, 1981 (In Japanese)

Ueda T, Masaoka T, Shibata H, K@ota Y, Saigo K, Takubo T, Nakamura H,

Yoshitake J, Iahigami S: Hepatic coma treated by plasma ● xchange during

treatment for hematological malignancies. In Oda T (edh therapeutic Plasmapheresis.n Stuttgart: F.K. Schattauer Verlag, 1981, pp 93-97

Yamarnoto H, Endo A, Yamamoto Y, Matwsmga S, Noguchi H, Nagasaki Y,

Nishioka S, Yataka I, Abe T: A case of severe hepatitis A with renal failure

treated by plasma exchange, hemodialysis and glucagon-irmlin therapy. in oda T

(edh therapeutic Plaamapheresis.” Stuttgart: F. K. Schattauer Verlag, 1981, pp

99-103

Sakamoto H, Shimuzu M, Harada H, Ohtake H, Tanaka S, Otbayashi A: Evaluation

of plasma exchange as a liver suppcm therapy for fulmhant hepatitis. Liver

21:723, 1980

Valbonesi M: Tb cdl separator in the therapy of hepatic comm Preliminary

experience in cases of viral hepatitis. Riv Emoter Immwmematol 27:51-56, 1980

Boland 3, et al: Fulminating hepatitis treated by plasmapheresis. Acta GaatroEnterol Belg 38:207-217, 1975

Jesipowicz M, et al: Termimtkm of hepatic coma complicating viral hepatitis by

means of ● xchange transfusion with plasmapheresis. Pol Tyg Lek 30:1265-1266,

1975

lesipowicz M, J akubowska M, Karski J, Osterowa K: Plasmapheresis and exchange

transfusion in the treatment of hepatic coma. Pol Tyg Lek 30:707, 1975
ARC Blood Services

Bibliography Supplement 2

TPB VII-2

ARC Blood Services

Bibliography Supplem

TPB VII-3

lent 2

Klebanoff G: A preliminary assessment of the efficacy of asanguineoushypothermic total body perfusion in the management of stage IV hepatic coma.

Am 3 Gastroenterol 60:105-113, 1973

Chang TMS: Hemoperfusion over microencapsulated adsorbent in a patient with

hepatic coma. Lancet 2:1371-1372, 1972

Haapanen E, Tiula E: Plasmapheresis with albumin as main substitute in acute

hepatic coma. Scand J Gastroenterol 7:75-83, 1972

Hauftova D, et al: P1asmapheresis in the treatment of hepatic coma (preliminary

report). Vnitr Lek 18:319-327, 1972

Sandu L, et al: Plasmapheresis with plasma replacement in the treatment of

tsspatic coma Anesth Analg (Paris) 28:1101-1107, 1971 (In French)

Graw RG, Buckner CD, Eisel R: Plasma exchange transfusion for hepatic coma

New technique. Transfusion 10:26, 1970

Durden WD, Siemsen AW, Briggs WA: Exchange transfusions in the treatment o;

ftdrninant hepatitis and coma Am 3 Gastroenterol 51:129-137, 1969

Szwed 33, MendenhaU CL, Grisell TW: Exchange transfusions for intractable

hepatic coma Arch Intern Med 123:$41-444, 1969

B. MisdkM(xIS

Balentin L, Lin J, Greenberg N, Abdou NI: Efficacy of plasmapheresis (PL) in

primary biliary-cirrhosis (PBC) - dissoci ation between correction of immune

parameters and clinical improvement. Clin Res 30: A279, 1982

Landini S, Coli U, Lucatello S, Fracasso A, Morachiello P, Righetto F, Bazzato G:

Plasma-exchange: Prevention and treatment of toxic acute hepato renal failure.

In International Symposium on Plasmapheresis: Therapeutic Applications and New

Techniques. n Cleveland: Int Soc Artif Organs, 1982, p 19

Landini S, Coli U, Lucatello S, Fracasso A, Morachiello P, Righetto F, Bazzato G:

Plasma-exchange in severe Ieptospirosis. In ‘International Symposium om Plasmapheresis Therapeutic Applications and New Techniques.” Clevelamk Int Sdc Artif

Organs, 1982, p 20

Le Pogamp C, et al: Cholestasis of pregnancy. A new indication for plasma

exchange. NOW Presse Med 11:457, 1982 (In French)

Amano I, Inagaki U, Tsuzuki K, Yamamoto T, Sugiyama T, Ide M, Kanoh H:

Experiences with plasma exchange for treatment of paraquat intoxication, SLE,

and acute liver failure. Artif Organs 10:563, 1981

Asanuma Y, et al: Chronic ambulatory liver support by membrane plasmapheresis

with on-line detoxification. Trans Am Soc Artif Intern Organs 27:416-422, 1981

Horak W, Polterauer P, Renner F, Silkerbauer K, Ftmovics 3, Muhlbacher F, Rauhs

R: Plasmapheresis in ftdminant hepatic failure. In Rainer H (cd): “cell Separation

and Cryobiology.” Stuttgart: F. K. Schattauer Verlag, 1981, p 101

Inoue N, Yamazaki Z, Yoshiba M, Ichikawa K, Sakai T, Oda T, Sanjo T, Wada T,

Inoue 3, Saoshiro T, Horiuchi T, Me K, Fujisaki Y : PIMma exchange using

membrane plasmapheresis in the treatment of acute tqxitic failure. Artif Organs

10:557, 1981

Inoue N, Yamazaki Z, Ycahiba M, Okada Y, Sanjo K, Oda T, Wada T: Membrane

plasmapheresis with plasma exchange in the treatment of acute liver failure. In

Oda~ (edh “Therapeutic Plasmapheresis.” Stuttgart: F. K. Schat*auer Verlag,

1981, pp 57-63

Keeling PW, Bull J, Kingston P, Thompson RP: Plasma exchange in primary biliary

cirrhosis. Postgrad Med 3 57:433-435, 1981

Landini S, et al: Plasma exchange in severe leptospirosis. Lancet 2:1119-1120,

1981

Mizokami M, Kano H, Amano I: Experience with plasma exchange in. hepatic

failure of hyperbilirubinemia and hyperalpha-fetoprotein (AFP) of hepatoma. In

Oda T (edk ‘Therapeutic Plasmapheresis.n Stuttgart: F. K. Schattauer Verlag,

1981, pp 89-92

Okamua 3, Horikawa S, Fujiyama T, Kambayashi J, Gotoh M, Sikujara O, Monden

M, Kosaki G, Sakurai M: Indication and ● ffect of plasma exchange on kpatic

failure. In Oda T (cd): Therapeutic Plasmapheresis.” Stuttgart: F. K. Sdattauer

Verlag, 1981, pp 71-75

Shimizu H, Yoshida S, Hosoya R, Eiraku K, Nishimura K: CliNcal trial of

plasmapheresis in hepatic failure. In Oda T (edk Therapeutic Plasmapheresis.n

Stuttgart: F. K. Schattauer Verlag, 1981, pp 83-88

Takayama M, Tomita Y, Okumura H, Katsuta Y, Satomura K, Aramaki T, Henmi H,

Murakami M, Koseki K: A case of fulminant hepatic failure treated with plasma

exchange: Problems and effectiveness. In Oda T (edh Therapeutic Plasmapheresis.” Stuttgart: F. K. Schatta&r Verlag, 1981, pp 77-82

Ueda K, et al: Effectiveness of plasma exchange in liver diseases and studies of

dose of plasma exchange. Rinsho Ketsueki 22:1636-1638, 1981 (In Japanese)

Maini R: A detoxification scheme for liver assist utilizing plasmapheresis,

biocompatible sorbents and dialysis. Artif Organs 3:153-155, 1979

Geerdink P, Snel P, Van Berge Henegouwen GP, Huybregts A, Tangerman A, Kunst

VA3 M, Van Tongeren 3HM: Treatment of intractable pruritus in patients with

cholestatic jaundice by plasma exchange and plasma perfusion. Neth J Med 21:239,

1978

Geerdink P, Van Berge Henegouwen GP, Hectors M, Huybregts A, Kuwt VA3 M,

Vartt Laar A, Snel P, Tangerman A, Van Tongeren IHM: Treatment of intractable

pruritus in patients with cholestatic jaundie by plasma exchange and plasma

perfusion. In Rainer H (edk ‘Cell Separation and Cryobiology.n Stuttgart: F. K.

Schattauer Verlag, 1978, p 111
ARC Blood Services

Bibliography Supplement 2

TPB VII-4

Balw G, et ah Exchange transfusion in acute liver failure. DtsdI Mad

WochemclY %:1329-1333, 1971

de Estable Puig RF, Eatable Puig JF$ Acute yellow atrophy in pregnancy: A case

treatad by plasrnaphereais and studied with the electron micros~pe. L’Union Mad

du Canada 99:1083-1093, 1970

Konsantinov VNt Effect of plasmapheresia on the protein-synthetic fmction of

the liver and several immunologic indices of reactivity of the donor orgsnism.

Probl Gematol Pereliv Krovi 15:50-51, 1970 (In Russian)

AMENCAN RED CROSS BLOOD SERVICU

Supplement 2

Therapeutic Pheresis Bibliography No. VW: Hemolytic Disease of the Newborn

Robirson EA: Potential for plasma exchange in Childen. Arch Dis Child

S7:300-308, 1982

Rock-C, Lafreniere I, Chan L, McCombie N: Plasma exchange in the treatment of

hemolytic disease of the newborn. In %Iternational Symposium on Plasmaphere*

Therapeutic Applications and New Techniques.N Cleveland: Int Soc Artif Organs,

198% p 38

Rubimtein P: Repeated small volume plasmapheresis in the management of

hemolytic disease of the newborn. In Frigoletto FD Jr, Jewett JF, Konugres AA

(edsh Wh Hemolytic Disease. New Strategy for Eradicatim.w Boston: G. K. Hall

Medical Publishers, 1982 pp 211-220

Kr”blo V, ● t al: Plasmapheresis in tk treatment of Rh ieoimm mizations during

gravidity. cask Gynekol 46:174-177, 1981 (English abstract)

Macchia A, et ah Bleed chemical parameters in newborn infants with fatal

erythroblaatosis during exchange transfusion. Minerva Gined 33:348-553, 1981

O1owe SA, et @: Exchange transfusion using G-6-PC deficient H*AS blood in

icteric neonates. 3 Natl Med Asaoc 79:81 1-819, 1981

S@ E, et al: Exchange transfusion in newborns via a peripheral -ry and veim

EU 3 Pediatr 137:283-284, 19S1

Simonovits I, Vedrodi K, 3olaIti I, Forgacs J, Gy & Plasmapheresis in R h

immmized pregnant womem Acta Haematol 12:65-67, 1981

Yoshids Y, Ymhida H, Tatsurni K, Asoh T, Nishimura T, Whim G: A new method

of selective antibody elimination for tlw treatment of severe M-incompatible

pregnancy. In Oda T (edb ~rapeutic PIasmapheresis.W Stuttgart: F. K.

Schattauer Verlag, 1981, pp 23S-239

Takahashi H, et al: Plasma exchange in the pregnant Rlwaensitized woman. Rimho

Ketsueki 22:1644-1647, 1981 (h Japanese)

Cregut R, et al: Theoretical model of epuratia by plasma exchan~ Application

to anti-~(D) immunization. Rev Fr Transfus 23:363-371, 1980

Heyns AduP, Odendaad H3, Slabber CR, Karshagen WF, Du Plessis HH3, Potgieter

GM: Severe Rh-isoimmtmization and intensive plasma exchange during pregnancy.

S Afr Med 3 58:884, 1980

Newland AC, Colvin BT, Dodd BE: Plasma exchange in severe rhksus haemolytic

disease. Br Mad] 2:45Z 1980
ARC Blood Services

Bibliography Supplement 2

TPB VIII-2

AMERICAN RED CROSS BLOOD SERVICES

Supplement 2

Tovey D, Robinson EAE: Effect of plasma exchange in rhesus immunization. Br

Mad 1 2:387, 1980

Wensley RT, Lee D, Fletcher S: Adverse effect of plasma exchange on anti-D

production. .Br Med3 2:619, 1980

Brossart Y: Incidents et accidents observd’s apres 200 hges plasmatiques chez

12 femmes enceintes, severement RH immunisees. Les echanges plasmatiques:

Pratiqw, r~sukats et perspectives. Bois Guillaume, March 1979

Graham-Poole 3: Exchange plasmapheresis for severe rhesus disease. Minneapolis:

Workshop on Therapeutic Plasma and Cytapheresis, April 1979, Mayo Clinic

Brossard Y, Bussel A, Cregut R, Benbunan M, Gerota I, Roberts JF: Massive

plasma exchange during pregnancy using the CFC blood cell separator in cases of

Rh-immmization. In Rainer H (ed)s all Separation and ~yobiology.” Stuttgart:

F. K. Schattauer VerIag, 1978, p 124

Tilz GP, Weisa P, Teuble I, Lamer G, Wollman H: Successful plasma exchange in

rhesus incompatibility and other clinical conditions. In Rainer H (ad): “Cell

Separation and Cryobiology.” Stuttgart: F. K. Schattauer Verlag, 1978, p 121

Correa N, et ah Immunologic aspects of plasmapheresis in series of Rh negative

pregnant women. Rev Chil Obstet Ginecol 41:257-258, 1976

.Fraser ID, et al: Proceedings: Anti-natal plasmapheresis in severe rhesus isoimmtstisation. Br J Haematol 28:147, 1974

Therapeutic Pheresis Bibliography No. IX: Cancer

Beyer J-H, Klee M, Kaboth U, Kehl A, K3stering H, Krieger G, Nagel GA :

Problems of plasma+ xchange solutions, gamma-globulin substitution, and tumor

en~ment in plasmapheresis of tumor patients. In Beyer 3 -H, Borberg H, Fuchs

Ch, Nagel GA (edsh ttpl=m+~m~ in lmm~lou and Oncology.” -1: S.

Karger, 1982, pp 204-217

Borghardt J, Beyer J+l, Nagel GA: Monitoring the course of CEA concentration in

tumcr patients receiving plasmapheresis. In Beyer J-H, Borberg H, Fuchs Ch,

Nagel GA (eds): ‘Plasmapheresis in Immmology and oncology.” Basek S. Karger,

1982, pp 260-266

Isrliel L, Edelstein R, Samak R: Repeated plasma exchanges in patients with

metastic cancer. In Beyer J-H, Borberg H, F U+ Ch, Nagel GA (edsb Wasmapheresis in Immwiology and Oncology.n Basal: S. Karger, 1982, pp 196-203

Klee M, Beyer 3-H, Schuff-Werner P, Nagel GA: The treatment of malignant

lymphomas with plasma exchange. In Bayer 3-H, Borberg H, Fuchs CL Nagel GA

(e&h Tlasmapheresis in Immunology and Oncmlogy.N Basel: S. Kqer, 1984 pp

251-259

K&tering H, Beyer J +i, Klee M, Kasten U, Schuff-Werner P, Nagel GA: Blood

coagulation changes induced by repeated plasmapheresia in 12 normal donors and 15

patients with rnali nomas. In Beyer 34-I, Borberg H, Fuchs Ch, Nagel GA (eds):

~asmapheresis in fmmunology and Oncology.w Basel: S. Karger, 1982, pp 218-231

Micksche M, Colot M, Kokoechek EM, Moser K, Rainer H: Plasmapheresis in

patients with advanced malignant disease - a pilot study. Oncology 39:146-151,

1982

S*uff-Werner P, Brattig N, Beyer 3+, Bartel J, Berg PA, Nagel GA: Bio-ass ays

as a tool for the demonstration of immune alteration in cancer patients Suppression of mitogen-induced lymphocyte proliferation by patients’ sera during plasma

exchange. Preliminary results in four patients. In Beyer J +1, Borberg H, Fuchs

Ch, Nagel GA (eds): Tlasmapheresis in Immunology and Oncology.n Basel: S.

Karger, 1982, pp 178-193

Beyer 3 -H, Schuff-Werner P, Kaboth U, Klee M, Koatering H, Krieger G, Nagel GA:

Combined plasmapheresis, chemotherapy and gammaglobulin-substitution in

patients with drug resistant malignant disease: Preliminary clinical results. In

Nydegger UE (edk ~mmunohematherapy. A Guide to lmmunoglobulin Prophylaxis

and Tbrapy.n London: Academic Press, 1981, pp 347-350

Beyer J-H, Schuff-Werner P, Kaboth U, Klee M, Kf3stering W, Nagd GA:

Plasmapherese: erste Klinische Ergebuisse bei malignen tumoren. Schweiz Med

Wochenschr 111:1522-1524, 1981
ARC Blood Services

Bibliography Supplement 2

TPB IX-2

Cupissol D, Ga~i L, Serrou B: Evaluation of a simplified plasma exchange therapy

in the treatment of advanced cancer - effects on the immune response. In Serrou

B, Rosenfeid C (ads): Tmmme Complexes snd Plasma Exchanges in Cancer

Patients.N New Yorlc Elsevier/North Holland Biomedical Press, 1981, p 329

Dimitrov NV, Rapaon C, McNutt R: Clinical results of multiple plasmapheresis in

patients with advanced cancer. In Serrou B, Rosenfeld C (eds): “Immune

Complexes and Plasma Exchanges in caner Patients.N New York: Elsevier/North

Holland Biomedical Press, 1981, p 293

Glassman AB: Gammopathies - clinical considerations related to plasmapheresis.

