ISSUEThis issue
Last Month’s Slides P.1
Monthly Case study P.1
Scientific feature - APL P.2-3
Monthly Quiz P.3
Top Tips P.3

April 2020
Slide Summaries
Slide 1
Myelocytes present andmild eosinophilia

Slide 2
Generally normal film

Slide 3Monthly Digital Case study
April 2020 Slide 6
Presentation

Slide review

Male (73 years old)
Multiple Instrument alarms (withWBCs in particular)

Hypergranular
blasts.
Multiple Auer rods.
Convoluted and folded
nuclei with fine chromatinstrands:

Lymphocytosis with smearcells. Indicative of CLLWBC
51.9* (10^3/mm3)RBC
2.48 (10^6/mm3)HGB
8.0 (g/dL)
HCT
20.9 (%)
MCV84 (fL)
MCH 32.0 (pg)
MCHC 38.1 (g/dL)
PLT
18* (10^3/mm3)

Slide 5Differential

Borderine monocytosis
Basophil identified

Slide 4

Occasional atypicallymphocyte

Slide 6
Acute Pro-Myelocytic
Leukemia
Neutropaenia
Thrombocytopaenia
Blasts +++(see case study opposite)

Neutrophils
0.7%
Lymphocytes
7.1%
Metamyelocytes 1.4%
Myelocytes
0.7%
Blasts90.1%

Diagnosis
Acute promyelocytic Leukemia(variant)
The patient presented as ahaematology emergency – sepsis
and haemorhagic
diseaseExamination of the blood film
confirms the low platelet count andalso shows the presence of
spherocytes as indicated by theraised MCHC

AcutePromyelocyticLeukaemia – In
Brief

MonthlyMorphology
Quiz
Name these cells.

An overview of theclinical features,
laboratory findings andtreatment
Introduction

Laboratory Findings

Acute Promyelocytic Leukaemia (APL)
is a differentiated variant of Acute
Myeloid Leukaemia (AML) thatusually (>95%) carries a t(15:17)
chromosomal translocation.
It accounts for around 10% of AML
cases and has a different treatment
protocol from AML..

Laboratory investigations, besides
FBC/Differential and blood film
morphology,
includethefollowing:• Bone Marrow Aspirate andTrephine• Immunophenotyping• Cytogenetic and mutation
analysis• Biochemistry(LFTs,U+E,Calcium, LDH)
• Coagulation Screening/ DDimer

Clinical Presentation

Look at the red cells in
the images above.
What abnormalities canyou see?
Name a condition
where you might see
this picture.
What other laboratory
tests could beindicated?

Answers in the nextedition.

The disease can be seen in either
gender and at any age but is mostcommon in middle-age. It frequently
presents with a severe haemorragic
syndrome.
• The following features may be
seen:• Symptoms of anaemia- leading tofatigue, pallor, tachycardia,
dyspnoea• Fever and infections due toneutropaenia• Symptoms relating to abnormal
platelet
functionandorcoagulopathy – severe bleeding
and or ecchymosis• Non-specific such as pain, slow
healing and unexplained weightloss

Haematologicalinvestigations
normally show normochromic
normocytic
anaemia
andthrombocytopaeniaonpresentation.
WBC is usually increased with avariable number of blast cells. Theconditionismorphologically
identified as M3 by the FAB
classification.
The bone marrow is hypercellular,
typically
containing
many
leukaemic blasts.
Morphology, immunophenotyping
and genetic analysis confirm thediagnosis.
Coagulopathy is often present inAPL.
Biochemistry tests are performed
as a baseline prior to treatment.
Raised Uric Acid and/or LDH may
be present.

Other News
Hematovision 5
Hematovision 5 is a freehaematology atlas that isavailable via the HORIBA
Medical website oroffline, as part of theHORIBA Medical app
dowloadable for IOs orAndroid devices

Bilbliography

Acute Promyelocytic Leukaemia Continued
Genetics

Treatment

The somatic mutation that causes
acute promyelocytic leukemia
involves two genes, the PML geneon chromosome 15 and the RARαgene on chromosome 17.

Treatment consists of supportive
therapy (maintaining haemoglobinand platelet count, treatment ofinfection and treatment of DIC(FFP)) and specific chemotherapy.

A rearrangement of genetic
material (translocation) between
chromosomes 15 and 17, written ast(15;17), fuses part of the PML genewith part of the RARα (retinoic acidreceptor α) gene. The protein
produced from this fused gene is
known as PML-RARα.

Treatment differs from that ofother acute myeloid leukaemia withthe addition of all-trans retinoic
acid (ATRA), often combined witharsenic trioxide or anthracycline

The RARα gene controls thematuration of WBCs which isblocked in APL

Prognosis
APL can be aggressive on
presentation but cells are relatively
sensitive to chemotherapy. Theaddition of ATRA and othertargeted therapies gives a >90%
prospect of remission.

This Month’s Q&A Morphology TipsQuick tips for making manual blood films. Problems andanswers
P Blood film extends right to the end of the slide

A Blood drop is too large or too small an angle between slide and spreader
P Blood film is too short
A Blood drop too small or too large an angle between slide and spreader
P The blood film is irregular with ridges and a long tail
A The edge of the spreader is dirty or chipped
P Holes appearing in the spread
A The slide is dirty/ greasy. Nb. Sometimes it can be lipaemia in the sampleHoffbrand’s Essential
Haematology 7th Edition
Ch.13. Wiley Blackwell
2015
QSP April 2020
Acute promyelocytic
leukemia: from highly
fatal to highly curable
Zhen-Yi Wang,Zhu Chen
Blood (2008) 111 (5):2505–2515

Editorial Team
Kelly Duffy
Mandy Campbell
Shubham Rastogi

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