bluuebunny/crossref_metadata_2025 huggingface dataset:
Acute transverse myelopathy successfully treated with plasmapheresis and prednisone in a patient with primary sjöugren's syndrome
Authors: Konttinen Yrjöu T. , Kinnunen Esko , Bonsdorff Martin Von , Lillqvist Petra , Immonen Ilkka , Bergroth Ville , Segerberg‐Konttinen Margaretha , Friman Claes
Published: February 2007

We report a case of acute transverse myelopathy in a patient with primary Sjögren's syndrome of 3 years duration. Our patient's acute transverse myelopathy developed within 1 week and resulted in complete paraparesis below the mamillary level. Extensive laboratory investigation ruled out viral, bacterial, and fungal etiology, Guillain‐Barré syndrome, poliomyelitis, and multiple sclerosis. At diagnosis, treatment was initiated immediately with prednisone (80 mg/day) and plasmapheresis, which was performed as a first‐aid measure. Improvement was noted as early as 10 days after the start of therapy. Within 5½ months of the first symptoms of paralysis, the patient walked without difficulty and returned to her normal activities. A causal relationship between plasmapheresis/prednisone therapy and recovery has not been proven but merits further consideration.
The extracellular control of intracellular aspirin hydrolysis
Authors: Costello Patrick B. , Green Floyd A.
Published: February 2007

We have previously presented evidence that an intra‐erythrocyte arylesterase is primarily responsible for the deacetylation of aspirin to salicylate. We now report studies on extracellular control factors. The fractional acetylsaticylic acid (ASA) hydrolysis at the completion of 20‐minute incubations in suspensions of washed red blood cells (RBC) with human serum albumin (HSA) decreased sharply, from 0.6 at 0 gm/dl HSA to 0.2 at 5.0 gm/dl HSA. In RBC suspensions with oleic, linoleic, and lauric acid, ASA hydrolysis increased as fatty acid:HSA ratios increased. The addition of salicylate (SA) also resulted in an increase in the fraction hydrolyzed. In a separate, more direct, ultracentrifugation assay, unbound ASA levels were similarly affected by HSA and the other ligands. When SA and oleic acid were incubated with ASA in RBC, additive competition for binding sites was apparent at relatively low levels of the fatty acid. In the presence of increasing concentrations of sodium SA, 5‐amino SA, and 4‐amino SA, ASA hydrolysis in RBC suspensions was increased by an average of 137%, 75%, and 54%, respectively. The most reasonable explanation for these findings is that the intact ASA molecule binds to albumin and that the binding of competing ligands can modulate the levels of free ASA in the circulation. This, in turn, affects the amount of drug available as substrate for penetration into the RBC and reaction with the intracellular hydrolase which catalyzes ASA deacetylation. Such factors controlling drug availability, if validated in vivo, could be important with regard to the antiinflammatory and anti‐platelet properties of aspirin.
Infective complications of plasma exchange: a prospective study
Authors: Singer Donald R. J. , Roberts Benita , Cohen Jonathan
Published: February 2007

We examined the incidence and types of infective complications which occurred in 41 patients whose medical management included plasma exchange (PX) by intermittent cannulation; femoral, subclavian, or internal jugular catheter; or arteriovenous shunt. A high incidence of positive cultures from vascular access catheters was demonstrated. Of 23 patients for whom data were available, 13 had positive cultures, and results on 3 of these showed > 1 species. Gram‐positive cocci were typically found. Of the 34 patients who received drug immunosuppression with PX, 1 patient developed severe shunt‐site infection, and an additional 4 developed bacteremia. Seven patients were given PX alone, and none of these developed clinically significant infection; however, this difference in infection rate did not reach statistical significance. Clinically significant access‐related infection remains an infrequent but potentially important hazard of therapeutic PX.
Tumoral calcinosis presenting as adhesive capsulitis: case report and literature review
Authors: Croock Alan D. , Silver Richard M.
Published: February 2007

Tumoral calcinosis (TC) is an uncommon disorder characterized by large calcific soft tissue deposits, usually adjacent to large joints. In the past, the etiology was unclear, but recently, TC has been considered to be an inherited metabolic disorder, characterized by elevated serum phosphorus and 1,25‐dihydroxyvitamin D levels, normocalcemia, and calcific deposits. However, these features have been shown to vary widely, with formes frustes of TC now being recognized. We report an unusual case of TC, which presented as an adhesive capsulitis, in an elderly North American black woman. The patient's nationality, late age of presentation, and multiple sites of involvement are uncommon features of TC. The clinicopathologic features and possible etiologies of this rare condition are briefly reviewed.
Differential reactivity of rheumatoid synovial cells and serum rheumatoid factors to human immunoglobulin g subclasses 1 and 3 and their CH3 domains in rheumatoid arthritis
Authors: Robbins Dick L. , Benisek William F. , Benjamini Eliezer , Wistar Richard
Published: February 2007