In Serrou B, Rosenfeld C (eds)s 7mmune complexes and Plasma Exchanges in

Cancer Patients.” New York: Elsevier/North Holland Biomedical Press, 1981, p

277

IsdIel L, Edelstein R: Repeated plssrna exchange in patients with metastic cancer.

cancer Immunol Parasite Immunol 97:75, 1981

Isrl!el L, Edelstein R, Samak R, Baudelot J, Breau 3L, Mannoni P, Radot E:

Clinical results of multiple plasmapheresis in patients with advanced cancer. In

Serou E$ Rosenfield C (eds): Tmmme Complexes and Plasma Exchanges in Cancer

Patients.n Amsterdam: Elsevier/Nonh Holland, 1981, pp 309-327

MacDumld 3S, Phillips TM, Smith FP, Lewis M, Isr8el L: The effect of aggressive

plasma exclymge on immune complex levels in plasma of patients with metastic

~r. In Serrou B, Rosenfeld C (eds): ‘Tmmme Complexes and Plasma

Exchanges in Patients with cancer.” New York: Elsevier/North Holland Biomedical Press, 1981, p 243

Rahr H, Kokoschka EM, Micksche M, Moser K, Colot M: Plasmapheresis for

therapy in patients with metastas’ung ‘ solid tumors. In Gurland HJ, Heinze V, Lee

HA (ads): ~rapeutic Plasma Exchange.N New York: Springer Verlag, 1981, pp

75-87

Retas S, Thomas CR, Chambers J D, Newton KA, Hobbs JR: The effect o f

plasmapheresis on tb clinical and immune status of patients with renal adenowcimma. In Serrou B, Rosenfeld C (eds): Tmmtme Complexes and Plasma

Exchanges in Patients with Cancer.N New York Elsevier/North Holland Biomedical Press, 1981, p 271

Salinaa FA, Silver HKB, Grossman L, Thomas J W: Plasmapheresis - a new approach

in the management of advanced malignant melanoma In Serrou B, Ro@6feld C

(eds): ‘Immme Complexes and Plasma Exchanges in Patients with Cancer.” New

York: Elsevier/North Holland Biomedical Press, 1981, p 253

Samak R, Edeistein R, IsrXel L, Bogucki D, Samak M: Repeated plasma exchange

in patients with advanced cancer - biological and immunological findings. In Serrou

B, Roaenfeld C (eds): qmmtne Complexes and Plasma Exchanges in Patients with

Cancer. n New York: Elsevier/North Holland Biomedical Press, 1981, p 22

Trotter J M, Shaw D, Carlyle E, Shephard 3, Calman KC: Nutritional aspects of

plasma exchange in cancer patients. In Serrou B, Rosenfeld C (eds): “Immune

Complexes and Plasma Exchanges in Cancer Patients.” New York: Elsevier/North

Holland Biomedical Press, 1981, p 209

ARC Blood Services

Bibliography Supplement 2

TPB IX-3

Ueda T, Masaoka T, Shibata H, K@ota Y, Saigo K, Takubo T, Nakamura H,

Yoshitake J, Ishigami S : Hepatic coma treated by plasma exchange during

treatment for hematological malignancies. In Ode T (cd): ‘Therapeutic Plasmapheresis.” Stuttgart: F.K. Schattauer Verlag, 1981, pp 93-97

Pedersen F, et al: Treatment of metastasizing renal adenocarcinoma with specific

plasma transfusion. A controlled trial of the effects on metastasis and survival

time. Ugeskr Laeger 142:3167, 1980

Rainer H, Kokcachka EM, Moser K: Plasmapherese als therapeutische Massnahme

bei patienten tit metastasierendem soliden tumor. Verh Dtsch Ges Inn Med

85:1303, 1979

Bottino J C, Rossen RD, Hersh EM, Rios A, Hester J P, McBrids CM: Response of

malignant melanoma to plasma exchange, surgical debulking and corynebacteria

parvum. 1nt 3 Artif Organs 1:53, 1978

Davidson WD, Isacoff WH, Block J B: Methotrexate %scapen using charcoal

hemoperfusion: An alternative to citrovorum %escue.n Trans Am Soc Artif Intern

Organs 6:16, 1977

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AMERICAN RED CROSS BLOOD SERVICES

Supplement 2

Therapeutic Pheresis Bibliography No. X: Skin Diseases

A. Pemphigus Vulgaris

Roujeau 3 C, Andre C, Revuz 3, Touraim R: Effects of various immunosuppressive

regimens cm the ‘rebound phenomenon” induced by plasma exchange in pemphigus.

In “International Sympasium on Plasmapheresis: Therapeutic Applications and New

Techniques.’” Cleveland: Int Soc Artif Organs, 1982, p 39

Roujeau 3 C, 3oneau-Fabre M, Revuz 3, Touraine R: Plasma exchange in the

management of pemphigus. In ‘lntematiorud Symposium on Plasmapheresis:

Therapeutic Applications and New Techniques.” Cleveland: Int Soc Artif Organs,

1983 p 40

Roujeau J C, et al: Plasma exchange in Corticosteroid-resistant pemphigus. Br 1

Dermatol 106:103-104, 1982

Hwmiker T, Schwarzenbach HR, Krebs A, Nydegger UE, Camponovo F, Hess M:

Plasma exchange in pemphigus vulgaris. Schweiz Med Wochenschr 111:1637-1642,

1981 (English abstract)

Matsumoto Y, Masaoka A, Kotoh Y: Plasma-exchange-regimes in the treatment of

autoimmune disorder= Systemic lupus erythematosus and pemphigus. In Oda T

(cd): “Therapeutic Plasmapheresis.W Stuttgart: F. K. Schattauer Verlagt 198 1~ PP

209-214

Takada M, et al: Case of pemphigus vulgaris with development of factor VIII

inhibitor: Successful treatment with plasma exchange. Rinsho Ketsueki 22:1605-

1610, 1981 (In Japanese)

Takamori K, ● t al: Plasma exchange in skin diseases, with special reference to

pemphigus vulgaris. Rinsho Ketsueki 22:1611-1615, 1981 (In Japanese)

T5rtik L, Borka 1, Reszler M, Toth E: Adjuvant therapy of pemphigus with

plasmapheresis. Orv Hetil 122:2349-2351, 1981 (In Htmgarian)

Amblard P, Reymond 3L, Beani 3 C, Chenais F, Arvieux J: BuUous pemphigoid.

Therapeutic efficacy and limitations of plasmapheresis. Nouv Presse Med 9:1446,

1980

Rifle G, Chalopin J, Tanter Y: Treatment of bullous pemphigoid by plasma

● xchange - two cases. Nouv Presse Med 9:1445-1446, 1980

Roujeau 3 C, Revuz J, Fabre M, Mannoni P, Touraine R: Plasma exchanges in

pemphigus vulgaris. NHK 9:148, 1980

ARC Blood Services

Bibliography Supplement 2

TPB X-2

Roujeau J C, Re :UZ 3, Tourairss R, Joneau-Fabre M, Mannoni P: Pemphigoide

bulleuse cortico-resistance: Succes des plasmaphereses. Nouv Presse Med 8:3362,

1979

C. Miscellaneous

Andersen E, Andersen R, Clemmens 02: Treatment of psoriasis with plasmapheresis. Arch Dermatol 118:74, 1982

Halevy S, Ideses C, Shohat B, Feuerman FJ: plasm~eresis for P$oritis. Arc h

Dermatol 118:292, 1982

Rebora A, et al: Plasma exchange in psoriatic erythroderm- Br J Dermatol

106:119-120, 1982

Steck WD, et al: Hemofiltration treatment of psoriasis. J Am ~cad Dermatol

6:346-349, 1982

Valbonesi M, Garelli S, Montani F, Levi L, Lampertico M, Ferrari A: Short-term

effects of plasma exchange treatment of psoriasis: Preliminary clinical and

immaochemical investigations. Plasma Ther Transfus Technol 3:177-181, 1982

valsecchi R, Bellavitz P, Cavagneri A, Cainelli T: Psoriasis improvement with

plasmapheresis. Int J Artif Organs 5:278, 1982

Wexler D, et ah Plasma exchange and dermatitis herpetiformis. Arch Dermatol

119:141-142, 1982

Asada H, Kobayashi S, Niwa T, Sezaki R, Kano K, Kawanishi A, Yokoyama M, Kishi

T, Kawaguchi S, Maeda K: Plasma exchange in the treatment of psoriasis pustulosa

and malignant rheumatoid arthritis. In oda T (cd): “tirapeutic pl=mapheresis.”

Stuttgart: F. K. Schattauer Verlag, 1981, pp 145-151

Kawagoe H, Matsubuchi T, Shinohara Y: Plasma exchange therap for WeberChristian’s disease and anti-factor VIII antibody disease. In oda T [ edh ~herapeutic Plasmapheresis.” Stuttgart: F. K. Schattauer Verlag, 1981, pp 113-118

Korotkii NG. et ah Hepatocyte state in psoriasis patients treated by hemosorption.

Vesm Dermatol Venerol 7:16-19, 1981 (English abstract)

Maeda K, Shinzato T, Usuda M, Sezaki R, Niwa T, Asada H, Kawaguchi S, Saito A,

Yamanaka N, Ohta K: Psoriasis treatment with hemofiltration and plasma

exchange. Int J Artif Organs 4:253, 1981

Maeda K, Saito A, Kawaguchi S, Niwa T, Sezaki R, Kobayashi K, Asada H,

Yamamoto Y, Ohta K: Psoriasis treatment with direct hemoperfusion. In Sideman

S, Chang TMS (eds): ‘t+emoperfusion. Kidney and Liver Support and Detoxification,n Part L Washington: Hemisphere Publishing Corporation, 1980, pp 349-354

Takamori K, et al: Plasma exchange in skin diseases, with special reference to

pemphigus vulgaris. Rinsho Ketsueki 22:1611-1615, 1981 (In Japanese)
ARC Blood Services

Bibliography Supplement 2

TPB X-3

Wallach D, Cottenot F, Bussel A, Palangie A, Pennec 3: Plasma exchange therapy

in Lucio’s phenomenon. Arch Dermatol 116:1101, 1980

Maeda K: Psoriasis hemodiafiltration and hernoperfusion. Int Soc Artif Organs, New

York, 1979

Wall;ch D, et al: Plasma ex~e in the treatment of Iepromatous leprosy. Acta

Leprol (Grieve) 76-77:283-290, 1979

AMERICAN RED CROSS BLOOD SERVICES

Sqplement 2

Therapeutic Pheresis Bibliography No. XI: Lipid Disorders (HYperlipickmia)

Dabels J, Preussine S, Brauer P, Wilmbuss H: 1st results of plasmapheresia in type2A homozygotic familiar hypercholesterolernia. Endokrinologie 80:75, 1982 (In

German)

Gerard A, Sdoone man F, Guine J M, Roche G, Canton P, Dureux 3 B, J anot C,

Streiff F: Treatment by plasma exchange of a patient with hyperlipidemia and

diabetic keto-acidosis with Iesional pulmonary adema and acute parcreatitis. Vox

Sang 43:147-150, 1982

3 an F, ● t al: Type It farniJiaJ hyperjipoproteinaen@ Vab of plasma ● xchange

treatment. Am Mad Interne (Paris) 133:110-113, 1982 (English abstract)

Postiglhxw A, et al: Increaeed blood flow to lower limbs after plasma exchange in

two patients with familial hypercholesterolemia ARhero6cleroais 41:421-425,

1982

H~ada M, et al: Pksmapheresia in familial hyperchoksterolemia and bone marrow

transplantation from an ~incompatibk donor. Rinsho Kemeki 22:1632- 163S,

1981 (English abstract)

Kikkawa T, Kishino a Fushirni H, Nishikawa M, Yamamoto A: Plasma exchange

therapy for homozygous familial hypercholeaterolernh In Oda T (ad): therapeutic

Piasmapheresia.W Stuttgart:F. K.Schattawr Verlag, 1981, ~ 127-130

Leonard JV, Clarke M, McCartney F3, Slack J: Progression of atheroma in

homozygous familial hypercholeaterolaemia during regular plasma exchange.

Lancet 2:811, 1981

Levy VG, Julien PE, Oppenheimer M, Denia 3, Opolon P: Treatment of cholestasis

by piasmapheresis. NOW Presse Mad 10:2588, 1981 OnFrench)

van de Wiel A, et al: Effects of plasma exchange on serum cholesterol levels in

heterozygous familial hypercholesterolemia Acta Mad Scand 21 OW61-465, 1981

Mwer H W, et al: Therapeutic trial of plasmapheresis in Refaum’s disease and in

Fabry disaase. Birth Defects 16:491-497, 1980

Pyaritz RE, et al: Plasma exchange removes glycosphingolipid in Fabry disease.

Am 3 Med Genet 7:301-307, 1980

Thompson GR: Long-term plasma exchange in severe familial hyperchoksteroIaernia. WorksImp on lltera~utic Plasma and Cytapheresis, Mayo CliniG April

1979

Tlmmpson GR: Therapeutic use of plasma exchange in familial hypercholeaterolaernia. In Crepaldi B, Lefebvre P2, Alberti KGMM (edsb ~iabetes, Obesity and

Hyperiipidernias.” Lcmdon: Academic Press, 1978, p 351
ARC Blood Services

Bibliography S~plement 2

TPB XI-2

Shafrir E, et al: Lipoprotein synthesis in hypoproteim~;a of experimental

nephrotic syndrome and pkamaplwmssis. b Bianti % et ~ k>’ ISb “P~ma Protein

Turnover.” Baltimore: University Park Press, 1974, pp 343-3:

AMERICAN RED CROSS BLOOD SERVICES

Supplement 2

Therapeutic Pheresis Bibliography No. XII: Immmological Disorders

A. Immtsmdeficiency

Plasrnapheresis techni~s advance in treatment of immwmlogically-mediated

diseases. Immunol Trib 4:3-6, 1982

Yamagata J, Shiozawa K, Tsuda H, Katayama S, Hashimoto H, Shiokawa Y:

Plasma exchange for immune disorders. In %mxnetional Symposium on Pksmapheresis: Therapeutic Applications and New Techniques.m Cleveland: Int Soc Artif

Organs, 1982 p 48

B. Immww Complex Disease

ChuchaIin AG, et al: Ltmg involvement in immme complex d&eases and let

clinical use of hemoaorption. Ter Arkh 53:15-18, 1981 (English abstract)

Schur PH: Immtne complexes. Clin Immtmol Newsletter 3:75-80, 1982

,

Valbonesi M, GareUi S, Montani F, Manca F, Cantarella S: Plasma exchange and

immme mmplex diseases: h predictability of immme complexes removal to

clinical response. VOX Sang 42:27-3% 1982

Geltner D! The place of pksmapheresis in immtne compkx disease. Harefuah

101:77-78, 1981 (In Hebrew)

Steven MM, et al: The effect of plasma exchange on the in vitro monocyle

function of patients with immune complex diseases. CIin Exp Immunol 45:240-245,

1981

Valbonesi M, ● t al: Patients with high titers of circulating immune complexes are

most likely to benefit from plasmapheresis treatment. Int J Artif Organs

4:234-237, 1981

Fassbinder W, Platzer E, Ernst W, Baldamus CA, Kock KM: Immme complex

elimination by plasma separation with membrane filtration. In Sieberth HG (cd):

‘Phsma Exchange. Plasmapheresis - Hasmaseparation.” s~t%art: F. K. ~ttauer Verlag, 1980, pp 107-112

Menini C, et al: Plasma exchange using a cell separator for immme complex

disease. Riv Emoter Immunoematol 27:38-50, 1980 (In Italian)

PUSS4 BA: The plasma exchange in irn.rnme complex *US and ~-~e’s

syndrome. Workshop on Therapeutic Plasma and Cytapheresis, Mayo Cliniq April

1979
AMERICAN RED CROSS BLOOD SERVICES

Supplement 2

Therapeutic Pheresis Bibliography No. XIII: Miscellaneous

A. Thyroid Storm

Diseases

Brehfi” G: Plasmapherese bei thyreotoxischer Krise. In Gurland HG, Heinze V, Lee

HA (eds): ‘Therapeutic Plasma Exchange.n New York: Springer Verlag, 1981, pp

99-103 (In German)

Glinder D, Gaham N, Sand G, Libert J, Grivegne A, Badjou R, Ermans AM: Use of

plasmapheresis in a case of Graves-disease with malignant ophthalmopathy. Ann

Endocrinol (Paris) 42:545-546, 1981 (In French)

van Hekelom LHS, et al: Plasmapheresis in L-thyroxine intoxication. Vet Hum

TOxiCOl 21:7, 1979

Wysk J, Stangel W, Korle J, Papastavrous S, Just S, Hesch RD: Treatment of

thyroid storm by continuous plasmapheresis. In Rainer H (cd): ‘Cell Separation

and Cryobiology.n Stuttgart: F. K. Schattauer Verlag, 1978, p 151

Suematsu H, Matsuda K, Shizume K, Nakao K: Effect of plasmapheresis on thyroid

hormone section. Endocrinology 86:1281, 1970

C. Hypertension

dlApice AJF, Shuikes AA, Skinner SL, Whitworth 3A, Kincaid-Smith P: Plasma

exchange: An antihypertensive procedure. Aust Soc Nephrol 8:227, 1979

D. Poisoning

Berlinger WG, Spector R, Flanigan MJ, Johnson GF, Groh MR:

phenylbutazone poisoning. Ann Jntern Med 96:334-33S, 1982

Cherskov M: Extracorporeal detoxification: Still debatable.

