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      AIDS-related bone marrow lesions--myelodysplastic features or predominant inflammatory-reactive changes (HIV-myelopathy)? A comparative morphometric study by immunohistochemistry with special emphasis on apoptosis and PCNA-labeling.

      Analytical cellular pathology : the journal of the European Society for Analytical Cellular Pathology
      Acquired Immunodeficiency Syndrome, complications, immunology, pathology, Adult, Apoptosis, Biopsy, Needle, Bone Marrow, chemistry, Cell Division, Diagnosis, Differential, Female, Hematopoiesis, Humans, Immunohistochemistry, Male, Myelitis, diagnosis, etiology, Myelodysplastic Syndromes, Proliferating Cell Nuclear Antigen, analysis, Stromal Cells, virology

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          Abstract

          There seems to be general agreement that AIDS-related bone marrow changes are consistent with myelodysplastic features. To re-evaluate this assumption more critically, a comparative study was performed on marrow smears and trephine biopsies in 20 patients presenting manifest stages of AIDS and in 30 patients with primary myelodysplastic syndromes (MDS). For an assessment of cytological atypias enzyme-(naphthol AS-D-chloroacetatesterase) and immuno-histochemical techniques including monoclonal antibodies directed against erythro-(Ret40f) and megakaryopoiesis (CD61), macrophages (PG-M1) and proliferating cell nuclear antigen-PCNA (PC10) were applied and staining results determined by morphometric analysis. The in situ end-labeling (ISEL) technique was used for the demonstration of cells undergoing apoptosis (programmed cell death). In the HIV-infected bone marrow the frequency of erythroid precursors and macrophages exceeded significantly the corresponding counts in MDS. In comparison with a control group, megakaryocytes were increased in both entities under study. However, MDS was characterized by a prevalence of atypical microforms. The small-sized megakaryocytes in MDS revealed striking abnormalities of nuclear-cytoplasmic organization. Severe defects of nuclear lobulation (pseudo-Pelger anomalies) of mature neutrophils or nuclear bridging of erythro-normoblasts were not conspicuous in AIDS. Whereas the incidence of apoptosis was significantly higher in MDS, no such differences could be found comparing the PCNA-labeling index of AIDS and MDS. On the other hand, both parameters were significantly increased in comparison with the controls. In the HIV-infected bone marrow alterations of the myeloid stroma were most prominently expressed. If well defined criteria for the diagnosis of (myelo-) dysplasia were applied, our findings in AIDS were not in keeping with the assumption of significant maturation defects comparable with MDS. Hence, bone marrow lessions accompanying AIDS should be separated from MDS and should be diagnosed as HIV-myelopathy.

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