19S IgM rheumatoid factors (RF) are polyclonal autoantibodies that may play an important pathogenic role in sustaining inflammatory synovitis in rheumatoid arthritis (RA). RF in RA have reactivity for as‐yet‐uncharacterized antigenic determinants in IgG Fc. We hypothesized that qualitative differences might exist between some of these RF molecules, and that differences such as reactivity and affinity might characterize more pathogenic RF molecules. Previous observations in our laboratory indicate that RF produced by rheumatoid synovial cells (RSC) have greater reactivity with human IgG and IgG3 subclass, in contrast to serum RF, which has greater reactivity with rabbit IgG and human IgG1. These observations were made using a complement‐dependent RF plaque‐forming cell assay. The purpose of this study was to validate and extend those observations. Therefore, we examined the reactivity of RSC and serum RF with human and rabbit IgG and the reactivity and avidity of RSC‐RF for IgG1 and IgG3 molecules and Fab, F(ab')2, and pFc' fragments thereof in a solid‐phase enzyme immunoassay. In particular, we found: 1) RSC‐RF had at least twice as much reactivity with human IgG as with rabbit IgG; 2) serum RF had approximately equal reactivity with human and rabbit IgG; 3) RSC‐RF had greater reactivity and avidity for IgG3 and IgG3 pFc' than for IgG1; and 4) RSC‐RF was nonreactive with Fab or F(ab')2 from either IgG1 or IgG3. These results suggest that the major antigenic determinant for RSC‐RF resides in the CH3 domain of the IgG3 molecule. Precise characterization of this epitope may provide further insight into the etiology and pathogenesis of RA.
Monocyte fc receptor function in rheumatoid arthritis. enhanced cell‐binding of igg induced by rheumatoid factors
Authors: Mackinnon Susan K. , Starkebaum Gordon
Published: February 2007

Monocytes from 11 patients with rheumatoid arthritis and 10 control subjects were purified by countercurrent elutriation. Rheumatoid arthritis monocytes had more cell‐associated IgG (P < 0.001) and bound more 125I‐labeled heat‐aggregated IgG in vitro (P < 0.02) than did monocytes from control subjects. Interaction of rheumatoid factor (RF) with monocytes was then investigated. Purified 125I‐labeled IgM‐RF and IgG‐RF bound directly to monocytes from normal individuals. Furthermore, preincubation of normal monocytes with RF augmented subsequent binding of aggregated IgG to the cells. We conclude that monocyte‐associated RF can enhance binding of IgG‐containing immune complexes to the cells and can exaggerate the measured number of Fc receptors. Such cell‐bound RF may affect clearance of immune complexes by the reticuloendothelial system in vivo.
The work dynamics of the person with rheumatoid arthritis
Authors: Yelin Edward , Henke Curtis , Epstein Wallace
Published: February 2007

This paper traces the work history of patients with rheumatoid arthritis (RA) from the year of diagnosis to 1985. The paper also describes the risk factors for work loss among patients with RA. It uses data from a panel of 698 RA patients, observed for 4 years, from the practices of a random sample of northern California rheumatologists. Of these 698, 353 had worked for pay at some point in their lives. Three hundred six of the 353 had worked when diagnosed as having RA. Of these 306, 157 (51%) were no longer working in 1985. Forty‐seven individuals started working after the onset of illness, but of these, approximately one‐third had stopped working by 1985. In all, 50% of RA patients with some work experience stopped working within a decade of diagnosis, 60% within 15 years, and 90% within 30 years. We found that the probability of work loss is lessened among persons in jobs that have few physical requirements, among those with high levels of discretion over the pace and activities of work, and among those who were able to stay on the job held when the diagnosis was made. The probability of work loss is increased among service workers. The findings of this longitudinal study, showing that work characteristics profoundly alter the probability of work loss among persons with RA, are consistent with the findings of our earlier cross‐sectional studies of work outcome and RA.
Viral and host genetic factors influence encephalomyocarditis virus—induced polymyositis in adult mice
Authors: Miller Frederick W. , Love Lori A. , Biswas Tapas , McClintock Patrick R. , Notkins Abner Louis , Plotz Paul H.
Published: February 2007

Recent research findings implicate picornaviruses in the etiology of human polymyositis/dermatomyositis and suggest that genetic factors play a role in susceptibility to these diseases. We compared 2 variants of encephalomyocarditis (EMC) virus for their ability to induce polymyositis in adult mice, and evaluated what role the genetic background of the host plays in the degree of myositis induced. While BALB/c mice developed minimal myositis when infected with a diabetogenic variant (EMC‐D), the same strain inoculated with a newly isolated myopathic variant (EMC‐221A) developed viral dose—dependent elevations in muscle‐associated enzymes, bilateral limb muscle weakness, and the histopathologic changes of severe polymyositis. Mice with different genetic backgrounds showed significantly different susceptibilities to EMC‐221A. These data suggest that the severity of polymyositis induced by EMC virus is influenced by both the viral and host genomes.
Activation of complement and coagulation in juvenile dermatomyositis
Authors: Scott John Paul , Arroyave Carlos
Published: February 2007

In patients with juvenile dermatomyositis (JDM), small vessel occlusion and thrombosis result in a decrease in the capillary: muscle fiber ratio. We studied 15 patients with JDM. Six of 7 patients with clinically active JDM had elevated levels of C3d. Moreover, concentrations of fibrinopeptide A and factor VIII‐related antigen were significantly increased in patients with clinically active JDM.
Atlantoaxial (C1‐C2) facet joint osteoarthritis: a distinctive clinical syndrome
Authors: Halla James T. , Hardin Joe G.
Published: February 2007

Osteoarthritis of the atlantoaxial facet joints was identified radiologically in 27 patients, and these comprised 4% of all outpatients with osteoarthritis or degenerative disease of the spine seen during a 36‐month period. These patients had a clinical syndrome which differed from those seen in patients who have subaxial degenerative disease of the spine or myofascial cervical pain. Occipital pain, occipital trigger points, crepitus in the occipital region, and a rotational head tilt deformity (in 13 patients, usually associated with collapse of 1 of the lateral masses [facets]), were the major features of this distinctive syndrome.
Is anticardiolipin activity a cross‐reaction of anti‐DNA or a separate entity?
Authors: Smeenk Ruud J. T. , Lucassen Wim A. M. , Swaak Tom J. G.
Published: February 2007