3048, 1982

Amano I, Inagaki U, Tsuzuki K, Yamamoto T, Sugiyama T,

Experiences with plasma ● xchange for treatment of paraquat

and acute liver failure. W Organs 10:563, 1981

Hemoperfusion for

3AMA 247:3047 -

Me M, Kanoh H:

intoxication, SLE,

GJ~ckner WM, Sieberth HG: Plasmaaustausch bei Digitalis-Jntoxikation. In

Gurland HJ, Heinze V, Lee HA (eds): ‘l?mra

r

tic Plasma Exchange.m New York:

Springer Verlag, 1981, pp 105-110 (In German

ARC Blood Services

Bibliography Supplement 2

TPB XIII-2

Sabto IK, Pierce RM, West RH, Gurr FW: Hemodialysis, peritoneal dialysis,

plasmapheresis and forced diuresis for the treatment of quinine overdose. Clin

N+’tWOi 16:264-268, 1981

Arsac Ph, Credoz D, Barret b Faure J: Digitalis poisoning treated by plasma

exchange. Nouv Resse Mad 9:41, 1980

Marin GA, Montoya CA, Sierra 31, Senior JR: Evaluation of corticosteroid and

exchange transfusion treatment of acute yellow-phosphorus intoxication. N Engl 3

Med 284:125-128, 1971

Kw”min DS, et al: Plasmapheresis in acute atropine poisoning (research experiment). Robl Gematol Pereliv Krovi 12:51-54, 1966

G. Miscellaneous

Berkman E: Issues in therapeutic apheresi~ N E@ 3 Med 306:1418-1420, 1982

Boral 11, Waid Ma Watson MJ, Muller VH: A mobile therapeutic apheresis

program at a regional blood center. Plasma Ther Transfus Technol 3:217-221, 1982

Feng CS: Therapeutic plasmapheresis - bloodletting makes a return. Postgrad Med

72:251-255, 1982

Garinger G: Legal issues for apheresis operators. Technical Forum. Plasma Ther

Transfus Technol 3:65-70, 1982

Ginder PA et al: PIaama@eresis: A therapeutic option for treatment of selected

patients. J Kans Med Soc 83:140-142, 1982

Kambic H, ~Y: !$pb.smapheresis: Historical Pefspective$ therapeutic app~cations and new frontiers.” Cleveland: International Center for Artificial Organs

and Transplantation, 1982

Kelly WF, Wensley RT: An evaluation of plasma exchange treatment of Graves

Ophthalmopathy. Boston: Haemonetics Advanced Component Seminar, 1982

(abstract)

Le Pogamp C, Le Pogamp P, Brissot P, 1A Berre C: Intensive plasma exc@ge: A

new treatment for chokstaais of pregnancy. In ‘International Symposium on

Piasmapheresis: Therapeutic Applications and New Techniques.” Cleveland: Int

Soc Artif Organs, 1982, p 23

Mamer B, Moknaar J, Nerup 3, Ludvigss 3, Lernmark A: Reliability of the indirect

immunofluorescence test for islet cell antibodies and an evaluation of the effects

of plasmapheresis on antibcdy-titers in type-l (insulin dependent) diabetes.

Diabetologia 23:185-186, 1982

Mamer B, ,Moelnaar J, N- J, Ludvigss J, Lernmark A: Reliability of the indirect

immunofluorescence test for islet cell antibodies and an evaluation of the effects

of plasmapheresis on antibody-titers. Acta Endocrinol 100:44, 1982
ARC Blood Services

Bibliography Supplement 2

TPB X111-3

Reuther P, Rohkamm R, Wiebeck D, Mertens HG: Plasma exchange in idiopathic

inflammatory myopathy. In “lnternational Symposium on Plasmapheresis: Therapeutic Applications and New Techniques.” Cleveland: Int Soc Artif Organs, 1982,

p 35

Samtleben W, Blumenstein M, Haberset R, Gurland HJ: Indications for the

application of plasmapheresis. Mt3n Med Wochenschr 124:641-645, 1982 (h

German)

Takahashi 1, Inoue T: Plasmapheresis: Present and perspective. ICU and CCU 6:1,

1982 (In Japanese)

Apheresis: Development, applications, and collection procedures. Rog Clin Biol

Res 65:1-66, 1981

~~:~tieo A, et al: Plasma exchange. Ann Med Interne (Paris) 132:89-92, 1981 (In

Cona 3A: Establishing a therapeutic pheresis program. Artif Organs 5:229-233,

1981

Cunio 3E: Plasma exchange therapy. Nephrol Nurse 3:35-38, 1981

Eliasson S, et al: Idiopathic inflammatory myopathy and plasmapheresis. Muscle

Nerve 4:446-447, 1981

Freireich E3: Future trends in apheresis. Prog Clin Biol Res 65:155-162, 1981

Gratwohl A, Comu P, Nissen C, Ruggero D, Ostervalder B, Speck B: Experience

with intensive plasma exchange. SChweiZ Med Wochenschr 110:1449-1451, 1981

(English abstract)

Hill N: Therapeutic studies on Ieukapheresis and plasmapheresis. Prog Clin Biol

Res 65:147-154, 1981

Holderman C, Schlesinger RG: Modified plasma therapy using the Haemonetics 30

blood processor. Plasma Ther Transfus Technol 2:31-33, 1981

Horiuchi T, Otsubo O, Uchima T, Kusaba R, Sugimoto H, Yanagisawa T, Inou T,

Nagata S, Tanaka S: Development of high performance membrane and optimum

design of plasma separator. Artif Organs 10:304, 1981 (In 3apanese)

Isbister 3P, et al: Fulminant lupus pneumonitis with acute renal failure and RBC

aplasia. Successful management with plasmapheresis and immunosuppression.

Arch Intern Med 141:1081-1083, 1981

Kalinin NN: Principles and methods of using apparatus for plasmacytapheresis with

donors and patients. Probl Gematol Pereliv Krovi 26:1 1-16, 1981 (In Russian)

Kater L: Indications and limitations of therapeutic plasmapheresis. Neth 3 Mad

24:206-208, 1981

Kuroda M, et al: Successful treatment of fulminating complications associated

with extensive rhabdomyolysis by plasma exchange. Artif Organs 5:372-378, 1981

ARC Blood Services

Bibliography Supplement 2

TPB XIII-4

Levy 3: The anatomy of the therapeutic plasma exchange. In Werner WL (cd):

“Plasma Forum IV, February 11-13, 1981.11 American Blood Resources Association,

1981, pp 81-85

Marconi M, et al: Approaching plasma-exchange mathematically. Int 3 Artif

Organs 4:295-299, 1981

Naito R: The begiming of plasmapheresis in Japan. In Oda T (cd): ‘Therapeutic

Plasmapheresis.” Stuttgart: F. K. Schattauer Verlag, 1981, pp 29-34

Olanow CW, Roses AD, Fay JW: The eff~t of plasmapheresis on post-thy mectomy

ocular dysfunction. Can 3 Neurol Sci 8:169-172, 1981

Ota K: Present status and future prospect of plasmapheresis. In Oda T (cd):

‘therapeutic Plasmapheresis.” Stuttgart: F. K. Schattauer Verlag, 1981, pp 15-25

Pekker S: Immunohematology: Plasmapheresis. Therapeutic possibilities. ZFA

(Stuttgart) 57:187-189, 1981 (In German)

Perveev VI: Plasmapheresis in severely burned patients. SoV Med 12:17-21, 1981

(English abstract)

Plasma exchange. W Presse Med 10:1493-1498, 1981 (In French)

Strauer Bq et ah Use of plasmapheresis and immunosuppressive therapy in

coronary microangiopathies. Bibl Haematologica 47:213-227, 1981

Symposium on plasma substitutes, volume replacement and hemodilution. Ann Clin

Rea 13 sUP@ 33:1-88, 1981

Terekhov NT, et al: Hemosorption and transfusion therapy in diffuse peritonitis.

Vesm Khir 127:62-65, 1981 (English abstract)

van de Wiel ~ Imhof 3W, Rommes JH: Plasmapheresis as a component of

treatment. Ned Tijdschr Geneeskd 125:1714-1718, 1981 (In Dutch)

Yamagata 2, et al: Therapeutic plasma exchange. Ryumachi 21:424-429, 1981 (In

Japanese)

Clark WF: Plasma exchange: A popular form of therapy. Dimens Health Serv

57:26-28, 1980

Frohlich CH, Schneider W: Plasmapherese: Therapeutische MoglichkeitenL’ Diagnostic und Intensivetherapie 5:89, 1980 (In German)

Hylland RG: Further evidence for plasmapheresis. Arthritis Rheum 23:129, 1980

Isbister JP: Blood letting reborn: Plasma exchange. Med J Aust 3:633, 1980

Koepke 3A: Plasma exchange at the University of Iowa hospitals and clinics. 3

Iowa Med Soc 70:510-512, 1980

Krebs JH: Plasmapheresis: A review. MMW 122:1755, 1980 (In German)

I
I s●

ARC Blood Services

Bibliography Supplement 2

TPB XIII-5

Verrier hnes J: Therapeutic plasmapheresis: An update. In Warner WL (cd):

‘Plasma Forum II, February 25-27, 1980.W American Blood Resources Assocm“ tion,

1980, pp 173-174

Wallach D, Cottenot F, Busael & Palangie A, Pennec 3: Plasma exchange therapy

in Lucio% phenomenon. Arch Dermatol 116:1101, 1980

Crispin JF: Medical ethics snd the morality of plasmapheresis. In Crouch RL (cd):

‘Plasma Forum.” McNally & Loftin, West: 1979, pp 39-51

Kriss 3P: Treatment of ● xophthalmos and pretibial myxoedema with plasmaphere% Br Med J 1:1149, 1979

Ncppert 3: Po&bilities of therapeutic plasmapheresis. Beitr lnfusionther KI~

Ernaehr 3:53-65, 1979 (In German)

Nowf Y, Malchesky PS: Therapeutic applications of plasmapheresh In Warner WL

(4): ‘plasma Forum. A Public Exchange of Views Regarding Plasmapheresis.”

American Blood Resources Association, 1979, pp 47-60

Pineda AA: Therapeutic plasma and qwqhresis (abstracts). Mayo Clinic

Workshop on Therapeutic Plasma and Cytapheresis, April 1979

Schareman WB, Tillotson JR, Taft EF, Wright E Plasmapheresis for meningococcemia with disseminated intravascular coqdation. N En@ J Med 300:1277,

1979

Smaller device tier triaI may widen plasmapheresis application. Hospital

Ractice, 1979, pp 29-33

Sussman LN, ● t al: Intensive plasmapheresis during pregmncy and spurious

amniotic fluid bilirubin. Am J Obatet Gynecol 135:156-157, 1979

Swisher SN: Plasmaphersis: A medical viewpoint. In Crouch RL (cd): ‘Plasma

Forum.” McNally & Loftin, West: 1979, pp 67-72

Warner WL (ad): ‘Plasma Forum. A Public Exchange of Views Regarding

Plasmapheresis.” American Blood Resowces Assoma“ tion, 1979

Buskard NA: Plasma exchange and plasmapheresis. CMA J 119:681, 1978

Sebahom G, Lefevre P, Carcassmne Y, Battaglmm“ “ I% Attempted clearance by

massive p&smaphe resia of an anti-HLA antibody in a patient who had received

multiple transfusions. Nouv Presae Mad 7:28, 1978

Bedry J, et al: Anti-tetanus immtnoglobulins and plasmapheresis. Rev Fr Transfus

Imnwnohematol 20:131, 1977

Thompson RN: Therapeutic pheresis. -on: Haemonetics Advanced Component

se*, 1977

Borberg H, Mulkr T, Lauterjung KIA Experimentelle tmd Klinische Erfakmgen

zur Plasmaphereses mit Blutzellaeparatoren. Verh Dtsh Ges Inn Med 82:1582, 1976

on German)

ARC Blood Services

Bibliography Supplement 2

TPB XIII-6

Baldassarre G, et al: Plasmaphereais: Method and value in extensive burns. Ann

Med NW (Itoma) 76:111, 1971.

Sandu L Nustalea N: ~ Therapeutical plasma~eresis in resuscitation. Cirurgia

20:845, 1971 (In Russian

Bystryn JC, Graf MW, Uhr JW: Regulation of antibody formation by serum

antibody. IL Removal of specific antibody by means of ● xchange transfusion. J

Exp Med 132:1278-1287, 1970

Mathes M: P~ for the isolation of mamlating plasma fractions. Folia

Haernatol 93:327-333, 1970 (In German)

MC M, e% al: Plasrnapheresis in puapral woman. Srps Arh Celok Lek 97:75-79,

1969

Sukunova LG, ● t al: Plasmapheresis and erytlrocyte reinfusion during the

restoration period following prolonged clinical death. RoM Gematol Pereliv Krovi

11:47-51, 1966 (In Russian)
AMERICAN RED CROSS BLOOD

supplement 2

SERVICES

Therapeutic Pheresis Bibliography No. XIV: Clinical Reactions, Complications

Aufeuvre 3P, Mortin-Hertel F, Cohen-%lal M, Lefloch A, Baudelot 3: Clinical

tolerance and hazards of plasma exchanges: A study of 6200 plasma exchanges in

1033~tients. In Beyer J-H, Borberg H, Fuchs Ch, Nagel GA (edsh “Pla$rnapheresis in Immunology and Oncology.” Basel: S Karger, 1982, PP 65-77

Beyer J-H, Klee M, Kaboth U, Kehl A, Kostering H, Krieger G, Nagel GA:

Problems of plasma-exchange solutions, gamma-globulin substitution, and turnor

enhancement in plasmapheresis of tumor patients. In Beyer 3-H, Borberg H, Fuchs

Ch, Nagel GA (eds): ‘Plasmapheresis in Immunology and Oncology.” Basel: S.

Karger, 1982, pp 204-217

Castelli D: Risiken and Komplikationen der therapeutischen Plasmapherese.

Therapeutische Umschau/Revue Therapeutique 39:555-557, 1982 (English abstract)

Connell 3M, et al: Self-poisoning with sustahed -release aminophylline: Secondary

rise in serum theophylline concentration after charcoal haemoperfusion. Br Med J

284:943, 1982

Huston DP, White M: Assessment of immtmoglobulin-G metabolism during plasmapheresis. Clin Res 30:A471, 1982

Keller F, Hauff A, Schultze G, Offermann G: Effect of repeated plasma exchange

on steady state kinetics of digoxin and digitoxin. In ‘International Symposium on

Plasmapheresis: Therapeutic Applications and New Techniques.” Cleveland: lnt

Soc Artif Organs, 1982, p 16

Kiprov DD, Dau PC: The effect of phsmapheresis and immunosuppressive drug

therapy on T cell subsets as defined by monoclinal antibodies. Boston: Haemonetics Advanced Component Seminar, 1982 (abstract)

Levy 3: Safety and standards in therapeutic apheresis. Plasma Ther Trmsfus

Technol 3:195-216, 1982

Rao AK, et al: The hemostatic system in children mdergoing intensive plasma

exchange. J Pediatr 100:69-75, 1982

Roberts WH, Kennedy MS, Doreen RE, Wanger GP: Acute copper deficiency in

patients undergoing plasma exchange. In “International Symposium on Plasmapheresis; Therapeutic Applications SIW’ :ew Techniques.n CleveIand: Int SOC Artif

Organs, 1982, p 36

Roujeau JC, Andre C, Revuz J, Touraine R: Effects of various immuncmqpressive

regimens on the %ebound phenomenon” induced by plasma exchange in pemphigus.

h-i ‘International Symposium on Plasmapheresis: Therapeutic Applications and New

Techniques.” Cleveland: Int Soc Artif Ggans, 1982, p 39

ARC Blood Services

Bibliography Supplement 2

TPB XIV-2

Samtkben W, Blurnenstein M, Habersetzer R, Gurland HJ: Indikationen nm

~tz der Plasmapherese. MIJn Med Wochenschr 124:641-645, 1982 (Englis h

abstract)

Schuff-Werner P, Brattig N, Beyer J-H, Bartel J, Berg PA, Nagel GA: Bio-assays

as a tool for the demonstration of immune alteration in cancer patients: Suppression of rnitogen-induced lymphocyte proliferation by patients’ sera during plasma

exchange. Preliminary results in four patients. h Beyer I-H! Borberg H) Fuchs

Ch, Nagel GA (eds): ‘Plasmapheresis in Immunology and oncology.” Basel: S.

