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The value of bone marrow biopsy in chronic myeloid leukaemia
Insights
This study differentiates chronic myeloid leukaemia (CML) subtypes, chronic granulocytic leukaemia (CGL) and chronic megakaryocytic granulocytic myelosis (CMGM), using clinical and bone marrow criteria. Distinguishing classical from atypical CML aids in understanding disease progression and Philadelphia chromosome presence.
Area of Science:
- Hematology
- Oncology
- Pathology
Background:
- Chronic myeloid leukaemia (CML) presents diagnostic challenges.
- Subclassification of CML is crucial for understanding disease heterogeneity.
Purpose of the Study:
- To differentiate between chronic granulocytic leukaemia (CGL) and chronic megakaryocytic granulocytic myelosis (CMGM) in CML patients.
- To identify reliable criteria for distinguishing classical CML from atypical myelosis.
- To investigate the correlation between CML subtypes, fibrosis, and Philadelphia chromosome presence.
Main Methods:
- Core biopsy analysis to classify CML patients into CGL and CMGM.
- Clinical assessment including ALP-Index, peripheral leukocyte and platelet counts, and bone marrow megakaryocyte estimation.
- Evaluation of fibrosis in bone marrow biopsies.
- Philadelphia chromosome detection in classical and atypical CML cases.
Main Results:
- Seventy-six CML patients were classified into CGL (n=24) and CMGM (n=52).
- Classical CML comprised 40% CGL and 60% CMGM; atypical myelosis consisted solely of CMGM with fibrosis.
- Fibrosis was present in 20% of classical CML and 50% of atypical myeloses.
- Philadelphia chromosome was detected in all CGL and 50% of myelofibrotic classical CML, but absent in atypical myeloses.
- Peripheral blood and bone marrow cytology distinguished CGL from CMGM in 70% of cases.
Conclusions:
- Clinical and bone marrow criteria effectively subdivide CML into CGL and CMGM.
- Distinguishing classical from atypical CML is possible using specific hematological and cytological parameters.
- Atypical myeloses, characterized by CMGM and fibrosis, lack the Philadelphia chromosome, suggesting distinct pathogenetic mechanisms.
Abstract:
Seventy-six patients with chronic myeloid leukaemia (CML) could be subdivided by core biopsy into chronic granulocytic leukaemia (CGL, n = 24) and chronic megakaryocytic granulocytic myelosis (CMGM, n = 52). By pure clinical definition 59 patients were grouped as classical CML and 17 showed a course which we termed atypical myelosis. The most reliable criteria for distinguishing between the classical and atypical forms were ALP-Index, peripheral leukocyte and platelet count and the estimated number of megakaryocytes in the bone marrow. The classical myeloses consisted of 40 per cent CGL and 60 per cent CMGM whereas the atypical consisted of CMGM only including all stages of fibrosis. Fibrosis was at the time of bone marrow biopsy found in 20 per cent of classical CML and in about 50 per cent of atypical myeloses. In classical CML Philadelphia chromosome could be detected in all the patients with CGL and in 50 per cent of those with myelofibrosis. Atypical myeloses did not exhibit Philadelphia chromosome. In 70 per cent of the cases it was possible to distinguish between CGL and CMGM by peripheral blood findings and bone marrow cytology.