Putative cross‐reactions between anti‐DNA and anticardiolipin activities were studied using sera of different patients and a panel of monoclonal antibodies to DNA. Sera were obtained from patients with systemic lupus erythematosus, from patients with syphilis, and from heroin addicts who showed a biologic false‐positive result on the serologic test for syphilis. While the patients with syphilis and the heroin addicts had elevated levels of anticardiolipin antibodies in their circulation, no reactivity with DNA was observed in these sera. Sera from systemic lupus erythematosus patients often showed both anti‐DNA and anticardiolipin activity. Although a correlation between anti‐DNA and anticardiolipin titers was found, this did not always result from cross‐reactivity of the same population of antibodies. In fact, we observed a relationship between cross‐reactivity and antibody avidity. Anti‐DNA of high avidity to DNA showed little cross‐reactivity with cardiolipin. Anticardiolipin activity in such sera was based on the presence of specific anticardiolipin antibodies. Anti‐DNA of low avidity was found to cross‐react with cardiolipin. Among monoclonal antibodies to DNA, we found that cross‐reactions with cardiolipin were rare: only 6 of 55 anti‐DNA clones produced antibodies that also reacted with cardiolipin.
D‐penicillamine therapy and interstitial lung disease in scleroderma. a long‐term followup study
Authors: Clerck Luc S. De , Dequeker Jan , Francx Luc , Demedts Maurits
Published: February 2007

Sequential lung function tests were performed on 17 scleroderma patients who were treated with D‐penicillamine (DP) (total of 66 treatment years) and on 10 control scleroderma patients who were not treated or were treated with low‐dose prednisone (total of 25 treatment years). Cusum plots showed significant differences between the 2 groups in their cumulative changes in carbon monoxide diffusing capacity (DLco) (P < 0.005) and in DLco/lung volume (P < 0.02). The end value of the DLco was > 10% lower than the initial value in 3 of the 17 DP‐treated patients versus 5 of the 10 control patients (P < 0.01, Fisher's exact probability test); in 3 DP‐treated patients and 8 control patients (P < 0.003, Fisher's exact probability test), the end value of the DLco/lung volume was >10% lower than the initial value. We conclude that DP has a beneficial effect on interstitial lung disease in patients with scleroderma.
T cytotoxic and helper cells are markedly increased, and t suppressor and inducer cells are markedly decreased, in rheumatoid synovial fluids
Authors: Goto Makoto , Miyamoto Terumasa , Nishioka Kusuki , Uchida Shoji
Published: February 2007

Synovial fluid lymphocytes and paired peripheral blood lymphocytes from 28 patients with rheumatoid arthritis were analyzed by 2‐dimensional flow cytometry. We found that the composition of the lymphocyte population is different in synovial fluid compared with that in peripheral blood, in that there were increased proportions of Ia+ Leu‐2a+/Leu‐15– (T cytotoxic) cells and Leu‐3a+/Leu‐8– (T helper) cells, together with marked decreases in Leu‐2a+/Leu‐15+ (T suppressor) cells and Leu‐3a+/Leu‐8+ (T inducer) cells. These findings suggest that the unique composition of synovial fluid lymphocytes might be the result of T cell activation by some mechanism that is not known.
HLA–D region epitopes associated with juvenile arthritis. recognition by alloreactive t cell clones and alloantisera
Authors: Myers Linda K. , Ball Edward J. , Nunez Gabriel , Fink Chester W. , Stastny Peter
Published: February 2007

The HLA–D region antigens DR5 (wll, w12), DRw6 (w13,w14), DRw8, DRw52, and DQw1 have previously been shown to be increased in frequency in subsets of patients with juvenile arthritis. Since the HLA–D region is complex (composed of at least 3 subregions encoding multiple molecules, each in turn presenting multiple alloantigenic epitopes), we sought to clarify whether one strongly associated factor might explain the previous findings. To search for the pertinent HLA–D region stimulatory epitopes, alloreactive T cells were primed against DR5 and DRw6 haplotypes and cloned by limiting dilution. Three T cell clones and 1 alloantiserum met the criteria for significant association with juvenile arthritis on patient testing, including DR5, DRw6, and DRw8 haplotypes. Monoclonal antibody blocking revealed that all 4 recognized epitopes on DR subregion products. For 2 of the clones, the relative risks for JA (10.5 and 9.4) were higher than the risks with any other previously described typing reagents.
Deficiency of the suppressor inducer subset of T lymphocytes in rheumatoid arthritis
Authors: Emery Paul , Gentry Kay C. , Mackay Ian R. , Muirden Ken D. , Rowley Merrill
Published: February 2007

New monoclonal antibodies allow CD4 lymphocytes to be categorized into helper/inducer (HI) CD4+ 4B4+, and suppressor inducer (SI) CD4+ 2H4+ subpopulations. Blood and synovial lymphocytes from 30 patients with rheumatoid arthritis (RA), 13 patients with other articular diseases, and 24 control subjects were exposed to these monoclonal antibodies and analyzed by flow cytometry. CD4:CD8 ratios were similar for the 3 groups. In RA patients, there was a depletion of SI cells in blood and synovial fluid, and the ratio of HI cells to SI cells was elevated, particularly in the synovial lymphocytes. These data provide new evidence for T cell dysregulation in the perpetuation of RA.
Peripheral blood and synovial fluid monocyte activation in inflammatory arthritis. i. a cytofluorographic study of monocyte differentiation antigens and class ii antigens and their regulation by γgm‐interferon
Authors: Firestein Gary S. , Zvaifler Nathan J.
Published: February 2007