Karger, 1982, pp 178-193

Senhauser DA, Westphal RG, Bohman 1~ NC IC: Immune system changes in

cytapheresis donors. Transfusion 22:302-304, 1982

Simon TL: Coagulation disorders with plasma exchange. Plasma lher Transfus

Technol 3:147-152, 1982

Spiva DA, Robinson CW Jr, Langley IW: Acute changes in antithrombin III levels

during apheresis procedures. Plasma Ther Transfus Technol 3:137-145, 1982

Tsokos CC, Balow la Huston DP, Wei N, Decker 3L: Effect of plasmapheresis on

lymphocyte-T and lymphocyte-B functions In patients with systemic @us-erythematosua - a double-blind study. Clin Exp Immunol 48:449-457, 1982

Urbaniak S3: Intensive plasma exchange - effects on haemostasis= In Collins 3A,

Shafer AW, Murawski K (eds): ‘Massive Transfusion in Surgery and Trauma.” New

York: Alan R. ~ Inc., 1982, pp 191-212

Volkin R~ Starz TW, Winkelstein A, Shadduck RK, Lewis JH, Hasiba U, Spero 3A:

Changes in coagulation factors complement, immunoglobulins, and immune complex concentrations with plasma exchange. Transfusion 22:54-58, 1982

Baudelot J, Aufeuvre 3P, ti-solal M, Estewes A : Technical aspects of

repeated plasmapheresis and plasma exchanges, and some of their clinical and

biological consequences. In Serrou % Rosenfeld C (eds): ~mmm complex= ad

Plasma Exchanges in Cancer patients.” New York: Elsevier/North Hollan d

Biomedical Ress, 1981, p 169-195

Borberg H: Roblems of plasma exchange therapy. In Gurland HJ, Heinze v, Lee

HA (eds): therapeutic Plasma Exchange.H New York: Springer-Verlag, 1981, pp

191-202

Brossard Y, et al: Severe complications of plasma exchange. Proposals for

attitudes to take in their prevention. Rev Fr Transfus Immunohernatol 24:701-708,

1981 (In French)

Dwyer J, Wade MJ, Katz W: Removal of thymic-derived lymphocytes dUring

pheresis procedures. Vox Sang 41:287-294, 1981

Fiala 1: Roblems in plasmapheresis (transfusions and c~nical aspects). Vnitr Lek

27:1131-1136, 1981 (English abstract)

Hester 3P, et al: Cross cellular contamination in plateletpheresi$. Ieukapheresis

and plasma exchange. Rog Clin Biol Res 65:109-121, 1981
ARC Blood Services

Bibliography Supplement 2

TPB XIV-3

3affe P, Mosher DF: Plasma antithrombin Ill and plasminogen levels in chronic

plasmapheresis. N Er@ J Med 304:789, 1981

3asso-Guti~rez ~ “Ruohern A, Delarosa L: Effects of ● xchange transfusion on

platelet counts. Arch Invest Med (Mex) 12:297-306, 1981

Kater L: Indications and limitations of therapeutic plasmapheresis. Neth J Med

24:206-208, 1981

Koepke 3A, Parks W,M, Goeken 3A, Klee GG, Strauss RG: The safety of weekly

plateletpheresis: Effect on the donor% lymphocyte population. Transfusion 21:59-

63, 1981

Kuroda M, et al: Successful treatment of fulminating complications associated

with extensive rhabdomyolysis by plasma exchange. Artif Organs 5:372-378, 1981

Isky LC, Lin AT, McCullough 33: Platelet counts before and after apheresis.

Transfusion 21:760-761, 1981

Pachl J, et al: Hemoperfusia and its pitfalls with children. Cesk Pediatr 36:511-

513, 1981 (English abstract)

Pieters R, Dequeker J: Infectious complications with plasma-exchange in connective tissue diseases. Abstract 643, 15th International Congress of Rheumatology, i%ris, lme 1981

Seiler F, Karges H, Geursen R, Sedlacek H: Possibilities, problems and tazards

with blood plasma substitution therapy, plasma exchange therapy. Proceedings

International Symposium, Wiesbaden. Georg-Thieme-Verlag, 1981, pp 37-52

Sunder—Plasmann L Hemodynamic changes during acutely induced hemodilution.

Ann Clin Res 13 SUppl 33:57, 1981

Talbert RL, et al: Propranolol plasma concentrations and plasmapheresis. Drug

Inteil Clin Pharm 15:993-996, 1981

Vasileva D: Effect of Ieukopheresis in donor hemopoiesis. Eksp Med Morfol

20:225-231, 1981 (English abstract)

Wright DG, Karsh 3, Fauci As K@@ 3H, Decker 3~ O*DonneU JF, Deisseroth

AB: Lymphocyte depletion and immunosuppression with repeated Ieukapheresis by

continuous flow centrifugation. Blood 58:451-458, 1981

Garelli S, et al: Studies on some coagulation parameters and platelet function in

Ieuko- and platelet-apheresed donors. Riv Emoter Irnmtmoematol 27:218-224, 1980

Gelabert A, Puig L, Maragall $ Monteaguido J, Castilio R: Coagulative alterations

during massive plasmapheresis. In Sieberth HG (cd): “Plasma Exchange. Plasmapheresis - Plasmaseparation.w Stuttgart: F. K. Schattauer Verlag, 1980, pp 71-75

Gltkkner WM, Sieberth HG, Dienst C, Vaith P, Mitrenga D, Kindler 3: Elimination

kinetics of antibodies and immune complexes in membrane plasma separation. In

Sieberth HG (cd): ‘Plasma Exchange. Plasmapheresis - Plasmaseparation.n Stuttgart: F. K. Schattauer Verlag, 1980, pp 121-124

ARC Blood Services

Bibliography Supplement 2

TPB XIV-4

Grgicevic D, Pistotnik M, Pende B: Observation of the changes of plasma proteins

after long term plasmapheresis. Dev Biol Stand 48:279-286, 1980

Grob PJ, GmUr J, Von Felten A, Frey-Wettstein M, Hartmann S, Gartmann 3:

Plasma exchange and non-specific immune parameters. Comparison of two methods. In Sieberth HG (ad): ‘Plasma Exchange. Plasmapheresis - PlasmaSeparation. w Stuttgart: F. K. Schattauer Verlag, 1980, pp 113-119

Keller AJ, Urbanhk SJ: Intensive plasma exchange on the cell separator: Effects

on serum immunoglobulins and complement components. Plasma Ther Transfus

Technol 1:1-10, 1980

Lundsgaard-Hansen F% Donor safety in plasrnapheresis. Dev Biol Stand 48:287-295,

1980

Rawer P, Sommerlad K-H, Goretzki K, Leber HW: Elimination of plasma proteina

during plasma separation using either centrifugation or membrane filtration and

selective removal of immumglobul,in G and immme complexes with immobilised

protein A. In siebe~ HG (ad): ‘Plasma Exchange. Plasmapheresis - Plasma-

$+=ati~.” s~ttgart: F. K. Schattauer Verlag, 1980, pp 65-70

Wing EJ, Bruns F3, Fraley DS, Segel DP, Adler S: Infectious complications with

plasmapheresia in rapidly progressive glomerulatephritis. JAMA 2ft4:2423-2426,

1980

Bussel A: Etudes des incidents ● t accidents observes au cours de 250 echanges

plasmatiques. Lea Echanges Plasrnatiqu- Pratique, Resultats et Perspectives.

Bois GuilIaume, March 1979

Busaard CM: llw eff~ of intensive plasmapheresis on plasma constituents in

donors and patients. PhD d“usertation, University Bern, 1979

Cohen E Possible immunological effects of long term plasmapheresis. In Warner

WL (cd): ‘Plasma Forum. A public Exchange of Views Regarding Plasmapheresi.%”

American Blood Resources Association, 1979, pp 5-20

Glassman AB: Immune responses: The rationale for plasmapheresis. Plasma Ther

Transfus Technol 1:13, 1979

Kimey NJ, Tarter R, Varga ~ Varga V, Sugerman AA, Milson S: Safety of

repeated weekly hemoperfusion. Clin Res 27:420A, 1979

Sideman S, Hoffer E: Biocompatibility and safety evaluation of hemoperfusion

devices. h Sideman S, Chang TMS (eds): ‘Hemoperfusion Workshop-Beit Oren.”

Samuel Newman Institute far Advanced Studies in Science and Technology, Israel,

1979

Sutton DMC, CaddIa CJ, Uldal.1 PR: some observations on tlw complications of

intensive plasma exchange. Boston: Haemonetics Research Institute, 1979

Engle WD, Jacobs JF, Swatz RD, Duff TE, Kelsch RC, Lane GA, Baublis 3W:

Severe coagulopathy complicating charcoal hemoperfusion in children with Reye

syndrome. 3 Pediatr 93:972-974, 1978

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ARC Blood Services ARC Blood Services

Bibliography Supplement 2 Bibliography Supplement 2

TPB XIV-5 TPB XIV-6

Gibson TP, Atkinson AJ: Effect of changes in intercompartment rate constants on

drug removal during hemoperfusion. J Pharmacol Sci 67:1 178, 1978

Fennimore 3, Kolthammer 3C, Lang SM: Evaluation of hemoperfusion systems in

vitro methods related to performance and safety. In Kenedi RM, Courtney J,

Gaylor JDS, GilChrist T (eds): ‘*Artificial Organs.” London: Macmillan Ress,

1977, PP 1$8-1S7

Gilcher RO, Hashiba U: Automated plasmapheresis (coagulation studies). Boston:

Haemonetics Advance Comportment Seminar, 1977

Lund<gaard-Hansen P: Volume Iimitatians of plasmapheresis. Vox Sang 32:20-25,

1977

Lynch R~ Buselmeier T3: Charcoal hernoperfusion - induced thrombocytopenia,

leukopenia, and serum chemistry alteration. Kidney Int 12:484, 1977

Rossen RD, Hersh EM, Sharp JT, McCredie KB, Gyorkey F, Suki WN, Eknoyan G,

Reisberg MA: Effect of plasma exchange on circulating immunocompiexes and

antibody formation in patients treated with cyclophosphamide and prednisone . Am

J Med 63:674, 1977

Scharschrnidt BF, Martin JF, Shapiro U: The use of calcium chelating agents and

prostaglandin El to eliminate platelet and white blood cell losses resulting from

hemoperfusion through uxoated charcoal albu -*o= gel ~ ne~al and

cation exchange resin. J Lab Clin Med 89:110-119, 1977

Friedman BA, et al: Plasrnaphe reais-induced hemodilution and its effects on serum

constituents. Transfusion 16:155-161, 1976

Koepke 3A, Wu KK, Hoak JC, Thompson 3S: Effects of long term plasmaphereais

on plasma proteins. Transfusion 16:191-192, 1976

Rimon O: Selective removal of metabolities from the blood serum by hemoperfusion. Thesis, Technicon, Haifa, 1976 (In Hebrew)

Winchester JF, Mackay JM, Forbes CD, Blakely Ej Prentice CRM, Kennedy AC:

Hemostatic changes induced in vitro by activated charcoal hemoperfusion. Throm

Diath 34:587, 1975

Konstantinov VN, ● t al: The effect of repeated plasmapheresis on the donors’

organism. Probl Gematol Pereiiv Krovi 16:25-27, 1971 (In Russian)

Ad Hoc committee: Safeguards for plasma donors in plasmapheresis programs.

3AMA 213:743, 1970

Cohen MA, Oberman HA: Safety and long term effects of plasmapheresis.

Transfusion 10:58, 1970

Oishi M: Studies a the regeneration of blood clotting factors following acute

plasrnapheresis. Acta Haernatol 3ap 33:226-244, 1970 (In Japanese)

Pacitti C, ● t al: Metabolic effects caused by blood protein restoration after

plasmapheresis. Arch Fisiol 67:215-223, 1969 (In Italian)

Daszynski 3, Klenowska Z: Preliminary investigations upon plasmapheresis in blood

dOiMXS. Pol Med J 6:857, 1967

Kliman A, Carbone PP, Gaydos LA, Freireich EJ: Effects of intensive plasmapheresis on normal blood donors. Blood 23:647-656, 1964

●
AMERICAN RED CROSS BLOOD SERVICES

Supplement 2

Therapeutic Pheresis Bibliography No. XV: Tectmical Aspects

Agishi 1: Dode filtration plasmapheresis and immmoadsorption: Tectmical

aspects. In Bayer J +1, Borberg H, Fuchs ~ Nagel GA (edsk Wlasmapheresis in

Immunology and Oncology.” Basal: S. Karger, 1982, pp 47-56

Borberg H: Tectmical aspects of atli-piasma separation and the elimination of

plastia-mponents ex vivo. In Bayer 3+1, Borberg H, Fuchs Ch, Nagel GA (eds):

Tlasmapheresis in Immwtology and Oncology.w Basel: S. Karger, 1982 pp 11-18

Leonard ff: The Shear-rate filtration rate relationship of membranes for

plasmapheresis. In %ternational Symposium on Plasmapheresis: Therapeutic

Applications and New Teclmi~s.W Cleveland: Int Soc Artif Organs, 1982, p 22

Randerson DH, et ah Mass transfer in membrane plasma exchange. Artif Organs

6:43-49, 1982

Kawai T, Yamagishi Y, N~ita Y, Yti M, Chiba A: Some pertinent factor s

involving biood v“ucometry. In ode T (edh 7herapautic Plesmapheresis.H Stuttgart: F. K. !k3Mttauar Verlag, 1981, w 41-46

Marinone G, et ah Mm marrow erytlrobiastic reaery after piasmapheresis in

acquired pure red cdl anemi~ case report. Heematologica (Pavia) 66:796-802,

1981

Mieike Gi 1 r, ● t ai: Tectmical and therapeutic applicatims of plasma exchange.

Prog Clin Biol Res 65:123-145, 1981

Qdlhorst & et al: How to prevent vasalar imtability: Haemofiltration. Pro c

Eur Dial Transplant Asaoc 18:243-249, 1981

Takahashi I, Otsti O, Horiuchi T, Nozaki H, Yanagisawa T, Maeda T, Seo S,

Yagata K, Inou T: F undamentai studies related to plasma exchange. In Oda T (edh

‘Tkrapeutic Plasmapheresis. Stuttgart: F. K. $dattauer Verlag, 1981, pp 35-40

Wenk RE, MWJC14 E, Brewer MK: Automated suspension of washed

3

hrocytes in

fresh-frozen plasma for exchange transfusion Obtaining a *si hamatocrit.

Transfusion 21:690-69~ 1981

Wood L, et al: The roie of continuou s-flow blood fraction separators in ciinical

practice. S Afr Med J 59x99-104, 1981

~oPC, Smit-S~ ChTS: Replamnant fluid in plasma exchange. Lancet 2:644,

Kleinman S, Thompaon-Breton R, Rifkind S, Goldfinger ~ Exdange red blood cell

pheresis in the management of complications of sickJe cell anemia. Plasma Ther

Transfus Technol 1:27, 1980

ARC Blood Services

Bibliography Supplement 2

TPB XV-2

Levine D3: Caiculaticm of volumes for ● xchange transfusions. J Pedhtr 97:870,

1980

Schurek HG, Heyde C vd, Velta H, Deicher H, Marghescu S, Stolte H: Different

application of plasma exchange. Optimal adaption of exchange procedure. NierenU. Hochdruckkrankht 9:149, 1980

Yamazaki Z, hmue N, Fujimori Y, Takahama T, Wada T, ode T, Ida K, Kataoka K,

Fujisaki Y: Biocompatibiiity of plasma separat~ of an improved cellulose acetate

hoilow fiber. In $ieberth HG (edk Wlaama Exchange. Piasmapheresis - Plasmaseparation.” Stuttgarm F. K. $chattauar Verlag, 1980, pp 45-51

N-’ Y, Maichesky PS: Therapeutic applicatims of plasmapharesis. In Warner WL

(edh Wasma Forurn. A Public Exchange of Views Regarding Plasmapheresis.n

American Biood Reaources Associatiat, 1979, pp 47-60

Buchholz DH, Bove 1 R, Charette 3 W Plasmapheresis using IBM 2991 blood ceil

processor. Transfusion 18:269-273, 1978

Gibson TP, Atkimon A2: Effects of changes in intercompartment rate constants on

drug removal during hemoparfusion. 3 Pharmacol Sci 67:1178-1179, 1978

Mtir 1: Interrelation of hemoperfusion plasma ciearanca and half life. In Chng

TMS (edh ‘Artifiaal Kidney, Artificial Liver, and Artificial Ceil&a New York:

Pienum press, 1978, pp 297-300

Panlilio AL, et ah Pheresia tecttniques in therapeutic procedures and preparation

of blood products. J Term Mad Assoc” 71:181- 1841978

Suaudeau 3, Kolobow T, Vsillancoum R, Carvalho A, ho Y, Erdmann A3: The Ito

‘flow-ttwough” centrifuge: A new devi~ for long-term (24 hours) plasmapharesis

wittmut platelet deterioratkm. Transfushm 18:312-319, 1978

Thompson GR: Clinical applicathm of plasma exchange. IBM Medicai Review,

1978

$dwnidt R, Faikenha gen D, Holtz M, Obsten B, Kmger E, Glasel E, Gottschail ST,

Ahrend KF, Bremer H, Tlesa D, Kiinkmann H: Harnoperfusion-Experimentelie and

Kliniscita ergebnisse. Dtsh Gesmdh-Wesen 32:2117-2122, 1977 @ German)

F arrelea FB, Summers T, Balder C, Bayer WL: Plasma exchange with plasma

protein fractkm and lactated Ringers solution using the ccmtinuous f~w =11

separator. Infusionstherapie 2:273-277, 1975

Raaenbaum 3L: Biocompatibility oi resin haemoperfushm. In Williams RS,

Murray-Lyons IM (edsb ‘Artifical Liver Support.” New York Pittman Press,

1975, p 118

Ayme G, et ai: An improved technique for polyacrylami~ gei electrophoresis:

Application for tha study of serum proteins during piasmapheresis. Prog Immwmbiol Stand 4:434-445, 1970 (In French)

-son SB, Rossing N: Metabolism of aibumin and G giobuiin during albumin

infusions and during plasmapheresis. Scand J Clin Lab Invest 20:183-184, 1%7
AMERICAN RED CROSS BLOOD SERVICES

Supplement 2

Therapeutic Pheresis Bibliography No. XVI: Alternative Methodologies

Agishi T, Kaneko I, Hasuo Y, Ota K, Amemiya H, Sugino N, Abe M: Automatic

control apparatus for membrane plasmapheresis. In International Symposium on

Plasrjyspheresm Therapeutic Appl.i=tions and New Techniques.” Cleveland: Int

%c Artif organs, 198% p 1

Bambauer R, 3 utzler GA, Keller HE, Stolz D: Clinical experience with a

technically simplified plasmapheresis system. In %ternational Symposium on

Plasmapheresis: Therapeutic Applicatiwm and New Techniques.” Cleveland: Int

Soc Artif Organs, 1982, p 3

Bambauer R, 3 utzler GA, Stolz D, Ranger A, Doenecke P: Detoxification: Using a

technically simplified plasma filtration system. In %itemational Symposium on

Plasmapheresis: Therapeutic Applicathns and New Techniques.W Cleveland: Int

Soc Artif Organs, 1982, p 4

Butylin Vi, et al: Use of th ISL-3 artificial circulathm apparatus for performing

hemosorption. Klin Khir 1:63-64, 1982 (In Russian)

Dmitriev M, et al: Evaluation of variants in tk approach to vessels in the

hemosorptkm operation in relation to the treatment regimen and procedure.

