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486 Chapter 12: Haematology and clinical immunology
and intramuscular L-asparginase. Phase 2 involves in-
travenous chemotherapy (cyclophosphamide and cy-
tosine) with oral 6-mercaptopurine.
Lymphoid Stem Cell Intensification: This involves intravenous metho-
trexate and folinic acid, with intramuscular L-
asparginase.
Lymphoblast
Consolidation: This involves several cycles of
chemotherapy at lower doses.
Maintenance: Therapy consists of 18 months of oral
cytotoxic therapy with intravenous vincristine given
Early T Cell Pre B Cell every 3 months.
CNS treatment involves a combination of intrathecal
methotrexate and cytosine and cranial irradiation.
Supportive treatment: Cytotoxic therapy and the
leukaemia itself depresses normal bone marrow func-
tion and causes a pancytopenia with resulting infection,
T Cell B Cell
anaemia and bleeding. Supportive therapy includes red
Figure 12.10 Lymphocyte development. cell concentrates, platelet transfusions, broad-spectrum
antibiotics and prophylaxis for pneumocystic pneumo-
nia.
papilloedema, cranial nerve palsies, testicular enlarge-
The role of early bone marrow and haemopoetic stem
ment and occasionally superior vena caval obstruction.
cell transplantation is currently under investigation.
Microscopy Prognosis
The normal marrow is replaced by abnormal Prognosisisrelatedtoage,subtypeandinverselypropor-
monotonous leukaemic cells of the lymphoid cell line. tionaltotheperipheralblastcount.Over90%ofchildren
The leukaemia is typed by cytochemical staining and respond to treatment, the rarer cases occurring in adults
monoclonal antibodies to look for cell surface mark- carry a worse prognosis.
ers. The FAB (French/American/British) classification is
based on morphology (FAB L1- homogenous popula-
tion of small cells, FAB L2 heterogeneous population Acute myeloid leukaemia
of cells, FAB L3 rare, cells similar to those in Burkitt’s Definition
lymphoma). Malignant expansion of cells from the myeloid cell line.
Investigations Age
Lymphoblasts are seen in a peripheral blood film. Full Most common in the middle aged and elderly
blood count shows a low haemoglobin, variable white
count,lowplateletcount.Bonemarrowaspirationshows Sex
increased cellularity with a high percentage of blast cells. M = F
Bone marrow cytogenetics and immunophenotyping is
used to type the ALL and look for prognostic indicators. Aetiology
Aetiology is largely unknown although previous expo-
Management sure to radiation, benzene or chemotherapy are known
The current treatment protocol is UKALL-12. Which to be precipitating factors.
consists of: FABsub classification (see Fig. 12.11)
Induction: Phase 1 involves intravenous chemother- M0 Undifferentiated myeloblasts
apy (daunorubicin and vincristine) oral prednisolone M1 Myelocytic leukaemia without differentiation