Recent study of the expression of monocyte differentiation antigens (MAg) and HLA–DR on peripheral blood monocytes (PBM) has led to the recognition of resting and activated monocyte phenotypes. The former is identified by the expression of large amounts of MAg (i.e., Mo2 and 63D3) and small amounts of HLA–DR, while the latter is identified by the reverse. We studied the phenotypes of PBM and synovial fluid monocytes (SFM) of patients with chronic inflammatory arthritis and found that PBM were primarily resting and SFM were usually activated. In addition, we measured the degree of modulation of MAg and HLA–DR by γ‐interferon (γ‐IFN). Patient PBM reacted the same as PBM from normal individuals (i.e., MAg decreased and HLA–DR increased after exposure to γ‐IFN). However, in patient SFM, HLA–DR did not increase with exposure to γ‐IFN because expression was already maximal. Interestingly, MAg could still be down‐regulated on γ‐IFN–treated SFM, even when expression began at a very low level (i.e., activated phenotype). This independent regulation of MAg and HLA–DR suggests that macrophage activating factors other than γ‐IFN may be responsible, in part, for the activated phenotypes observed.
Hla–Dr4 and Gm 1;21 haplotypes are associated with pseudolupus induced by venopyronum dragéeaes
Authors: Grosse‐Wilde Hans , Genth Ekkehard , ühl Audrey Grevesm , Vögeler Udo , Zarnowski Hanabela , Mierau Rudolf , Doxiadis Gabriele , Doxiadis Ilias , Maas Dieter
Published: February 2007

The phenotypic frequencies of human major histocompatibility complex class I, II, and III antigens and immunoglobulin allotypes (Gm factors) were determined in 56 patients (55 women, 1 man) who had lupus‐like disease induced by Venopyronum dragées. The findings in these patients were compared with those of a control group. We found a significant increase of HLA‐DR4 (57.1% versus 26.5%, relative risk [RR] 3.7) and a decrease of HLA‐DR3 (3.6% versus 19.1%, RR 0.16) in the patient group. In addition, the haplotype Gm 1;21 (60.7% versus 32.9%, RR 3.2), and the phenotype Gm 1,3;5,21 (46.4% versus 25.8%, RR 2.5) were significantly increased. Both the haplotype Gm 1;21 and the phenotype Gm 1,3;5,21 are associated with HLA–DR4 in pseudolupus patients but not in controls. The coincidence of HLA–DR4 and Gm 1;21 markedly increases the risk of acquiring pseudolupus (RR 6.9). We conclude that the pathogenesis of pseudolupus is influenced by at least 2 independent genetic factors, A similar HLA association has been described in hydralazine‐induced lupus, and this suggests a common pathogenic mechanism.
Association of a 9.2‐kilobase pvu ii class i major histocompatibility complex restriction fragment length polymorphism with ankylosing spondylitis
Authors: McDaniel D. Olga , Acton Ronald T. , Barger Bruce O. , Koopman William J. , Reveille John D.
Published: February 2007

We analyzed DNA restriction fragment length polymorphism (RFLP) in 53 white ankylosing spondylitis (AS) patients and 92 healthy controls, utilizing a full‐length HLA‐B7 complementary DNA probe. A 9.2‐kilobase (kb) Pvu II fragment was found to be significantly increased in frequency in B27 positive AS patients compared with the B27 positive control group (P = 0.00085, relative risk = 7.2). The presence of both B27 and the 9.2‐kb RFLP in an individual conferred a relative risk for AS of 297, compared with a relative risk of 119 in those who had B27 alone. The 9.2‐kb RFLP appears to be a marker for AS which, with HLA–B27, contributes further to susceptibility to the disease. Our findings indicate that this fragment and HLA–B27 segregate independently in familial studies of AS.
The prevalence of knee osteoarthritis in the elderly. the framingham osteoarthritis study
Authors: Felson David T. , Naimark Allan , Anderson Jennifer , Kazis Lewis , Castelli William , Meenan Robert F.
Published: February 2007

To investigate the prevalence of osteoarthritis (OA) of the knee in elderly subjects, we studied the Framingham Heart Study cohort, a population‐based group. During the eighteenth biennial examination, we evaluated the cohort members for OA of the knee by use of medical history, physical examination, and anteroposterior (standing) radiograph of the knees. Radiographs were obtained on 1,424 of the 1,805 subjects (79%). Their ages ranged from 63–94 years (mean 73). Radiographs were read by a radiologist who specializes in bone and joint radiology, and were graded 0–4 according to the scale described by Kellgren and Lawrence. OA was defined as grade 2 changes (definite osteophytes), or higher, in either knee. Radiographic evidence of OA increased with age, from 27% in subjects younger than age 70, to 44% in subjects age 80 or older. There was a slightly higher prevalence of radiographic changes of OA in women than in men (34% versus 31%); however, there was a significantly higher proportion of women with symptomatic disease (11% of all women versus 7% of all men; P = 0.003). The age‐associated increase in OA was almost entirely the result of the marked age‐associated increase in the incidence of OA in the women studied. This study extends current knowledge about OA of the knee to include elderly subjects, and shows that the prevalence of knee OA increases with age throughout the elderly years.
Metabolism of C4 and linkage analysis in a kindred with hereditary incomplete C4 deficiency
Authors: Wisnieski Jeffrey J. , Nathanson Michael H. , Anderson Jeanne E. , Davis Iii Alvin E. , Alper Chester A. , Naff George B.
Published: February 2007

We studied a kindred in which C4 deficiency had been discovered. Unlike families with total absence of C4, in this kindred C4 deficiency was found to be incomplete, autosomal dominant, not caused by null alleles, and not associated with a high incidence of systemic lupus erythematosus. The deficient state was caused by hyposynthesis of C4, not by hypercatabolism. The locus for incomplete C4 deficiency was not closely linked to the major histocompatibility complex. The abnormal autosomal dominant allele is, apparently, rare, and how it causes decreased synthesis of C4 is unknown.
Restricted heterogeneity of polyclonal rheumatoid factors
Authors: Bouvet Jean‐Pierre , Xin Wu Yu , Pillot Jacques
Published: February 2007