Anesteziol Reanirnatol 1:35-37, 1982 (En@h @$traa)

Falkenhagen D, Gottachall S, Esther G, Courtney JM, Klinkmann H: In vitro

assessment of darcoal and resin hemoadsorbents. Cantrib Nephrol 29:23-33, 1982

Falke

Y&r

n D, Schmitt % Schneider P, Behm E, Tessenow W, Klinkrnann H:

Plaema- ption - an alternative way to treat intoxications? In %ternational

Symposim on PISmapheresis: Therapeutic Applications and New Tectmiques.”

Cleveland: Int Soc Artif Organs, 1982, p 11

Gurland HG, Noe4 Y, ASanUfM Y, Bhmenstein M, thkhe$ky PS, Samtleben W,

Schmidt B, Zawicld h Membrane-plasma filwation. In Bayer 34, Mberg H,

Fuchs Ch, Nagel GA (edsb ~lasmapheresis in Immunology and Onmlogy.” Baseh

S. Karger, 1983 pp 2-10

Khatri ~ A tedmique for easy vascular access in patients mdergoing plasmapheresis. J Clin Apheresis 1:55, 1982

Kimwa G, et ah A computerized model to analyze tranw=llular fluid shift during

hemofiltration. Artif Organs 6:31-3Q 1982

Krakauer RS, Aaanuma Y, Zawicki 1, Calabrese L Malchesky P, Naae Y: Circuiting immune complexes in rheumatoid arthritis: Selective removal by cryogelation

with membrane filtration. Arch Intern Med 142:395-397, 1982

ARC Blood Services

Bibliography Supplement 2

TPB XVI-2

L eonard EF: The Shear-rate filtration rate relationship of membranes f=

plasmapheresis. In qntemational Symposium on Plasmapheresi= Therapeutic

Applicatias and New Techniques.” Clevelamh Int Soc Artif Organs, 1982, p 22

Lopot F, et ah Haemofiltration - a new method of treatment far chronic renal

failure. Cas Lek Cesk 121:210-213, 1982 (English abatract)

Lysaght M3: Factors governing mass transport in filters for membrane phssm~

pheresis. In ‘Internaticmal Symposium on Plasrnapheresk Therapeutic Applicatiotu and New Techniques.N Cleveland Int Soc Artif Organs, 1982, p 25

Maldwsky I%: Membrane plasma separatkn. In ~ntematianal Symposium on

Plasmapheresiss Thempeutic Application and New TechNquee.” Cleveland Int

Soc Artif Organs, 1982, p 27

Millward BL, Hoeltge GA: The historical -Velopment of automated hemapheresis.

J Clin Apheresis 1:25-3Z 1982

ONeil GD, Ksrp DD, H~ LE, Mwtel J, Gorgone BC, Ervin TJ: Preliminary

results of t!rombocytaphereais using a sqe pump. Boatom Haemonetics

Advanced Component Sernhr, 1982 (abstract)

Pourrat 3P, Sanchez V, Espenan P, Dueymea JM, Conte 33: On-1ine separati~ of

plasma proteh by convective elecuophoresh An alternative to plasma-exchange.

Boatora Haemonetics Advanced Component Seminar, 1982 (abstract)

Rawer P, Sommded K-H, Gocetzky K, L- HW: A comparative stdy of the

efficacy of two methods of plasrnapheresk Centrifugation with ACD or heparin

and membrane filtration with two diff~ent celluhxe dketate hollow-fiber

membranes. In Bayer J-H, Borbert H, Fuchs Ch, Nagd GA (ads> Tlaamapheresie

in Immmology and Oncology.n Basek S. Karger, 1982, pp 28-36

Schreiner = Clinical hemoperfuaiom Contrib Neptrol 2%7- 10, 1982

Shettiger UR, et ah PortaMe artificial Id&ey with advantages of hemodialysis,

hereof iltradon, and hemoperfueion. Artif Organs 617-231982

Sueoka A, Wojcicki 3, Maldwsky P, Need Y: PVA membranes for plasma

separation. In %tternational Symposium on Pl=mapheresiss Therapeutic Applications and New Techniques.w Cleveland Int Soc Artlf Organs, 198Z p 42

Vanholder R, DeClippele M, Wulfmnk, Deschrijvcr A, Ringoir S Urdptaacture

membrane plasmapheresis. In %tternaticsud Sympoaium on Plasmapheresis Therapeutic Application and New Techniques.W Cleveland 1nt Soc Artif Organs, 1983

p46

Asmurna Y, et ah Clronic ambulatory liver stpport by membrane plasmapheresis

with on-line detoxification. Trans Am Soc Artif Intern Organs 27:416-422 1981

Bussel A: Comparative study of the various technics used in plasma exchange.

Rev Fr Transfus Immmohematoi 24:691-699, 1981 (b French)

Cavalier 3: Gcsteral parameters in the technology of plasma filtration using a

membrane. Rev Fr Transfus tmmtmohematol 24:633-64 1, 1981 on French)
ARC Blood Services

Bibliography Supplement 2

TPB XVI-3

Chmiel H: Technoiogkhe ~kte zur Membranplasmapherese. In Gurland HJ,

Heinze V, Lee HA (eds): therapeutic Plasma Exchange.” New York: SpringerVerlag, 1981, w 15-21 (In German)

Cunio 3E, hderson WW : Continuous flow plasma exchange utilizing %ingle

needle” techniques. Trana Am Soc Artif $tem Organs 27:550-553, 1981

Elghouzzi MH, et al: Technical, immunological and clinical study of the performance of blood filtration using Erypur filters. Rev Fr Transfus Immunohernatol

24:579-595, 1981 (English abstract)

Gajd66s Ph, Simon N, Elkharrat D, Goulon M: Testing a cellulose diacetate

membrane for plasma exchange. NOUV Presse Mad 10:3469-3471, 1981 (English

abstract)

Hughes RD, ● t al: Selection of an adaorlm’tt and hemoperfusion column design. lnt

J Artif Organs 4Q24-229, 1981

Inoue N, Yarnazah“ i& Yoshiba M, Ichikawa K, Sakai T, ode T, Sanp T, Wada T,

Inoue 3, Saoshiro T, tkxiuchi T, Ida K, Fujisaki Y : Plasma exchange using

membrane plasmapheresis in the treatment of acute hepatic failure. Artif Organs

10:557, 1981

Kanamono T, 1wata H, Yasuhara N, TAahashi $ Satoh K, Ohishi Y, Nakagawa M,

Yamanaka N, Kohyarna M, Saitoh A, Ota K: Long-term experience of plasma

exchange using herno-filter. in Oda T (cd): ~peutic Plasmapheresis.W Stuttgart: F. K. Schattauer Verlag, 1981, pp 139-144

Kaneko 1, Agishi T, Hasuo Y, Era K, Om K, Abe M: Automatic controlling system

for double filtration pbmaphe resis. Artif Organs 100i284, 1981 (In Japanese )

Kayashima K, et al: Simple on-line filters for the therapeutic removal of

lymphocytes from blood. Trana Am Soc Artif Intern Organs 27:559-562, 1981

Kourilsky O, ● t al: Plasma exchange by membrane filtration.

T

ience of the

Tenon Hospital. Rev Fr Transfus Immunohematol 24:643-655, 1981 In French)

Mathez D, et al: A new plasma exchange techni ue: Coagulation studies. Nouv

Rev Fr Hernatol 23:285-289, 1981 (English abstract1

No*’ Y, Malchesky PS: Therapeutic membrane plasmapheresis. In Oda T (cd):

%rapeutic PiasmapheresisW Suttgart: F. K. Schattauer Verlag, 1981, pp 3-14

Pierides AM, et al: Two year experience with over 500 sessions of postdiluthm

hemofiltration. Trana Am Soc Artif intern Organa 27:618-622, 1981

Pineda AA Taswell HF: Selective plasma component removal: Alternatives to

plasma exchange. H Organs 5:23A240, 1981

Piskin ~ et al: The best mating material for hemoperfusion: Comparison of

cellulose nitrate with cellulose acetate and derivatives. bit J Artif Organs 4*6-88,

1981

ARC Blood Services

Bibliography Supplement 2

TPB XVI-4

Radcliffe DR~ et al: Sorption kinetics in haernoperfusion columns. part 2:

ModeUing COhllllfl Performancee. Mad Biol Eng Comput 19:627-637, 1981

Radcliffe D% et al: sorption kinatics in haemoperfusion columns. Part 1:

Estimation of mass-transfer parameters. Med Biol Eng Comput 19:617-626, 1981

Ramperez P, ● t ah Economic preparation of starile pyrogen free infusate for

haemofiltration. Roc Eur Dial Transplant Aasoc 18:293-296, 1981

Sakai & Matsumoto & Nishimuta & Imamura N, Amemiya M, Fujimaki H,

Nakamura Mj Ochiai H, Miyahara T: p~=i$ @W two ho~w fibef$ of

callulo5e4iacetate membrane of different pore size. In Oda T (ad): ‘Therapeutic

p~r=i$.” St-: F. K. ~~ Verlag, 1981, pp 177-183

SchhdMm K, et ah Mass transfer chmcteristics of plasma filtration membranes.

Trans Am Soc Artif Intern Organa 27:554-558, 1981

ShaMon $ et a h Mixed hemofiltration (MHF): 18 months experience with

ultrdmrt treatment time. Trana Am Soc Artif Intern Organa 27:610-612, 1981

Shimizu H, Hoaoya R, Yahida $ Eiraku K, Niahimura K: Efficiency of blood cell

~a~~ and clinical evaluation of IBM 2997 CFCS Artif organs 10:316, 1981 (In

Shirno K, Suzuta T, Suztdti M, No# Y: Basic and clinical studies on continuous

cryofiltratiom A new treatment for rheumatoid arthrith Rheumachi 21:61, 1981

& et al: Accessible plasma exchange using membrana filter - a

successfully treated case of TTP with repeated plasma 45tchanges. Artif Organs

5Q48-253, 1981

Simon P, et al: Plasma exchange using filtrathm. Experience at the apropos of 21

patients. Rev Fr Transfus Immunohematol 24:671-690, 1981 (In French)

smith 3W, Wyaenbeek AJ, Kmkauer RSz Plasmapheresis h Membrane filtration

methods. Plasma Ther Transfua Technol 2:53-60, 1981

Solomon BA: Membrane separations: Technological principles and issues. Trans

Am Soc Artif Intern Organs 27:345-350, 1981

Verrier 3ones J: @ntrifugal separation of plasma: Techniques and applications.

Trans Am Soc Artif Intern Organa 27:351-355, 1981

Werynaki & Makhesky PS; Sueoka A, Asanuma Y, Smith JW, Kayashirna K, Herw

E, Sato H, -Y: Membrane plasma separation: Toward improved clinical

operation. Trana mSoc Artif Jntem Organs 27:539-543, 1981

2hang X: Regress in he~filtration research. Chung Hua Nei Ko Tsa Chih

20:439-44~ 1981 (In Chinese

Agishi T, Kaneko 3, Hasuoi Y, Sanaka T, Ota K, Amemika H, Sugino N: Double

filtration plasmapheresis with no or minimal amount of blood derivative for

substitution. In Sieberth HG (ad): ‘Plasma Exchange. Pla.smapheresia - Plasmaseparation.” Stuttgart: F. K. Schattauer Verlag, 1980, pp 53-57

Asaba H, Lofquist B, Wehle a Bergstrom J: Plasma exchange with a membrane

plasma filter (plasmaflo). Nieren+. Hochdruckkrankht 9:136, 1980
w

Cn

I

al

N

w

o

cm

w

. .

ARC Blood Services

Bibliography Supplement 2

TPB XVI-5

Blaha M, et al: Case report of hyperviscosity syndrome treatment with plasma

● xchange using the “Aminco” separator. Vnitr Lek 26:786-791, 1980 (In Czechoslovakian)

Brunner G, Harstick K, Holloway C3: Agarose-encapsulated absorbents: A new

material for haemoperfusion. in Sideman S, Chang TMS (eds): ‘HemoperfWion.

Kidney and Liver Support and Detoxification,w Part L Washington: Hemisphere

Publishing Corporation, 1980, pp 37-44

Chang TMS: Present status and prospective of artificial cells in hemoperfusion.

In Sideman S, Chang TMS (eds): ‘Hemoperfusion. Kidney and Liver mPPort and

Deto~ification.m Washington, DC: Hemisphere Publishing Corporation, 1980, pp

93-104

Burton BT, Chang TMS, Nose Y, Rosenbaum 3L, Sideman S: Pa@ Discussion:

Resent and future of hernoperfusion. In Sideman $ Chang TMS (eds): ‘Hemoperfusion. Kidney and Liver Support and Detoxification.” Washington, DC:

Hemisphere Publishing Corporation, 1980, pp 399-401

Farrell PC, Schindhelm K, Roberts CG: Membrane plasma separation. In Sieberth

HG (cd): “Plasma Exchange. Plasmapheresis - Plasmaseparation.n Stuttgart: F.

K. Schattauer Verlag, 1980, pp 37-44

Gibson TP: Pharmacokinetic deterrnhnts of the efficacy of hemoperfusion. In

Sideman % Chang TMS (eds): “Hernoperfuaion. Kidney and Liver Support and

fkJo2~~ication,” Part I. Washington: Hemisphere Publishing Corporation, 1980, pp

Inoue N, Yoshiba M, Yamazaki ~ Sakai T, Sanjo K, Okada K, Oda T, Wada T, hue

T: Continuous flow membrane plasmapheresis utilizing cellulose acetate hollow

fiber in hepatic failure. In Brwmer G, Schmidt FW (ads): “Artificial Liver

support.” New York: Springer Verlag, 1980, p 175

Kaneko 1, Agishi T, Hasuo Y, Hoshimo T, Era K, Ota K, Abe M, Hayasaka Y, Kawai

S, Yamane T: Technical feasibility of double filtration plasmapheresis. Artif

Organs 9:443, 1980 (In hpanese)

Mor LA, Sideman & Mor I+ Brandes JM: Analysis of hemoperfusion columns:

Selective removal of protein-bound metabolizes. in Sideman $ Chang TMS (eds):

“Hemoperfusion. Kidney and Liver Support and Detoxification,” Part I. Washington: Hemisphere Publishing Corporation, 1980, pp 175-188

Nakabayashi N, Masuhara E, Nakagawa S, Koshikawa S, Nakashima T, Takakura K:

Preparation of poly-hema coated spherical activated charcoal for direct hemoperfusion. In Sideman S, Chang TMS (eds): ‘Hemoperfusion. Kidney and Liver

Sqpport and Detoxification.” Washington, DC: Hemisphere Publishing Corporation,

1980, pp 57-61

Odaka M, Hirasawa H, Kobayashi H, Ohkawa M, Soeda K, Tabata Y, Soma M, Sato

H: Clinical and fundamental studies of cellulose coated bead-shaped charcoal

haemoperfusion in chronic renal failure. In Sideman Sj Chang TMS (eds):

‘Hemoperfusion. Kidney and Liver Support and Detoxification.” Washington, DC:

Hemisphere Publishing Corporation, 1980, pp 45-55

ARC Blood Services

Bibliography S~plement 2

TPB XVI-6

Samtleben W, Hillebrand G, Krumme D, Gurland HJ: Membrane Plasma separation:

Clinical experience with more than 120 plasma exchanges. In ‘Sieberth ‘HG (cd):

“Plasma Exchange. Ph.smapheresis - Plasrnaseparation.” Stuttgart: F. K.

