Page 380 - Textbook of Pathology, 6th Edition

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Figure 14.14 PBF findings in a case of acute myeloblastic leukaemia (AML).
SECTION II
when the marrow is so much filled with leukaemic cells 2. Sudan Black: Positive in immature cells in AML.
that they cannot be aspirated because the cells are adhesive 3. Periodic acid-Schiff (PAS): Positive in immature
and enmeshed in reticulin fibres. In such cases, trephine lymphoid cells and in erythroleukaemia (M6).
biopsy should be done. 4. Non-specific esterase (NSE): Positive in monocytic
2. Leukaemic cells. The bone marrow is generally tightly series (M4 and M5).
packed with leukaemic blast cells. The diagnosis of the 5. Acid phosphatase: Focal positivity in leukaemic blasts
type of leukaemic cells, according to FAB classification, is in ALL and diffuse reaction in monocytic cells (M4 and
generally possible with routine Romanowsky stains but M5).
cytochemical stains may be employed as an adjunct to
Romanowsky staining for determining the type of IV. BIOCHEMICAL INVESTIGATIONS. These may be
leukaemia. The essential criteria for diagnosis of AML, as of some help:
per FAB classification, was the presence of at least 30% 1. Serum muramidase. Serum levels of lysozyme (i.e.
blasts in the bone marrow. However, as per WHO muramidase) are elevated in myelomonocytic (M4) and
classification, these criteria have been revised and lowered monocytic (M5) leukaemias.
to 20% blasts in the marrow for labelling and treating a 2. Serum uric acid. Because of rapidly growing number
case as AML. of leukaemic cells, serum uric acid level is frequently
3. Erythropoiesis. Erythropoietic cells are reduced. increased. The levels are further raised after treatment
Dyserythropoiesis, megaloblastic features and ring with cytotoxic drugs because of increased cell breakdown.
sideroblasts are commonly present.
4. Megakaryocytes. They are usually reduced or absent.
5. Cytogenetics. Chromosomal analysis of dividing leuka- Treatment and Complications
Haematology and Lymphoreticular Tissues
emic cells in the marrow shows karyotypic abnormalities The management of acute leukaemia involves the following
in 75% of cases which may have a relationship to aspects:
prognosis. WHO classification emphasises on the
categorisation of AML on the basis of cytogenetic I. TREATMENT OF ANAEMIA AND HAEMORRHAGE.
abnormalities. Two of the most consistent cytogenetic Anaemia and haemorrhage are managed by fresh blood
abnormalities in specific FAB groups are as under: transfusions and platelet concentrates. Patients with severe
i) M3 cases have t(15;17)(q22;q12). thrombocytopenia (platelet count below 20,000/μl) require
regular platelet transfusions since haemorrhage is an
ii) M4E0 (E for abnormal eosinophils in the bone marrow) important cause of death in these cases.
cases have inv(16)(p13q22).
6. Immunophenotyping. AML cells express CD13 and II. TREATMENT AND PROPHYLAXIS OF INFECTION.
CD33 antigens. M7 shows CD41 and CD42 positivity. Neutropenia due to bone marrow replacement by leukaemic
blasts and as a result of intensive cytotoxic therapy renders
III. CYTOCHEMISTRY. Some of the commonly emplo- these patients highly susceptible to infection. The infections
yed cytochemical stains, as an aid to classify the type of are predominantly bacterial but viral, fungal, and protozoal
AML are as under (also see Table 14.5): infections also occur. For prophylaxis against infection in
1. Myeloperoxidase: Positive in immature myeloid cells such cases, the patient should be isolated and preferably
containing granules and Auer rods but negative in M0 placed in laminar airflow rooms. Efforts are made to reduce
myeloblasts. the gut and other commensal flora which are the usual source