The electrophoretic pattern of rheumatoid factor (RF) was investigated in 40 polyclonal sera, by using radiolabeled IgG. Thirty sera specifically bound IgG aggregates, correlating with their RF titer. The binding pattern was monoclonal or oligoclonal. The molecules responsible were classic RF antibodies, as shown by using purified IgM, inhibition experiments, and by the optimal size of aggregates (2,000–4,000 kd). These data show that RF heterogeneity is restricted in polyclonal sera, and this can have a bearing on several mechanisms.
Effects of gold sodium thiomalate on interferon stimulation of C2 synthesis and HLA–DR expression by human monocytes
Authors: Sanders Karen M. , Carlson Patricia L. , Littman Bruce H.
Published: February 2007

Gamma‐interferon (γ‐IFN) is a T cell–derived lymphokine that has potent macrophage‐activating properties. It increases Fc receptor density, increases the formation and release of reactive oxygen intermediates, increases the synthesis and release of complement cascade proteins, especially C2 and factor B, and increases class II (HLA–DR) antigen expression. These effects may play a role in the potentiation of inflammation in rheumatoid arthritis. We examined the possibility that gold sodium thiomalate (GST), an effective treatment for rheumatoid arthritis, would inhibit γ‐IFN–mediated stimulation of monocyte/macrophages. GST in concentrations attainable in vivo was shown to inhibit both spontaneous and γ‐IFN–stimulated C2 production up to 50%. GST inhibition could be only partially overcome with increasing concentrations of γ‐IFN. In addition, GST inhibited γ‐IFN–stimulated HLA‐DR expression at the highest concentrations tested (20–50 μg/ml). GST alone in low concentrations (0.1–5 μg/ml) was found to increase HLA‐DR antigen expression as quantitated by several methods, including flow cytometry, cell surface enzyme‐linked immunosorbent assay, and Western blotting. This GST‐stimulated increase in HLA‐DR antigen expression paralleled an increased ability of monocytes to present antigen. The mechanism by which low concentrations of GST stimulate HLA‐DR antigen expression is unclear, but was shown by 35S‐methionine cell labeling not to involve increased HLA‐DR protein synthesis.
Lentivirus infection augments concurrent antigen‐induced arthritis
Authors: Banks Keith L. , Jacobs Cindy A. , Michaels Frank H. , Cheevers William P.
Published: February 2007

Experimental antigen–induced arthritis was compared in normal goats and goats infected with caprine arthritis‐encephalitis virus. Although acute arthritis was the same in infected and uninfected animals, the disease lasted 16 weeks longer in the caprine arthritis‐encephalitis virus–infected goats. Our findings suggest that the arthritis caused by this virus is due to events other than, or in addition to, the immune reaction to viral antigens.
Analyses of hla linkage in white families with multiple cases of seropositive rheumatoid arthritis
Authors: C. P.Go Rodney , Alarcón Graciela S. , Acton Ronald T. , Koopman William J. , Vittor Virginia J. , Barger Bruce O.
Published: February 2007

Families with multiple cases of seropositive rheumatoid arthritis (RA), identified through 2 probands with the disease, were analyzed for genetic linkage between an autosomal susceptibility gene for RA and the HLA loci. These analyses were carried out over a wide range of penetrances (0.1–0.4), with prevalence for the disease fixed at 0.01 or 0.04. In some models, a sporadic frequency of 20% was assumed. Close linkage to the HLA loci was ruled out for all models where the gene was autosomal dominant, except for those with low penetrance and with prevalence set at 0.04. The models in which the gene was autosomal recessive produced results similar to those in models where it was autosomal dominant when prevalence was set at 0.01, and close linkage was ruled out, except at very low penetrances. With prevalence set at 0.04, the autosomal recessive gene model produced log odds scores which were all negative (−2.6 to −0.3). Therefore, the evidence in these families does not support close linkage with HLA, even though a significant DR4 RA population association exists. The data suggest that non‐major histocompatibility complex (MHC) genes may contribute to the development of RA and, therefore, disease susceptibility may involve the genetic interaction of one or more MHC genes and non‐MHC genes, in addition to environmental agents.
Serum concentrations of salicylate and naproxen during concurrent therapy in patients with rheumatoid arthritis
Authors: Furst Daniel E. , Sarkissian Edmund , Blocka Kenneth , Cassell Sidney , Dromgoole Sydney , Harris E. Robert , Hirschberg Joel M. , Josephson Nathan , Paulus Harold E.
Published: February 2007

The kinetic interaction between salicylate and naproxen was investigated in 25 rheumatoid arthritis patients. Kinetic interactions were tested in serum after patients had been on each drug regimen for 1 month. Salicylate decreased serum naproxen concentration from 89.5 mg/liter to 65.9 mg/liter (P < 0.001) and increased serum naproxen clearance by 56%. Naproxen had minimal effect on serum salicylate concentrations.
Charge‐charge interactions between articular cartilage and cationic antibodies, antigens, and immune complexes
Authors: Zatarain‐Rios Ernesto , Mannik Mart
Published: February 2007

