ISSUE

This issue
Last Month’s Slides P.1
Monthly Case study P.1
Scientific feature - APL P.2-3

April 2020 Monthly Quiz P.3

Top Tips P.3

Slide Summaries

Slide 1 Monthly Digital Case study

Myelocytes present and April 2020 Slide 6
mild eosinophilia
Presentation Slide review
Slide 2 Male (73 years old)
Hypergranular blasts.
Generally normal film Multiple Auer rods.
Multiple Instrument alarms (with Convoluted and folded
WBCs in particular) nuclei with fine chromatin
Slide 3 WBC 51.9* (10^3/mm3) strands:
Borderine monocytosis RBC 2.48 (10^6/mm3)
Basophil identified HGB 8.0 (g/dL)
HCT 20.9 (%)
MCV 84 (fL)
Slide 4 MCH 32.0 (pg)
Lymphocytosis with smear MCHC 38.1 (g/dL)
cells. Indicative of CLL PLT 18* (10^3/mm3)

Slide 5 Differential
Occasional atypical
lymphocyte Neutrophils 0.7% Examination of the blood film
Lymphocytes 7.1% confirms the low platelet count and
Metamyelocytes 1.4% also shows the presence of
Slide 6 Myelocytes 0.7% spherocytes as indicated by the
Acute Pro-Myelocytic Blasts 90.1%
raised MCHC
Leukemia
Neutropaenia Diagnosis
Thrombocytopaenia
Blasts +++
(see case study opposite) Acute promyelocytic Leukemia
(variant)
The patient presented as a
haematology emergency – sepsis
and haemorhagic
disease
Monthly Acute
Morphology Promyelocytic
Quiz Leukaemia – In
Name these cells. Brief
An overview of the
clinical features,
laboratory findings and
treatment

Introduction Laboratory Findings

Acute Promyelocytic Leukaemia (APL) Laboratory investigations, besides
is a differentiated variant of Acute FBC/Differential and blood film
Myeloid Leukaemia (AML) that morphology, include the
usually (>95%) carries a t(15:17) following:
chromosomal translocation. • Bone Marrow Aspirate and
It accounts for around 10% of AML Trephine
cases and has a different treatment • Immunophenotyping
protocol from AML.. • Cytogenetic and mutation
analysis
Clinical Presentation • Biochemistry (LFTs, U+E,
The disease can be seen in either Calcium, LDH)
gender and at any age but is most • Coagulation Screening/ D-
common in middle-age. It frequently Dimer
presents with a severe haemorragic
Look at the red cells in
syndrome. Haematological investigations
the images above. normally show normochromic
• The following features may be normocytic anaemia and
seen: thrombocytopaenia on
What abnormalities can
presentation.
you see? • Symptoms of anaemia- leading to WBC is usually increased with a
fatigue, pallor, tachycardia, variable number of blast cells. The
Name a condition dyspnoea condition is morphologically
identified as M3 by the FAB
where you might see • Fever and infections due to classification.
neutropaenia The bone marrow is hypercellular,
this picture. typically containing many
• Symptoms relating to abnormal leukaemic blasts.
What other laboratory platelet function and or Morphology, immunophenotyping
coagulopathy – severe bleeding and genetic analysis confirm the
tests could be and or ecchymosis diagnosis.
indicated? Coagulopathy is often present in
• Non-specific such as pain, slow APL.
healing and unexplained weight Biochemistry tests are performed
loss as a baseline prior to treatment.
Raised Uric Acid and/or LDH may
Answers in the next be present.
edition.
 Other News
Hematovision 5
Hematovision 5 is a free
haematology atlas that is
available via the HORIBA
Medical website or
offline, as part of the
HORIBA Medical app
dowloadable for IOs or
Android devices

Bilbliography
Acute Promyelocytic Leukaemia Continued Hoffbrand’s Essential
Haematology 7th Edition
Genetics Treatment Ch.13. Wiley Blackwell
The somatic mutation that causes Treatment consists of supportive 2015
acute promyelocytic leukemia therapy (maintaining haemoglobin
involves two genes, the PML gene and platelet count, treatment of QSP April 2020
on chromosome 15 and the RARα infection and treatment of DIC
gene on chromosome 17. (FFP)) and specific chemotherapy. Acute promyelocytic
leukemia: from highly
A rearrangement of genetic Treatment differs from that of fatal to highly curable
material (translocation) between Zhen-Yi Wang,
other acute myeloid leukaemia with
Zhu Chen
chromosomes 15 and 17, written as the addition of all-trans retinoic Blood (2008) 111 (5):
t(15;17), fuses part of the PML gene acid (ATRA), often combined with 2505–2515
with part of the RARα (retinoic acid arsenic trioxide or anthracycline
receptor α) gene. The protein
produced from this fused gene is Prognosis Editorial Team
known as PML-RARα. APL can be aggressive on
Kelly Duffy
presentation but cells are relatively
The RARα gene controls the Mandy Campbell
sensitive to chemotherapy. The Shubham Rastogi
maturation of WBCs which is addition of ATRA and other
blocked in APL targeted therapies gives a >90%
prospect of remission. About us
HORIBA UK Limited
This Month’s Q&A Morphology Tips Kyoto Close
Moulton Park
Northampton, UK
Quick tips for making manual blood films. Problems and NN3 6FL
answers
HORIBA Medical
P Blood film extends right to the end of the slide Parc Euromédecine,
A Blood drop is too large or too small an angle between slide and spreader 390 Rue du Caducée,
34790, France
P Blood film is too short
A Blood drop too small or too large an angle between slide and spreader www.horiba.com/medical

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 sample