Schattauer Verlag, 1980, pp 175-178

Sideman S, Hoffer ~ Better OS, Lupovitch S: Development of a hemoperfusion

system for phosphate removal. In Sideman & Chang TMS (eds): “Hemoperfusion.

Kidney and Liver Support and Detoxification,” Part L Washington: Hemisphere

Publishing Corporation, 1980, pp 81-89

Asanuma Y, Smith JW, Malchesky PS, Hermann RE, Carey WD, Nose Y: Preclinical evaluation of membrane plasmapheresis with on-line bilirubin removal.

Artif organs (in press), 1979

Chang TMS: &sessment of clinical trials of charcoal hemoperfusion in uremic

patients. Nephrol 11:11 1-119, 1979

Cooney DD, Daly 3S: Mass transfer characteristics of hollow-fiber dialyzers and

hemoperfusion devices. Artif Crgans 3:253-258, 1979

Garciape 33, Redondor M, Torresra A, Mendezpe ML, Meceirac B, Buenogom 3:

Hemoperfusion over sorbent materials. Rev Clin Rea 152:331-335, 1979

Grabensee BH, Gobel K, Hofmann E, Schnurr g Schroder E: Tierexperimenteile

untersuchungen zur Behandlung Schwere Schlamittelvergiftungen mit Hamoperfusion durch Adaorberharz. Verh Dtsch Ges km Med 80:1571, 1979

Malcheaky PS, Asanurna Y, Smith 3W, Zawicki I, ~’ Y: Membrane plasmapheresis with on-line plasma treatment. Artif Organs 3:359, 1979

Nakabayashi N, Maauhara 5 Nakagawa % Koshikaw Ss Encapsulation of spherical

activated charcoals with Poly-Hema for direct hemoperfusion. Kobunsh-Ron

36:279-286, 1979

Rossi PL: Therapeutic value of the ceil separator: Review and case reports.

Minerva Med 70:1289-1298, 1979

Smith JW, Asanuma Y, Suwa S, HaraSaki. H, Zawicki I, Malchesky PS, Nose Y:

Blood compatibility studies of hoUow fiber plasma filtration for hepatic assist.

Trans Am Soc Artif Intern Organs 25:476, 1979

Tijsaen J, Bantjes A, van Doom AWJ, Feijen J, van Dijk B, Vonk CR, Dijkhais JC:

A hemoperfusion coIumn based on carbon granules coated with an ultrathin

membrane of cellulose acetate. Artif Organs 3:11, 1979

Uldall RP, Dyck RF, Woods F, Merchant N, Martin GS, Cardella C3, Sutton D, de

Veber GA: Subclavim cannula for temporary vascular access for haemoldialysis or

plasmapheresis. Dial Transplant 9:963, 1979

Amano I, Kano H, Takahira H, Yamarnoto Y, Itoh K, Iwatsuki S, Maeda K, Ohta K:

Hepatic assist system using bead-type charcoal. In Chang TMS (cd): “Artificial

Kidney, Artificial Liver, and Artificial Cells.” New York: Plenum Ress, 1978, PP

89-98
ARC Blood Services

Bibliography Supplement 2

TPB XVI-7

Chang TMS: Adsorbent hemoperfusion - general discussion. In Chang TMS (cd):

“Artificial Kidney, Artificial Liver, and Artificial Cells.” New York: Plenum

Ress, 1978, pp 301-304

Chang TMS: A 1978 perspective of adsorbent hemoperfusion, artificial organs.

Artif Organs 2:363-366, 197?

Cooney DD, Infantolino W, Kane R: Comparative studies of hemoperfusion

devices. 1. In vitro clearance characteristics. Biomater Med Devices Artif Organs

6:199-213, 1978

Grab@nsee BH, Konigshausen TH, Schnurr E : Behandh.mg Schwerer Schlafmittelver-giftungen durch extrakorporale hamoperfusion. Dtsch Med Woschenschr

101:158-162, 1978

Gundermann KJ, Lie TS: Moglichkeiten zur Vermeidung der Adsorption physioIogische substanzen bei der Aktivkohlehamoperf usion. Res Exp Med (Berl) 173:

105-111, 1978

Hampel G, Widdop B, GouJding R: Adsorptive capacities of hemoperfusion devices

in clinical use. Artif Organs 2:363-366, 1978

Hellwig G, Chmiel H: Theoretical concepts of absorbents for hemoperfusion.

Haemoperfusion, Dialysate and Diafiltrate Purification Symposium, Tutzing,

Germany, 1978 (abstract)

Hughes RD, Ton HY, Langley PG, “Silk DBA, Williams R: The use of ‘an in vitro

hemoperfusion circuit to evaluate the blood compatibility of albumin<oated

amberlite XAD-7 resin. Int J Artif Organs 1:129, 1978

Inwe N, Yamazaki Z, Sakai T, Fujiwara K, Oda T, Sanjo K, Wada T, Abe T, Furuta

T, Inagaki K, Korninami N, Kataoka K, Fujisaki Y: Clinical application of a new

method for plasmapheresis using cellulose acetate hollow fiber as a plasma

separator. ~if Organs 7:1095, 1978

Klein g Holland FF, Eberle K, Marton FC, Cabasso I: Sorbent filled hollow fibers

for hemoperfusion. Trans Am Soc Artif Intern Organs 24:127-130, 1978

KuJpmann WR, Oelleric M, Blume V, Schmidt E, Barthels M: In vitro evaluation of

absorbents used in hemoperfusion. Klin Wochenschr 56:1 171-1178, 1978

bwyer C, Aitchison 3, Sutton 3, Beunett W: Treatment of theophylline neurotoxicity with resin hemoperfusion. Ann lntem Med 88:516-517, 1978

Losgen H, Brunner G, Holloway CJ, Buttelmann, B, Husmann S, Scharff P, Siehoff

A: Large agarose beads for extracorporeal detoxification systems. L Preparation

and some properties of the large beads in haemoperfusion. Biomater Med Devices

Artif Organs 6:151-173, 1978

Maini R: Plasmapheresis/dialysis through high porosity protein ~rmeable membrane with sorbent detoxification. Haemoperfusion, Dialysate, and Diafiltrate

Purification Symposium, Tutzing, Germany, 1978 (abstract)

ARC Blood Services

Bibliography Supplement 2

TPB XVI-8

Martin AM, Gilbbons JK, Oduro A, Herbert R: Clinical experience with cellulose

coated carbon haemoperfusion. In Chang TMS (cd): “Artificial Kidney, Artificial

Liver, and Artificial Cells.n New York: Plenum Ress, 1978, pp 143-151

Piatkiewicz W, Malchesky P$ Ouchi A, Asanuma Y, Nose Y: Mechanical aspects

of the plasma separation by microporom membrane filters. Proc Annu Conf Eng

Med Biol 23:300, 1978

Silk DBA, Williams R: Experiences in the treatment of fulminant hepatic failure

by conservative therapy, charcoal hemoperfusion, and polyacrylonitrile hemodialy -

SiS. Int J Artif Organs 1:29, 1978

Silk DBA, Williams R: Treatment of fulminant hepatic failure with charcoal

haemoperfusion and polyacrylonitrile haemodialysis. In Chang TMS (cd): “Artificial Kidney, Artificial Liver, and Artificial Cells.n New York: Plenum Ress, 1978,

pp 125-134

Suaudeau J, Kolobow T, Vaillancourl R, Carvalho A, Ito Y, &dmann Ad: The Ito

Wlow-throughn centrifuge: A new device for long-term (24 hours) plasmapheresis

without platelet deterioration. Transfusion 18:312-319, 1978

Trafford A, Ireland R, Evans R: The use of hemoperfusicm as an adjunct to

hemodiaiysis. Artif Organs 3:249-253, 1978

Winchester JF, Gelfand MC, Knepshield JH, Schreiner GE: Resent and future uses

of hemoperfusion with sorbents. Artif Organs 2:353-358, 1978

Winchester JF, Gelfand MC, Knepghield JH, Schreiner GE: Present and future

uses of sorbent hemoperfusion. Hemoperfusion, Dialysate md Diafiltrate Purification Symposium, TutZing, Germany, 1978

Winchester JF, Mackay JM, Forbes CD, Courtney JM, Gilchrist T, Rentice CRM:

Hemostatic changes induced in vitro by hemoperfusion over activated charcoal.

Artif Organs 2:293, 1978

Yamazaki ~ Fujimori Y, Sanjo K, Kojima Y, Sugiura M, Wada T, Inoue N, Sakai T,

Oda T, Kominami N, Fujisaki U, Kataoka K: New artificial liver support system

(plasma-perfusion detoxification) for hepatic coma. Arti.f Ggans 2 (suppl):273,

1978

Berk PD: A computer simulation study relating to the treatment of fulminant

hepatic failure by hemoperfusion. Roc Soc Exp Biol Med 155:535-539, 1977-z

Castro LA, Hampel G, Gebhardt R, Fateh A, Gurland HJ: Combinatica of

hemodialysis and hemoperfusion in a single hollow-fiber unit for treatment of

uremia In Chang TMS (cd): “Artificial Kidney, Artificial Liver and Artificial

Cells.” New York: Plenum Ress, 1977, pp 193-197

Chang TMS: Criteria, evaluation and perspectives of some charcoal hemoperfusion

systems. 3 Dial Transplant 5:50-54, 1977

Chang TMS: Criteria, evaluation, and prospective of various microencapsulated

charcoal hemoperfusion systems. 3 Dial Transplant 6:21, 1977

.
ARC Blood Services

Bibliography Supplement 2

TPB XVI-9

Chang TMS, Chirito E, Barre P, Cole C, Lister C, Resurrection E: Clinical

evaluation of the clearance profiles of a portable compact dialysate-free system

incorporating microencapsulated charcoal hemoperfusion for blood purification

with ultrafiltration for fluid removal. J Dial 1:239-259, 1977

Denti E, Walker 3M, Brancaccio D, Tessore V: Evaluation of novel sorbent systems

for joint hemodialysis and hemoperfusion. Med Instrum 11:212, 1977

Gilcher RO, Hashiba U: Automated plasmapheresis (coagulation studies). Haemonetics Advanced Component Seminar, Boston, MA, 1977

Holldd FF, Donnand A, Gidden HE, Klein E: Methods of measurement of mass

transfer rates and capacities of hemoperfusion cartridges. Trans Am Soc Artif

Intern Organs 23:573-581, 1977

Malchesky PS, Ouchi K, Piatkiewicz W, No=’ Y: Recent developments in the

design of an extracorporeal system for total hepatic assist. NIH Conference on

Fulminant Hepatic Failure, Bethesda, February 1977

Martin AM, Gibbons 3K, Honsson E, Trinder P: The clinical use of carbon

haemoperfusion column. In Kenedi RM, Coutiney 3M, Gaylor JDS, Gilchrist T

(eds): “Artificial Organs.” London: Macmillan Press, 1977, p 196

Ouchi K, Malchesky PS, Piatkiewicz W, Herrmann RE, N=’ Y: Improved

hemoperfusion sorbent and plasma filtration system for hepatic assist. Roc

ACEMB 19:439, 1977

Oules R, Asaba H, Neuhauser M, Yajiel V, Gurmarsson B, Bergstrom J, Furst P:

Removal of uremic small and middle molecules and free amino acids by carbon

hemoperfusion. Trans Am Soc Artif Intern Organs 23:583, 1977

Siernsen AW: Augmentation of hernodialysis by charcoal hemoperfusion. Kidney

Int 12:490, 1977

Chang TMS, Chirito E, Barre P, Resurrection E: The use of ACAC micro-

● ncapsulate charcoal hemoperfusion in series with Amicon ultrafiltration for

patients with chronic renal failure. Trans Am Soc Artif intern Organs 5:15, 1976

Malchesky PS, Vames WG, Nokoff R, No=” Y: The charcoal capillary hemoperfusion system. Roc Eur Dial Transplant Assoc 13:242, 1976

Odaka M, Tabata Y, Kobayashi H, Nomura Y, Soma H, Hirasawa H, Sata H,

Suenage E, Nageta K: Three-hour maintenance dialysis combining direct haemoperfusiion and haemodialysis. Proc Eur Dial Transplant Assoc 13:257, 1976

Temple AR, Walker 3, Done GA: A comparative evaluation of activated charcoal

hernoperfusion devices. Meeting of the AM Acad Clin Toxicol. The Am ASSOC

Poison Control Centers and the Can Acad Clin Toxicol, Seattle, WA, 1976

Walker 3M, Denti E, Wagenen RV, Andrade JD: Evaluation ancl =Jectlon of

activated carbon for hemoperfu$lon. Kidney Int 10: S320-327, 1976 #

Yamanki Z, Fujimoto Y, Sanjo K, Kojima Y, Sugiura M, Wada T, Inoue N, Oda T,

Kominami N, Fujsaki U, Kataoka K: New artificial liver support system (plasma

perfusion detoxification) for hepatic coma. Artif Organs 5:227, 1976 (In Japanese)

ARC Blood Services

Bibliography Supplement 2

TPB XVI-10

Chang TMS: Biocompatible microencapsulated (coated) charcoal for hemoperfusion

in patients. In Williams R (cd): “Artificial Support Systems for Acute Hepatic

Failure.” London: Whitefriars Press, 1975, pp 94-103

Chang TMS, Chirito E, Barre P, Cole C, Hewish M : Clinical performance

characteristics of a new combined system for simultaneous hemoperfusion-hemodialysis-ultrafiltration in series. Trans Am Soc Artif Intern Organs 21:502-508,

1975

Dunea G, Rizvi 2A, Anicama HG, Mamdani BH, Majurkar SD: Charcoal hemoperfusion: In-vivo and in-vitro studies. Am Soc Nephrol 8:28, 1975

Farrales FB, Summers T, Belcher C, Bayer WL: Plasma exchange with plasma

protein fraction and lactated Ringer’s solution using the continuous flow cell

separator. Infusionstherapie 2:273-277, 1975

Lsakov IUF, Lopukhin UM, Burkov IV, Mashkow OA, Lutsky I, Mosharov OP,

Kazyukow VD, Isotov BN, Macheret NA: First experience with the use of

extracorporeal hemoperfusion through activated charcoal in children. Eksp Khir

Anestexiol 4:52, 1975

Ito Y, Suaudeau 3, Bowman RL: New flow-through centrifuge without rotating

seals applied to plasmapheresis. Science 189:999-1000, 1975

Maini R: Hemoperfusion over ion-exchange resins and polymeric absorbents. Int 3

Artif Organs 1:196-201, 1975

Scharschmidt BF, Martin 3F, Shapiro L3, Plotz PH, Berk PD: Use of calcium

chelating agents and protaglandin El (PGE1) to eliminate platelet losses during

hemoperfusion through various absorbents. Gastroenterology 69:A64, 1975

Weston MJ, Mellon PJ, Langley PG, Hughes RD, Dunlop EH, Gazzard BG, Williams

R: Resin column perfusion with whole blood or plasma separated by the continuous

flow centrifuge. Clin Sci Molec Med 48:187-192, 1975

Winchester 3F, Apiliga MT, Mackay 3, Kennedy AC: Haemodialysis with charcoal

haemoperfusion. Roc Eur Dial Transplant Assoc 12:526-533, 1975

Davis TA, Cowsar DR, Harrison SD, Tanquari AC: Artificial carbon fibers for

hemoperfusion. Trans Am Soc Artif Intern Organs 20:356, 1974

Gilchrist T, Honsson E, Martin AM, Naucler L, Cameron A, Courtney 3M:

Development of the Strathclyde hemoperfusion system. In Williams R, MurrayLyons [M (eds): “Artificial Liver, Artificial Kidney, and Artificial Ceils.” London:

Pittman Medical, 1974, p 319

Hill JB, Palaia FL, Horres CR: The design of a charcoal haemoperfusion system.

In Kenedi RM, Courtney JM, Gaylor JDS, Gilchrist T (eds): “Artificial organs.”

London: Macmillan Press, 1974, p 123

Courtney JM, Gilchrist T, Walker JM, Edwards RO: A new coated adsorbent for

blood perfusion. Digest IOth Int Conf Med Biol Eng, Dresden, Germany, 1973
ARC Blood Services

Bibliography Supplement 2

TPB XVI-11

Holland FF, Donnaud A, Giddeon HE, Mein E: Methods of measurement of mass

transfer rates and capacities of hemoperfusion cartridges. Trans Am Soc Artif

Intern Organs 18:573-582, 1973

Andrade 3D, van Wagenen R, Chen C, Ghamavian M, Voider 3, Kirkham R, Koli

WR: Coated absorbents for dire blood perfusion. Trans Am Soc Artif Intern

Organs 18:473-483, 1972

Evenson MA, de Vos D: Direct contact (membraneless) haemoperfusion through

oils. Ciin Chem 18:554-562, 1972

Andrade 3D, Kunimoto K, van Wagene R, Kastigir B, Gough S, Kolff W3: Coated

adsoriknts for direct blood perfusion Herna/activated charcoal. Trans Am Soc

Artif Intern Organs 17:222-228, 1971

Chang TMS, Pent A, Johnson LJ, Malave N: Response to intermittent extracorporeal perfusion through shunts containing semipermeable microcapsules. Trans

Am Soc Artif Intern organs 15:163-168, 1%8

Pozniakow VA, ● t al: Method and technic of plasmapheresis by use of glass flasks.