Bovine articular cartilage was used to examine the binding of cationized antibodies, antigens, and immune complexes to articular cartilage by charge‐charge interactions. Rabbit antibodies to human serum albumin (anti‐HSA) and HSA were cationized to various degrees by the addition of amino groups. When approximately 20 or more new amino groups were added to HSA and approximately 25 or more amino groups were added to anti‐HSA, the proteins readily bound to cartilage and penetrated into the matrix. Soluble immune complexes made with the cationic antibodies, including small‐latticed complexes, bound only to the surface of the cartilage. When cationic HSA was bound to the matrix of the cartilage, unaltered antibodies bound only to the antigen at the surface and did not penetrate the matrix. This model system defines the manner in which cationic antigens and antibodies bind to and penetrate into the articular cartilage.
Quantitation of retroviral gp70 antigen, autoantibodies, and immune complexes in extravascular space in arthritic mrl‐lpr/lpr mice. use of a subcutaneously implanted tissue cage model
Authors: Dayer Eric , Yoshida Haruyoshi , Izui Shozo , Lambert Paul‐Henri
Published: February 2007

MRL‐lpr/lpr (MRL/1) mice spontaneously develop a disease that is characterized by glomerulonephritis, diffuse vasculitis, and arthritis associated with high levels of autoantibodies that include IgG rheumatoid factor (RF). To define the immunopathogenic mechanisms that lead to the development of extravascular lesions such as arthritis, we implanted a tissue cage subcutaneously in arthritic MRL/1 mice and compared components of the tissue cage fluid, which resembles the extravascular fluid, with those of sera. When compared with those of sera, tissue cage fluids from arthritic MRL/1 mice had similar levels of RF and one‐third the amount of Clq immune complexes. In contrast, anti‐DNA activities in tissue cage fluids corresponded to only 10% of the serum activities and, most strikingly, nephritogenic retroviral gp70‐anti‐gp70 immune complexes were almost undetectable in tissue cage fluids. This was also the case for another strain of autoimmune mice, (New Zealand black x New Zealand white)F1 mice, although they did not produce RF. The absence of gp70 immune complexes in tissue cage fluids could be due to markedly limited diffusion of gp70 antigen in these fluids. These results strongly suggest that serum proteins, including autoantigen and autoantibodies, appear in extravascular fluid in a selective manner, depending on their size and charge. Their specific properties in sera or extravascular fluid could partly account for the different manifestations of vascular and extravascular lesions observed in autoimmune mice.
Measuring disease activity: comparison of joint tenderness, swelling, and ultrasonography in rheumatoid arthritis
Authors: Spiegel Timothy M. , Iii William King , Weiner Steven R. , Paulus Harold E.
Published: February 2007

In a prospective study of 6 patients with classic rheumatoid arthritis, we evaluated 3 measures of disease activity: comprehensive joint swelling and joint tenderness counts, and ultrasonography of joints. After baseline data were obtained on these 6 patients, therapy with fenbufen, a new nonsteroidal antiinflammatory drug, was begun. Followup examinations were performed at 4 weeks and 24 weeks after baseline. There were statistically significant differences between joint tenderness and joint swelling findings and between joint tenderness and joint ultrasonography findings (P < 0.05 by kappa test statistic). In comparisons of joint swelling and ultrasonography, no difference was found (P > 0.05). When measures of changes over 6 months were compared, there was a high concordance between improvement in joint swelling and improvement in joint ultrasonography (P < 0.01). Our results demonstrate that clinical assessment of joint swelling provides an accurate measure of synovial effusion, as confirmed by the more objective ultrasound measurements.
Connective tissue activation. xxxii. structural and biologic characteristics of mesenchymal cell—derived connective tissue activating peptide—v
Authors: Cabral A. R. , Cole L. A. , Walz D. A. , Castor C. W.
Published: February 2007

Connective tissue activating peptide—V (CTAP‐V) is a single‐chain, mesenchymal cell—derived anionic protein with large and small molecular forms (Mr of 28,000 and 16,000, respectively), as defined by sodium dodecyl sulfate—polyacrylamide gel electrophoresis. The proteins have similar specific activities with respect to stimulation of hyaluronic acid and DNA formation in human synovial fibroblast cultures. S‐carboxymethylation or removal of sialic acid residues did not modify CTAP‐V biologic activity. Rabbit antibodies raised separately against each of the purified CTAP‐V proteins reacted, on immunodiffusion and on Western blot, with each antigen and neutralized mitogenic activity. The amino‐terminal amino acid sequence of the CTAP‐V proteins, determined by 2 laboratories, confirmed their structural similarities. The amino‐terminal sequence through 37 residues was demonstrated for the smaller protein. The first 10 residues of CTAP‐V (28 kd) were identical to the N‐terminal decapeptide of CTAP‐V (16 kd). The C‐terminal sequence, determined by carboxy‐peptidase Y digestion, was the same for both CTAP‐V molecular species. The 2 CTAP‐V peptides had similar amino acid compositions, whether residues were expressed as a percent of the total or were normalized to mannose. Reduction of native CTAP‐V protein released sulfhydryl groups in a protein:disulfide ratio of 1:2; this suggests that CTAP‐V contains 2 intramolecular disulfide bonds. Clearly, CTAP‐V is a glycoprotein. The carbohydrate content of CTAP‐V (16 kd) and CTAP‐V (28 kd) is 27% and 25%, respectively. CTAP‐V may have significance in relation to autocrine mechanisms for growth regulation of connective tissue cells and other cell types.
Acute arthritis occurring in association with subcutaneous dirofilaria tenuis infection
Authors: Corman Lourdes C.
Published: February 2007

A patient who developed a self‐limited acute migratory arthritis in association with subcutaneous infection with Dirofilaria tenuis is described. There have been several reports of parasitic rheumatism and the possible association between arthritis and parasitic infection. Parasitic rheumatism in a patient infected with D tenuis has not been previously reported, however.
Increased helper inducer and decreased suppressor inducer phenotypes in the rheumatoid joint
Authors: Lasky H. Paul , Bauer Kenneth , Pope Richard M.
Published: February 2007

