Page 201 - Essential Haematology

Chapter 13 Acute myeloid leukaemia / 187

Remission
induction
Consolidation
Relapse
Complete
remission 100
10 12 Bone Severe
marrow
failure Mild
10
Conventional detection level
10 10 5
Detection level by molecular or
immunological techniques
1
Number of leukaemic cells 10 6 4 (chemo±TBI) chemotherapy Resistant disease 0.1 % leukaemic cells in bone marrow
8
10
Maintenance
(biochemical,
(ALL)
anatomical,
biological
SCT
resistance)
0.01
10
10 2 0.001

10 0 0.0001
Time

Figure 13.8 Acute leukaemia: principles of therapy. ALL, acute lymphoblastic leukaemia; SCT, stem cell

transplantation; TBI, total body irradiation.

Induction
e.g. daunorubicin, cytosine arabinoside,
thioguanine or etoposide
An important concept developing in AML
therapy is that of basing the treatment schedule of
Consolidation individual patients on their risk group. Favourable
e.g. daunorubicin, cytosine arabinoside,
thioguanine or etoposide cytogenetics and remission after one course of
chemotherapy both predict for a better prognosis.
In contrast, monosomy 5 or 7 abnormalities, blast
Consolidation cells with the FLT3 internal tandem duplication
e.g. m-AMSA, etoposide, mutation or poorly responsive disease places patients
cytosine arabinoside
into poor risk groups which need more intensive
treatments (Table 13.3 ).
Possible stem cell Further consolidation Monitoring of minimal residual disease during
transplantation, e.g. mitoxantrone, idarubicin,
allogeneic or autologous high dose cytosine and after chemotherapy is being investigated as a
arabinoside, anti-CD33 means to guide appropriate treatment. It may be
antibody
performed by polymerase chain reaction (PCR) or

flow cytometric analysis of the abnormal ‘ leukaemia -

Figure 13.9 Acute myeloid leukaemia: fl ow chart associated immunophenotype ’ that is seen in over
illustrating typical treatment regimen. 90% of cases.