Robl Gematol Pereliv Krovi 13:62-63, 1968 (In Russian)

Moore RJ, Lehman TH, Hodges CV: Treatment of acute hyperkalaernia utilizing

extracorporeal perfusion of blood through cation-exchange resin columns. Surg

Gynaecol Obstet 112:67-74, 1961

AMERICAN RED CROSS BLOOD SERVICES

Supplement 2

Therapeutic Pheresis Bibliography No. XVII: Texts, Symposia

Beyer 3-H, Borberg H, Fuchs Ch, Nagel GA (eds): “Plasmapheresis in Immunology

and Oncology.” Bad: S Karger, 1982

Bono~ini V, Chang TMS (eds): ‘Hemoperfusion.” Basel: S Karger, 1982 (Listed in

Bibliography as Contrib Nephrol, Vol. 29)

Horiuchi T, Kambic H, ?akatani S, Nose Y: Topics in plasmapheresis: A

bibliography of therapeutic applications and new techniques. Cleveland: Charles

E. Spahr Information Center of the International Center for Artificial Organs and

Transplantation, 1982

“International Symposium on Plasmapheresis: Therapeutic Applications and New

Techniques.” Cleveland: Int Soc Artif Organs, 1982 (collection of abstracts)

Gurland 3G, Heinze V, Lee HA (eds): therapeutic Plasma Exchange.n New York:

Springer-Verlag, 1981

Ota T (ad): therapeutic Plasmapheresis.N Stuttgart: F. K. Schattauer Verlag,

1981

Serrou B, Rosenfield C (ads): ‘Immune Complexes and Plasma Exchanges in

Patients with Cancer.n New York: Elsevier/North Holland Biomedical Ress, 1981

Sideman S, Chang TMS (eds): ‘Hemoperfusion. Kidney and Liver Support and

Detoxification,” Part L Washington: Hemisphere Publishing Corporation, 1980
References
References

1.

2.

3.

4.

5.

6.

7.

8.

9.

10.

11.

12.

Abel, J., Rowntree, L. G., and Turner, B. B.,

“Plasma Removal With Return of Corpuscles, ”

J. Pharmacol. L&p. Ther. 5:625-641, 1914 .

Altman, L. K., “Bloodletting Is Revived for a

Wide Variety of Modern Ills, ” New York Times,

sec. C., p. 1, Apr. 27, 1982.

Altman, S. H., and Blendon, R. (eds.), Medical

Technology: The Culprit Behind Health Care

Costs, proceedings of the 1977 Sun Valley Forum

on National Health, DHEW publication No.

(PHS) 79-3216 (Washington, D. C.: Government

Printing Office, August 1977).

American College of Physicians, Clinical Efficacy

Assessment Project, “Apheresis for the Treatment

of Goodpasture’s Syndrome, Systemic Lupus

Erythematosus, Membranous and Proliferative

Glomuleronephritides, Multiple Sclerosis, Potentially Life-Threatening Complications of Rheumatic Diseases, and Thrombotic Thrombocytopenic Purpura, ” unpublished draft statement,

Philadelphia, Pa., July 20, 1982.

American Medical Association, Council on Scientific and Medical Affairs, Apheresis Panel, “Minutes of the Apheresis Panel, ” Chicago, Ill., June

19, 1982.

American Society of Hematology, “On the Use

of Apheresis for Treatment of Hematologic Disorders, ” prepared for the National Center for

Health Care Technology, Office of the Assistant

Secretary for Health, Department of Health and

Human Services, Rockville, Md., September

1981.

American Society of Hematology, “Statement by

the American Society of Hematology on the Use

of Aphemsis for Treatment of Hematologic Disorders, ” unpublished, Thorofare, N. J., 1981.

Anthony, J., Baxter Travenol Laboratories, Inc.,

Deerfield, Ill., personal communication, December 1982.

Arthritis Foundation, “Recommendations of the

Arthritis Foundation and the American Rheumatism Association on Plasrnapheresis in Rheumatic

Diseases, ” unpublished, Atlanta, Ga., February

1981.

Asbury, A., Fisher, R., McKhann, G. M., et al.,

“Guillain-BarrE Syndrome: Is There a Role for

Plasmapheresis?” IVeuroZogy 30:1112, 1980.

Beattie, T. J., Murphy, A. V., Willoughby, M.

L. N., et al., “Plasmapheresis in the HemolyticUraemic Syndrome in Children,” Br. Med. J

282:1667-1668, 1981.

Berkman, E., “Issues in Therapeutic Apheresis, ”

editorial, IV. Engl. J. Med. 306(23):1418-1420,

1982.

13.

14.

15.

16.

17.

18.

19.

20.

21.

22.

23.

24.

25.

26.

27.

Borberg, H., “Problems of Plasma Exchange

Therapy,” in Therapeutic PZasma &change, H.

J. Gurland, V. Heinze, and H. A. Lee (eds. ) (Berlin: Springer-Verlag, 1981).

Bowman, J. M., Peddle, L. J., and Anderson, C.,

“Plasmapheresis in Severe Rh-iso-immunization,”

VOX Sang. 15:272, 1968.

Brettle, R. P., Gross, M., Legg, N. J., et al.,

“Treatment of Acute Polyneuropathy by Plasma

Exchange, ” letter, Lmcet 2:1100, 1971.

Buco, M., Blue Cross-Blue Shield Association,

Chicago, Ill., letter to Travenol Laboratories,

Inc., Deerfield, 111., Oct. 27, 1982.

Bunker, J. P., Hinkle, D., and McDermott, W.

v., “Surgical Innovation and Its Evaluation, ”

science 200:937-941, 1978.

Burton, R., Anatomy of Melancholy (New York:

Vintage Books, Random House, 1977).

Center for the Analysis of Health Practices, Harvard School of Public Health, “Impact on Health

Costs of NCHCT Recommendations for Nonreimbursement for Medical Procedures, ” prepared

for the National Center for Health Care Technology, Department of Health and Human Services, Rockville, Md., Apr. 15, 1981.

Ciarkowski, A. A., Food and Drug Administration, Department of Health and Human Services,

Silver Spring, Md., personal communication,

August 1982.

Ciarkowski, A. A., Food and Drug Administration, Department of Health and Human Services,

Silver Spring, Md., personal communication, December 1982.

Ciuryla, V. T., E. I. du Pent de Nemours & Co.,

Inc., Wilmington, Del., personal communication,

December 1982.

Cobcroft, R., Tamagnini, G., and Dorrnandy, K.

M., “Serial Plasmapheresis in a Hemophiliac

With Antibodies to Factor VIII,” J. CZin. Pathol.

30:763-765, 1977.

Collins, R. M., Cobe Laboratories, Inc., Lakewood, Colo., personal communication, December 1982.

Cook, T. D., and Campbell, D. T., Quasi-&perimentation: lkign and Analysis of Research in

Field Settings (Chicago: Rand McNally, 1979).

Cook, T. D,, Tindall R. A. S., Walker, J., et al.,

“Plasma Exchange as a Treatment of Acute and

Chronic Idiopathic Autoimmune Polyneuropathy: Limited Success,” Neurology 30:361, 1980.

Corachan, M., Talonu, T., Oldfield, E., et al.,

“Treatment of Acute Severe Guillain-BarrE Syndrome by Plasmapheresis, Papua New Guinea

Med. J. 23:146-147, 1980.

159
IW . Hea/th Technology -se Study 23: The Safety, Efficacy, and Cost Effectiveness of Therapeutic Apheresis

28,

29,

30.

31,

32.

33.

34.

35.

36.

37.

38.

39.

40.

41.

42.

Cotter, D., Office of Health Technology Assessment, Department of Health and Human Services, Rockville, Md., personal communication,

March 1983.

Cotter, D., Office of the Assistant Secretary for

Health, Department of Health and Human Services, Rockville, Md., pemonal communication,

July 1982.

Dau, P. C., Children’s Hospital, San Francisco,

Calif., 1981, as reported by Travenol Laboratories, Inc., Deerfield, Ill., personal communication, December 1982.

Dau, P. C., Miller, R. G., and Denys, E. H., “Experience With Plasmapheresis in 153 Necrologic

Patients,” lht. J Artif. Org. 5(1):37-46, 1982.

Douma, A. J., American Medical Association,

Chicago, Ill., personal communication, August

1982.

Durward, W. F., Burnett, A. K., Watkins, R.,

et al., “Plasma Exchange in Guillain-Barr6 Syndrome,” Br. Med. J. 283:794, 1981.

Edelson, E., “Cleansing the Blood,” Science 82

(American Association for the Advancement of

Science, Washington, D.C.), 3(8):72-77, October

1982.

Edmondson, F. W., Travenol Laboratories, Inc.,

Dmrfield, Ill., personal communication, July

1982.

Edson, J. R., McArthur, J. R., Branda, R. F., et

al., “Successful Management of a Subdural

Hematoma in a Hemophiliac With an Anti-Factor

VIII Antibody,” Blood 41:113122, 1973.

Erskine, J. G., Burnett, A. K., Walker, I. D., et

al., “Plasma Exchange in Non-Haemophiliac Patients With Inhibitors to Factor VIII, ” Br. Med.

J. 283:760, 1981.

F&deral Register, 46(116):31770, June 17, 1981.

Food and Drug Administration, Department of

Health and Human Services, “Apheresis: Medical

Therapy for the 80s,” unpublished internal document (no date, Rockville, Md. ) sent to the National Center for Health Care Technology, Department of Health and Human Services, Rockville, Md., May 26, 1982.

Foreman, R. M., National Kidney Foundation,

Inc., New York, letter to the National Center for

Health Care Technology, Department of Health

and Human Services, Rockville, Md., no date.

Friedman, L., American Red Cross, Bethesda,

Md., personal communication, December 1982.

Frost & Sullivan, Inc., “In-Vivo Hemodetoxification and Hemoprocessing Markets in the U.S., ”

unpublished, New York, June 1981.

43.

44.

45.

46.

47.

48.

49.

50.

51.

52.

53.

54.

55.

Goldstein, M., National Institute of Neurological

and Communication Disorders and Stroke, National Institutes of Health, Department of Health

and Human Services, Bethesda, Md., personal

communication, December 1982.

Grady, D., “Pumping Plasma,” Discover, pp.

70-72, November 1980.

Gross, M. L. P., Sweny, P., and Legg, N. J.,

“Successful Plasmapheresis in the Miller-Fisher

Syndrome,” Br. Med. J. 282:1159, 1981.

Haemonetics Research Institute, “Guidelines for

Therapeutic Apheresis,” unpublished, Braintree,

Mass., 1980.

Hamburger, M. I., Washington, D. C., personal

communication, November 1982.

Hamburger, M. I., letter to Stephen HeySe, National Center for Health Care Technology, Department of Health and Human Services, Rockville, Md., no date.

Hambu~er, M. I., State University of New York,

Stony Brook, N. Y., personal communication,

January 1983.

Harden, L. B., Bluck R. S., and Salcedo, J. R.,

“Simultaneous Hemodialysis and Exchange

Transfusion in Hemolytic Uremic Syndrome, ”

Clin. Pediatr. 19:640-642, 1980.

Health Care Financing Administration, Department of Health and Human Services, Meai”care

Hospital ManuaZ, Coverage Issues Appendix,

Sec. 35-50: Pheresis, Baltimore, Md., revision of

Dec. 9, 1980.

Health Care Finanang Administration, Department of Health and Human Services, Medicare

~ospital Manual, Coverage Issues Appendix:

Sec. 35-5o: Pheresis, Baltimore, Md., Sept. 15,

1981.

Health Policy Alternatives, Inc., “Public and Private Payer Views on Reimbursement for Therapeutic Apheresis,” unpublished, Washington,

D. C., Jan. 20, 1982.

Heyse, S. P., National Center for Health Care

Technology, Department of Health and Human

Services, Rockville, Md., memorandum on “Coverage of Plasmapheresis, ” to Deputy Director,

Office of Coverage Policy, Bureau of Program

Policy, Health Care Financing Administration,

Department of Health and Human Services, Baltimore, Md., Feb. 11, 1981.

HeySe, S. P., National Center for Health Care

Technology, Department of Health and Human

Services, Rockville, Md., memorandum on

“Medicare Coverage Instruction on Pheresis,” to

Deputy Director, Office of Coverage Policy, Bu-
References ● 161

56.

57.

58.

59,

60,

61

62.

63.

64.

65.

66,

67.

68,

69,

reau of Program Policy, Health Care Financing

Administration, Department of Health and Human Services, Baltimore, Md., Apr, 2, 1981.

Heyse, S. P., National Center for Health Care

Technology, Department of Health and Human

Services, Rockville, Md., memorandum on “Plasmapheresis—Your Memorandum of October 24,

1980,” to Deputy Director, Office of Coverage

Policy, Bureau of Program Policy, Health Care

Financing Administration, Department of Health

and Human Services, Baltimore, Md., Nov. 6,

1980.

Heyse, S. P., National Institutes for Arthritis,

Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Department of Health

and Human Services, Bethesda, Md., personal

communication, December 1982.

Heyse, S. P., National Institutes for Arthritis,

Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Department of Health

and Human Services, Bethesda, Md., personal

communication, July 1982.

Heyse, S. P., Renault, P. R., and Perry, S., “National Center for Health Care Technology Assessment of Therapeutic Apheresis for Rheumatoid

Arthritis, 1981,” J. Clin. Aphemsis 1:50-54, 1982.

Hiatt, B., “Mutation Studies Go High-Tech., ”

Research News (University of Michigan), 33(6/7),

June/July 1982.

Hollis, T., Blue Cross-Blue Shield of Massachusetts, Boston, Mass., personal communication, February 1983.

Hughes, R. A. C., Newsom-Davis, J., Armitage,

P., et al., letter, Br. Med. J. 282:2056, 1981.

Hughes, R. A. C., Newsom-Davis, J. M., Perkin,

G. D., et al., “Controlled Trial of Prenisolone in

Acute Polyneuropathy,” Lmcet 2:750-753, 1978.

Irvine, A. T., and Tibbles, J., “Treatment of

Fisher’s Variant of Guillain- Barr6 Syndrome by

Exchange Transfusion, ” J. Can. Ski. IVeurol

8:49-50, 1981.

Isselbacher, K. J., Harrison’s Principles of Internal A4edicine, 9th ed. (New York: McGraw-Hill,

1980),

Jones, J. V., Claugh, J. D., Klinenberg, J. R., et

al., “The Role of Therapeutic Plasmapheresis in

the Rheumatic Diseases, ” J. Lab. Med. 97:589-

598, 1981.

Jones, J. V,, “Plasmapheresis in SLE,” Clinics in

Z?heum. Dis. 8(1):243-260, 1982,

Jones, J. V., et al., “Rape and Heresy,” Plasma

Therapy (Laux Co., Inc., Harvard, Mass.)

1(4):3-4, 1980.

Jones, R. J., American Medical Association, Chicago, 111., letter to the National Center for Health

70.

71.

72.

73.

74,

75.

76.

77.

78.

79.

80.

81.

82.

Care Technology, Department of Health and Human Services, Rockville, Md., June 1, 1981.

Kambic, H., and NosE, Y., Plasmapheresis: Historical Perspective, Therapeutic Applications,

and N&v Frontiers (Cleveland, Ohio: International Center for Artificial Organs and Transplantation, 1982).

Kaplan, B. S., and Drummond, K. N., “The

Hemolytic-Ummic Syndrome is a Syndrome,” N.

Engl. J. Med. 298:964-966, 1978.

Kingsley, G. F., Haemonetics Corp., Braintree,

Mass., letter to the National Center for Health

Care Technology, Office of the Assistant Secretary for Health, Department of Health and

Human Services, Rockville, Md., Sept. 14,1981.

LeCocq, J., “Therapeutic Apheresis Update:

Report on the International Symposium on Plasmapheresis, ” unpublished, Montgomery Securities, San Francisco, June 15, 1982.

Levy, J., Immunogenetics, Sherman Oaks, Calif.,

personal communication, January 1983.

Levy, J., Immunogenetics, Sherman Oaks, Calif.,

letter to P. Renault, National Center for Health

Care Technology, Office of the Assistant Secretary for Health, Department of Health and Human Services, Rockville, Md., July 14, 1980.

Levy, R. L., Newkirk, R., and Ochoa, J.,

“Treating Chronic Relapsing Guillain-Barr6 Syndrome by Plasma Exchange, ” Lancet 2:259-

260, 1979.

Littlewood, R., and Bajada, S., “Successful Plasmapheresis in the Miller-Fisher Syndrome, ” Br.

Med. J. 282:778, 1981.

Maisey, D. N., and Olczak, S. A., “Successful

Plasmapheresis in the Miller-Fisher Syndrome,”

Br. Med. J. 282:2055, 1981.

Martini, J. A., Blue Cross/Blue Shield of

Massachusetts, Boston, Mass., letter to S. P.

HeySe, National Center for Health Care Technology, Department of Health and Human Services, Rockville, Md., Aug. 3, 1981.

Marwick, C., “New Blood Washing Therapy:

Catching on Big Despite Lack of Controlled Studies,” Med. World N. 22:47-59, June 8, 1981.