Cells isolated from the joints of patients with rheumatoid arthritis (RA) exhibit functional immune abnormalities, such as diminished suppressor activity, depressed response to mitogens, and enhanced immunoglobulin production. We sought to characterize the T lymphocyte subsets in the synovial fluid (SF) and peripheral blood (PB) of RA patients in an attempt to clarify the mechanism(s) responsible for these functional immune abnormalities. We used dual‐immunofluorescence staining techniques with several combinations of monoclonal antibodies, including anti‐4B4 and anti‐2H4, which define, respectively, the helper inducer and suppressor inducer subsets of CD4+ (Leu‐3+ and T4+) cells. Mononuclear cells from normal PB (n = 9), RA PB (n = 6), and RA SF (n = 9) were analyzed, after staining, by flow cytometry. We observed a significant increase (P < 0.0002) in the number of cells bearing the helper inducer phenotype (CD4+, 4B4+), and a significant decrease (P < 0.0002) in the number of cells bearing the suppressor inducer phenotype (CD4+, 2H4+), in RA SF compared with the levels in PB from RA patients or normal control subjects. We also observed that the CD8+, 2H4+ subset was significantly decreased (P < 0.0001) in SF compared with that in PB. There was no significant difference in the lymphocyte subset levels in PB from RA patients and from normal subjects. These observations may account, in part, for the reduced suppressor activity, the poor response to mitogens, and the autologous mixed lymphocyte reaction, as well as the enhanced production of Ig and rheumatoid factor, that are observed in the rheumatoid joint.
Monoclonal rheumatoid factor–igg immune complexes. poor fixation of opsonic c4 and c3 despite efficient complement activation
Authors: Ng Yin C. , Peters D. Keith , Walport Mark J.
Published: February 2007

Monoclonal IgM rheumatoid factor forms complexes with IgG in essential mixed cryoglobulinemia. We demonstrate that such complexes fix C3 and C4 poorly, although efficient fluid‐phase C3 conversion can occur. Fixation of small amounts of C4 may be sufficient to generate a C3 convertase, but may prevent subsequent fixation of C3 by competing for binding sites on the complex. These complexes bind inefficiently to normal erythrocyte complement receptor type 1 (CR1) in vitro, and are undetectable on erythrocytes of patients with essential mixed cryoglobulinemia in vivo. Clearance of such phlogistic complexes from tissues by CR1‐bearing cells may be inefficient.
A new autoantibody in patients with rheumatoid arthritis: characterization of the anti–hat‐1 antibody system
Authors: Abe Yoichi , Inada Shinichi , Torikai Katsutaka
Published: February 2007

A unique, new autoantibody, anti–HaT‐1, has been identified in the serum of patients with rheumatoid arthritis (RA). Anti–HaT‐1 antibody is predominantly IgM, and reacts by double immunodiffusion with HaT‐1 antigen, an acidic protein in human and rat liver supernatant (MW ∼ 150,000). It was detected in 9 of 38 patients with RA, 2 of 15 patients with RA and Sjögren's syndrome, and none of 92 patients with other connective tissue diseases, indicating that this autoantibody is highly specific for RA.
Radiographic assessment and psychologic variables as predictors of pain and functional impairment in osteoarthritis of the knee or hip
Authors: Summers Mary N. , Haley William E. , Reveille John D. , AlarcOan Graciela S.
Published: February 2007

Sixty‐five outpatients with osteoarthritis of the knee and/or hip were assessed using radiographic ratings of disease severity, measures of psychologic coping, and multidimensional clinical outcomes of degree of pain and functional impairment. Disease severity accounted for little of the individual variability in clinical outcomes. Even after controlling for disease severity, psychologic variables remained strong predictors of individual differences in functional impairment and pain. Psychologic processes deserve greater clinical and research attention as potential mediators between disease severity and clinical outcome.
Articular responses to purified cartilage proteoglycans
Authors: Boniface Raymond J. , Cain Paul R. , Evans Christopher H.
Published: February 2007

To examine whether proteoglycans (PGs) liberated from cartilage might contribute to articular changes in arthritis, cartilage PGs were injected intraarticularly into rabbit knee joints. Twice‐weekly injections of PG (2.5 mg) provoked synovial hypertrophy, synovitis, erosion of the articulating surfaces, and loss of metachromasia of the articular cartilage. These changes were accompanied by a marked elevation in the production of neutral collagenase and gelatinase by both synoviocytes and chondrocytes. The synoviocytes of experimental knee joints also produced factor(s), possibly related to interleukin‐1, which provoked the activation of chondrocytes. Our data are consistent with the idea that free PG fragments mediate some of the pathophysiologic changes that occur in arthritic joints. This property may be particularly important in osteoarthritis.
Acquired immunodeficiency syndrome mimicking sjögren's syndrome and systemic lupus erythematosus
Authors: De Clerck Luc S. , Couttenye Marie M. , De Broe Marc E. , Stevens Wim J.
Published: February 2007

We describe a patient in whom the diagnosis of transfusion‐associated acquired immunodeficiency syndrome (AIDS) was delayed because her clinical symptoms were similar to those of systemic lupus erythematosus and Sjögren's syndrome and because of a false‐negative result on a Western blot test for human immunodeficiency virus. The importance of using different diagnostic tests for AIDS and the pitfalls in diagnosing AIDS in patients who appear to have connective tissue disease are discussed.
Degenerative spondylolisthesis, synovial cyst of the zygapophyseal joints, and sciatic syndrome: report of two cases and review of the literature
Authors: Reust Pierre , Wendling Daniel , Lagier RenEa , Pageaut GEarard , Reverdin Alain , Jacquet Guy , Guidet Michel , Fallet Georges H.
Published: February 2007

