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As Dr Marsh and her colleagues point out, there is growing evidence of intrinsic abnormality in the haematopoietic progenitor cell function at least in some of the patients and this is reflected in our experience that included atypical blast colony formation over pre-formed stroma, decreased adhesiveness and impaired response to recombinant growth factors. It is therefore not surprising that the mature blood elements may be quantitatively abnormal in this disease (De Planque et a/. 1989). Although our own data is still inconclusive, a hypothesis could be proposed that in some cases of aplastic anaemia the haematopoietic defect may be present before the onset of the pancytopenia which is the result of an immunologically mediated surveillance mechanism mounted to suppress the abnormal haematopoiesis. Biological immune response modulation, with antilymphocyte globulin, leads to an improvement in the peripheral blood count values as well as in marrow cellularity but is unlikely to correct the underlying defect.
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Guinot et al. (1991) studied this question.
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