Mayr, U., Rumpl, E., Hackl, J. M., et al., “Treatment of Guillain-BarrF Syndrome by Plasma Exchange, in Plasma Ekchange Therapy, H. Borberg

and P. Reuther (eds. ) (Stuttgart: Georg Thieme

Verlag, 1981).

Mishler, J. M., Blood Resources Branch, Division

of Blood Diseases and Resources, memorandum

on “Apheresis” to Director, National Heart,

Lung, and Blood Institute, National Institutes of

Health, Department of Health and Human Services, Bethesda, Md., Feb. 13, 1981.
162 ● Hea/th Technology Case Study 23: The Safety, Efficacy, and Cost Effectiveness of Therapeutic Apheresis

83.

84.

85.

86.

87.

88.

89.

90.

91.

92.

93,

Mishler, J. M., Blood Resources Branch, Division

of Blood Diseases and Resources, memorandum

on “Therapeutic Apheresis, ” to Director, National Heart, Lung, and Blood Institute, National

Institutes of Health, Department of Health and

Human Services, Bethesda, Md., Mar. 2, 1981.

Misiani, R., Trevisan, F., Marchesi, D., et. al.,

“Plasmapheresis and Plasma Infusion in the

Treatment of Hemolytic-Uremic Syndrome, ”

I-Iemostasis, ProstogZandins and Renal D“sease

(New York: Raven Press, 1980).

Murt, H., “Therapeutic Plasmapheresis: A Medical Innovation in Search of Applications, ” unpublished, School of Public Health, University

of Michigan, Ann Arbor, Mich., 1982.

National Center for Health Care Technology,

“Apheresis in the Treatment of Rheumatoid Arthritis,” Assessment Report %ries, vol. 1, No. 6,

Department of Health and Human Services, 1981.

National Institutes of Health—Progress Report,

“Plasmapheresis Treatment of Acute GuillainBarrE,” grant No. IRO1-NS 17053-01, 1981.

Nightingale, S. L., Acting Associate Commissioner for Health Affairs, Food and Drug Administration, memorandum on “Apheresis in the

Treatment of Disease, ” to the National Center for

Health Care Technology, Department of Health

and Human Services, Rockville, Md., July 29,

1981,

Norris, F. H., Denys, E. H., and Mielke, C. H.,

“Plasmapheresis in Amyotrophic Lateral Sclerosis, ” in Plasmapheresis and tkImmunobiology

of Myasthenia Gravis, P. Dau (cd. ) (Boston:

Houghton Mifflin Professional Publishers, 1979).

Nos6, Y., and Malchesky, P. S., “Therapeutic

Application of Plasrnapheresis,” Plasma Q 1(4),

1979.

Office of Health Research, Statistics, and Technology, “Apheresis for Multiple Sclerosis, ” Assessment Report Series, vol. 2, No. 11, Department of Health and Human Services, Rockville,

Md., 1982.

Office of Health Research, Statistics, and Technology, “Plasmapheresis and Plasma Exchange

for Treatment of Thrombotic Thrombocytopenic

Purpura,” Assessment Report Series, vol. 2, No.

13, Department of Health and Human Services,

Rockville, Md., 1982.

Office of Health Research, Statistics, and Technology, “Rheumatoid Vasculitis Therapeutic

Apheresis,” Assessment Report Series, vol. 2, No.

8, Department of Health and Human Services,

Rockville, Md., 1982.

94.

95.

96.

97.

98,

99.

100.

101.

102.

103.

104.

Office of Health Technology Assessment,

“Apheresis for the Treatment of Goodpasture’s

Syndrome and Membranous Proliferative Glomerulonephritides,” Assessment Report Series,

vol. 3, Nos. 2 and 3, Department of Health and

Human Services, Rockville, Md., 1983.

Office of Technology Assessment, U.S. Congress,

Assessing the Efficacy and Safety of Medical

Technologies, Washington, D. C., OTA-H-7S,

September 1978.

Office of Technology Assessment, U.S. Congress,

lkelopment of Medical Technology: @portunities for Assessment, OTA-H-34, Washington,

D. C., August 1976.

Office of Technology Assessment, U.S. Congress,

“The Impacts of Randomized Clinical Trials on

Health Policy and Medical Practice,” preliminary

draft, Washington, D. C., March 1983.

Office of Technology Assessment, U.S. Congress,

The Implications of Cost-Effectiveness Analysis

of Medical Techno~ogy, OTA-H-126, Washington, D. C., August 1980.

Office of Technology Assessment, U.S. Congress,

The Implications of Cost-Effectiveness Analysis

of Medical Technology/Background Paper #l:

Methodological Issues and Literature Review,

OTA-BP-H-5, Washington, D. C., September

1980.

Office of Technology Assessment, U.S. Congress,

The Implications of Cost-Effectiveness Analysis

of Medical Technology/Background Paper #2:

Case Studies of Medical Technologies, 17 individually published case studies, Washington,

D. C., 1980-1982.

Office of Technology Assessment, U.S. Congress,

The Implications of Cost-Effectiveness Analysis

of Medical Technology/Background Paper #3:

The Efficacy and Cost Effectiveness of Psychotherapy, OTA-BP-H-6, Washington, D. C., October 1980.

Office of Technology Assessment, U.S. Congress,

Medical Technology and the Costs of the Medicare Program/Health Technology Case Study

#22: The Effectiveness and Costs of Alcoholism

Treatment, OTA-HCS-22, Washington, D. C.,

March 1983.

Office of Technology Assessment, U.S. Congress,

“The National Center for Health Care Technology and Medical Technology Assessment Policy,”

unpublished staff paper, Washington, D. C.,

March 17, 1981.

Office of Technology Assessment, U.S. Congress,

Strategies for Medical Technology Assessment,
References ● 163

105,

106<

107,

108,

109(

110.

111.

112.

113.

114.

115.

116.

OTA-H-181, Washington, D. C., September

1982.

Oldham, Robert K., National Cancer Institute,

National Institutes of Health, Bethesda, Md., personal communication, December 1982.

Parries, B., Duke, V. E., Simon, N. M., et al.,

“Adult Hemolytic-Uremic Syndrome Successfully

Treated With Plasma Exchange,” Plasma Tlzerapy 3:57-61, 1981.

Pease, E. A., “Report From NCHCT: Evaluation

of Therapeutic Apheresis for Rheumatoid Arthritis,” J. A.M.A. 246(10):1053, 1981.

Phillips L, Scoville Associates, Therapeutic

PZasmapheresis: Review and Market Forecast,

Greenville, S. C., February 1981.

Piller, G., Hocker, P., Ludwig, E., et al., “Plasmapheresis: Its Role in the Management of Inhibitor Patients, “ in Workshop on Inhibitors of

Factors VIII and IX, January 26th and27th, 1976

(Vienna: Facultas-Verlas, 1977).

Pineda, A. A., Brzica, S. M., and Taswell, H.

F “Continuous-, and Semicontinuous-Flow

B~ood Centrifuge Systems: Therapeutic Applications With Plasma-, Platelet-, Lympha-, and

Eosinpheresis, ” Transfusion 17:407-416, 1977.

Pintado, T., Taswell, H. F., and Bowie, E. J.,

“Treatment of Life-Threatening Hemorrhage Due

to Acquired Factor VIII Inhibitor, ” Blood

46:535-541, 1975.

Powell, L. C., “Intense Plasmapheresis in the

Pregnant Rh-Sensitized Woman,” Am. J. Obstet.

GynecoZ. 101:153, 1968.

Rettig, R. A., “End-Stage Renal Disease and the

‘Cost’ of Medical Technology,” in Medical Technology: The Culprit Behind Health Care Costs,

proceedings of the 1977 Sun Valley Forum on National Health, S. H. Altman and R. Blendon

(eds.), DHEW publication No. (PHS) 79-3216

(Washington, D. C.: U.S. Government Printing

Office, August 1977).

Ri%6sz, T., M5tyus, J., Goldschmidt, B., et al.,

“Control of Life-Threatening Bleeding by Combined Plasmapheresis and Immunosuppressive

Treatment in a Hemophiliac With Inhibitors, ”

Arch. Dis. Child. 55:641-643, 1980.

Riegelman, R. K., “Plasmapheresis in GuillainBarr6 Syndrome, ” prepared for the Office of

Technology Assessment, U.S. Congress, September 1982.

Robbins, F., “Assessing the Consequences of Biomedical Research, ” in Medical Technology: The

Culprit Behind Health Care Costs, proceedings

of the 1977 Sun Valley Forum on National

Health, S. H. Altman and R. Blendon (eds. ),

117.

118.

119.

120.

121.

122.

123.

124.

125.

126.

127.

128.

129.

130.

DHEW publication No. (PHS) 79-3216 (Washington, D. C.: U.S. Government Printing Office,

August 1977).

L. F. Rothschild, Unterberg, Towbin, “Therapeutic Apheresis, ” unpublished, New York,

Sept. 11, 1981.

Rothwell, R. S., Davis, P., Gordon, P. A., et al.,

“A Controlled Study of Plasma Exchange in the

Treatment of Severe Rheumatoid Arthritis, ”

Arth. & Rheumat. 23:785-790, 1980.

Rumpl, E., et al., “Treatment of Guillain-Barr<

Syndrome by Plasma Exchange,” J. IVeuroZ. 225:

207-217, 1981.

Samtleben, W., Blumenstein, M., Liebl, L., et al.,

“Membrane Plasma Separates for Treatment of

Immunologically Medicated Disease, ” Trans.

Am. Soc, of Artif Int. Org. 26:12-16, 1980.

Sandier, G. S., American Red Cross, Washington, D. C., personal communication, December 1982.

Saxe, L., and Fine, M., SociaZE@eriments: Methods for &s&n and Evaluation (Beverly Hills,

Calif.: Sage Publications, Inc., 1981).

Schooneman, F., Janet, C., Streiff, F., et al.,

“Plasma Exchange in Guillain-Barr~ Syndrome:

Ten Cases,” Plasma Ther. 2:117-121, 1981.

Schweitzer, S., and Foxman, B. H., UCLA School

of Public Health, “The Effect of Third Party Reimbursement on Expenditures for Medical Care, ”

prepared at the request of the National Center for

Health Care Technology, Department of Health

and Human Services, Rockville, Md,, Sept. 1s,

1981.

Scoville, P., Greenville, S. C., personal communication, December 1982.

Seger, R., Joller, P., and Baerlocher, K. ,

“Hemolytic-Uremic Syndrome Associated With

Neuraminidase-Producing Micro-Organisms:

Treatment by Plasma Exchange, ” HeIv. Paediatr.

Act. 35:359-367, 1980.

Simon, T., “Overview of the Efficacy of Therapeutic Apheresis, ” presented at Plasma Forum

V, Washington, D. C., June 1982.

Simon, T., United Blood Services, Albuquerque,

N. M., letter to S. P. Heyse, National Center for

Health Care Technology, Department of Health

and Human Services, Rockville, Md., Sept. 11,

1981.

Slocombe, G. W., Newland, A. C., and Colvin,

M. P., “The Role of Intensive Plasma Exchange

in the Prevention and Management of Hemorrhage in Patients With Inhibitors to Factor VIII, ”

Br. J. Haematol. 47:577-585, 1981.

Sutton, D. M. C., Cardella, C. J., Udall, P. R,,
I&# ● Hea/th Technology Case Study 23: The Safety, Efficacy, and Cost Effectiveness of Therapeutic Apheresis

131.

132.

133.

134,

135.

136.

137.

138.

139.

140.

141.

142.

143.

144,

145

et al., “Complications of Intensive Plasma Exchange, “ Plasma Ther. 2:19-23, 1981.

Sweny, P., Winning, A., Gross, M., et al.,

“Plasmapheresis in the Haemolytic-Uraemic Syndrome in Children,” Br. Med. J. 282:2137, 1981.

Taft, E. G., and Baldwin, S. T., “Plasma Exchange Transfusion, ” Skmin. Tkomb. Hemostas.

7:15-21, 1981.

Thomas, L., Lives of a Cell (New York: Viking

Press, 1974).

Valbonesi, M., Mosconi, L., Garelli, S., et al.,

“Successful Treatment by Plasma Exchange in

Guillain-BarrE Syndrome With Immune Complexes,” Vox Sang. 38:181-184, 1980.

Viatel, P., Chenais, F., Dechelette, D., et al.,

“Adult Hemolytic Uremic Syndrome Successfully Treated With Plasma Exchange,” Kidney ht.

15:453, 1979.

Vibert, G. J., Parker-Hannifin Corp., Irvine,

Calif., personal communication, August 1982.

Waldenstrom, J. G., “Plasmapheresis-Bloodletting Revived and Refined,” Acta Med. Scand.,

208:1-4, 1980.

Wallace, D. J., Goldfinger, D., and Gatti, R.,

“Plasmapheresis and Lymphoplasmapheresis in

the Management of Rheumatoid Arthritis,” Arth.

& Rheumat. 22:703-710, 1979.

Wallace, D. J., Goldfinger, D., Lowe, C., et al.,

“A Double-Blind, Controlled Study of Lymphoplasmapheresis Versus Sham Apheresis in Rheumatoid Arthritis, ” N. Engl. J. Med.

306(23):1406-1410, 1982.

Wallace, D. J., Goldfinger, D., ThompsonBreton, R., et al., “Advances in the Use of Therapeutic Pheresis for the Management of Rheumatic Diseases, ” Sem. Arth. & Rheumat.

10:81-91, 1980.

Warner, K. E., “A ‘Desperation-Reaction’ Model

of Medical Diffusion,” 14eakh Serv. Res. 10:369-

383, 1975.

Warner, W. L, (cd.), Plasma Forum IV.. l+bruary

21-13, 1981, American Blood Resources Association, no city, no date.

Wensley, R. T., Stevens, R. F., Burn, A. M., et

al., “Plasma Exchange and Human Factor VIII

Concentrate in Managing Hemophilia A With

Factor VIII Inhibitors,” Br. Med. J. 281:1388-

1389, 1980.

Wenz, B., and Barland, P., “Therapeutic Intensive Plasmapheresis, ” %m. HematoZ. 18(2):147-

162, 1981.

Wohlreich, J. J., Travenol Laboratories, Inc., letter to the National Center for Health Care Tech146.

147.

148,

149,

150.

151.

152.

153.

nology, Department of Health and Human Services, Rockville, Md., Sept. 14, 1981.

Wortmart, P. M., and Murt, H. (in collaboration

with Bruce Friedman), “Plasmapheresis for

Hemolytic-Uremic Syndrome and Factor VIII Inhibitor,” prepared for the Office of Technology

Assessment, U.S. Congress, October 1982.

Wortman, P. M., and Saxe, L., ‘The Assessment

of Medical Technology: Methodological Considerations, ” prepared for the Office of Technology

Assessment, U.S. Congress, Appendix C in Strategies for Medical Twhnology Assessment, OTAH-181, Washington, D. C., September 1981.

Wyngaarden, J. B., and Smith, L. H. (eds.), CeciZ

Textbook of Medicine, 16th ed. (Philadelphia,

Pa.: W. B. Saunders Co., 1982).

Young, D. A., Deputy Director, Office of Coverage Policy, Bureau of Program Policy, Health

Care Financing Administration, Department of

Health and Human Services, Baltimore, Md.,

memorandum on “Coverage of Apheresis” to

Associate Director for Medical and Scientific

Evaluation, National Center for Health Care

Technology, Department of Health and Human

Services, Rockville, Md., May 11, 1981.

Young, D. A., Deputy Director, Office of Coverage Policy, Bureau of Program Policy, Health

Care Financing Administration, Department of

Health and Human Services, Baltimore, Md.,

memorandum on “Coverage of Plasmapheresis, ”

to Director, National Center for Health Care

Technology, Department of Health and Human

Services, Rockville, Md., Jan. 13, 1981.

Young, D. A., Deputy Director, Office of Coverage Policy, Bureau of Program Policy, Health

Care Financing Administration, Baltimore, Md.,

memorandum on “Medicare Coverage Instructions on Pheresis, ” to Director, National Center

for Health Care Technology, Department of

Health and Human Services, Rockville, Md.,

Dec. 12, 1980.

Young, D. A., Deputy Director, Office of Coverage Policy, Bureau of Program Policy, Health

Care Financing Administration, Department of

Health and Human Services, Baltimore, Md.,

memorandum on ‘WCHCT Regarding Plasmapheresis in the Treatment of Rheumatoid Arthritis, ” to Associate Director for Medical and

Scientific Evaluation, National Center for Health

Care Technology, Department of Health and

Human Services, Rockville, Md., June 1s, 1981.

Young, D. A., Deputy Director, Office of Coverage Policy, Bureau of Program Policy, Health
preferences ● 765

154.

Care Financing Administration, Department of

Health and Human Services, Baltimore, Md.,

memorandum on “Medicare Coverage Instructions on Pheresis, ” to Director, National Center

for Health Care Technology, Department of

Health and Human Services, Rockville, Md.,

Mar. 11, 1981.

Young, D. A., Office of Coverage Policy, Bureau

of Program Policy, Health Care Financing Administration, Department of Health and Human

Services, Baltimore, Md., memorandum on

“Plasmapheresis- Memorandum of August 25,

1980” to Associate Director for Medical and

Scientific Evaluation, National Center for Health

Care Technology, Department of Health and

Human Services, Rockville, Md., Oct. 24, 1980.

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