Two cases of sciatica secondary to nerve root compression by a “synovial cyst” of a zygapophyseal joint are described. In light of these 2 cases and on reviewing the literature, it appears that zygapophyseal joint osteoarthritis with degenerative (or articular) spondylolisthesis can be a predisposing factor to the formation of such synovial expansions and, consequently, the cause of nerve root compression. The coexistence of a lumbar degenerative spondylolisthesis with a radicular syndrome should therefore encourage early investigation by computed tomography scan, so that conservative treatment would not be unnecessarily prolonged.
Clinical associations of anticentromere antibodies and antibodies to topoisomerase i. a study of 355 patients
Authors: Weiner E. S. , Earnshaw W. C. , SeneAcal J.‐L. , Bordwell B. , Johnson P. , Rothfield N. F.
Published: February 2007

Anticentromere antibodies (ACA) and anti–topoisomerase I (anti–topo I) were assayed in serum samples from 355 patients: 89 with proximal scleroderma; 54 with CREST syndrome (calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, telangiectasias), without proximal scleroderma; 154 with primary and secondary Raynaud's disease; and 58 with other rheumatic diseases, without Raynaud's disease. Sera from healthy control subjects were also assayed. Using immunoblotting techniques, anti‐topo I was detected in 28% of the patients with proximal scleroderma; using immunodiffusion techniques, this antibody was found in only 20% of the same group of patients. Anti–topo I and ACA were found primarily in patients with scleroderma, CREST syndrome, and Raynaud's phenomenon. ACA identified patients with less severe disease, whereas anti–topo I identified patients with skin and cardiac involvement and patients with malignancies.
Epidemiology of reiter's syndrome in rochester, minnesota: 1950–1980
Authors: Michet Clement J. , Machado E. B. V. , Ballard David J. , Mckenna Charles H.
Published: February 2007

The incidence of Reiter's syndrome in a predominantly white, community‐based population is reported. The age‐adjusted annual incidence rate for males younger than age 50 was 3.5 per 100,000. No female cases were identified. Over time, a greater proportion of cases have been identified among younger males. In 63% of the patients, either a prolonged or relapsing disease course occurred.
Common tests for rheumatoid factors: poorly standardized but ubiquitous
Authors: Goddard David H. , Moore Mary E.
Published: February 2007

Rheumatoid factor (RF) test results reported in the College of American Pathologists' surveys for 1983–1985 lacked inter‐laboratory reliability and mutual validity. Using the 4 most popular commercial kits for RF testing, participating laboratories consistently identified as “positive” or “negative” all but the weakly positive samples. A wide range of titers was reported on qualitative testing, however. One popular kit using a modified sheep red blood cell agglutination technique yielded results that differed markedly from those with other kits. Investigators apparently have paid little attention to these discrepancies. In Arthritis & Rheumatism, from 1983 to 1985, over 50% of the articles that referred directly or indirectly to RFs omitted details of RF methodology. Until a reliable RF test is adopted, it is essential that such methodologic information be specified.
Correlates between autoantibodies to nucleolar antigens and clinical features in patients with systemic sclerosis (scleroderma)
Authors: Reimer Georg , Steen Virginia D. , Penning Carol A. , Medsger Thomas A. , Tan Eng M.
Published: February 2007

Immunofluorescence on rat liver sections was used to select high‐titer antinucleolar antibodies (ANoA) in the sera of patients with systemic sclerosis (scleroderma). In 646 patients, 53 ANoA sera (8%) were identified, and of these, 46 were available in sufficient quantities for further analysis. The complex of RNA polymerase I was immunoprecipitated by 7 sera (15%), which uniformly produced punctate nucleolar staining. The PM‐Scl antigen, a particle consisting of 11 polypep‐tides, was immunoprecipitated by 8 sera (17%), all of which displayed homogeneous nucleolar staining. A 34‐kd nucleolar protein (fibrillarin) of the U3 RNP complex was positive in immunoblotting of 22 sera (48%), which characteristically produced clumpy nucleolar staining. Antibodies against RNA polymerase I were associated with diffuse scleroderma of short duration, which was characterized by a high prevalence of internal organ involvement, including renal crisis. Anti‐U3 RNP antibodies had a high prevalence in men with significantly less joint involvement, compared with ANoA‐negative patients. Anti–PM‐Scl antibodies identified a group of scleroderma patients with a high prevalence of concomitant myositis and renal involvement.
Spontaneous cartilage degeneration in guinea pigs
Authors: Bendele A. M. , Hulman J. F.
Published: February 2007

Spontaneous degeneration of the knee joint cartilage in male Hartley guinea pigs was studied by light microscopy in animals aged 3–18 months. Unilateral focal degeneration, characterized by chondrocyte death and proteoglycan loss with surface fibrillation, was observed on the medial tibial plateau in 2 of 5 guinea pigs that were 3 months old. The incidence and severity of the lesions increased with age, and by 12–18 months of age, all animals had moderate‐to‐severe degeneration of the medial tibial plateau, femoral condyle, and meniscus. Lesions were not present on the lateral aspect of the knee joint in any of the animals.
Hairy cell leukemia presenting as a lupus‐like illness
Authors: Strickland Roger W. , Limmani Alex , Wall James G. , Krishnan Jayashree
Published: February 2007

We describe a young Hispanic man who presented with features suggestive of a diagnosis of systemic lupus erythematosus. Eventually, a bone marrow biopsy was performed, and it revealed the presence of hairy cell leukemia. This case of a lupus‐like syndrome should be added to the list of reported rheumatic syndromes that are associated with hairy cell leukemia.