Thiele J, Hoffmann I, Bertsch H P, Fischer R
Institute of Pathology, University of Cologne, Germany.
Virchows Arch A Pathol Anat Histopathol. 1993;423(1):33-8. doi: 10.1007/BF01606429.
An immunohistochemical and morphometric analysis was performed on bone marrow trephine biopsies in 40 patients with primary myelodysplastic syndromes (MDS) to evaluate the proliferative activity in erythropoiesis and the endoreduplicative capacity of megakaryocytes. Control groups included normal bone marrow and marrow from cases presenting with pernicious anaemia. Double-immunostaining was applied with a monoclonal antibody (PC10) directed against proliferating cell nuclear antigen (PCNA), followed by antibodies against glycophorin C (Ret40f) or platelet glycoprotein IIIa (Y2/51-CD61) for the identification of the erythroid and megakaryocytic cell lineage. Comparison with normal bone marrow showed a reduction of erythropoiesis accompanied by an increase in atypical (micro-) megakaryocytes. Erythroid precursors displayed significant enhancement of PCNA-immunostaining. Megakaryocytes showed no increase in the relative frequency of PC10-positive cells (PCNA-labelling index). In pernicious anaemia, predominance of macrocytic-megaloblastoid erythropoiesis was associated with a striking increase in PCNA-labelling. Cell kinetic studies in this disorder revealed an abnormal arrest, particularly in S-phase which generates an over-expression of PCNA. Similar conditions were believed to be present in MDS with secondary folate deficiency. This mechanism explains the relatively high rate of positively-reacting pro- and erythroblasts which is not invariably accompanied by an increase in cell proliferation. Determination of megakaryocyte size and PCNA-staining capacity resulted in a significant increase in PC10-positive cells among micromegakaryocytes. Our findings on this cell lineage are in keeping with the assumption of a block in endoreduplicative activity at higher ploidy levels, associated with an apparently not-deregulated endomitosis in small-sized megakaryocytes of lower ploidy stages.
对40例原发性骨髓增生异常综合征(MDS)患者的骨髓环钻活检组织进行了免疫组织化学和形态计量分析,以评估红细胞生成的增殖活性和巨核细胞的核内复制能力。对照组包括正常骨髓和恶性贫血患者的骨髓。采用针对增殖细胞核抗原(PCNA)的单克隆抗体(PC10)进行双重免疫染色,随后使用抗血型糖蛋白C(Ret40f)或血小板糖蛋白IIIa(Y2/51-CD61)抗体来鉴定红系和巨核细胞系。与正常骨髓相比,红细胞生成减少,同时非典型(微)巨核细胞增多。红系前体细胞的PCNA免疫染色显著增强。巨核细胞中PC10阳性细胞的相对频率(PCNA标记指数)没有增加。在恶性贫血中,大细胞-巨幼样红细胞生成占优势与PCNA标记的显著增加有关。该疾病的细胞动力学研究显示存在异常停滞,尤其是在产生PCNA过表达的S期。MDS伴继发性叶酸缺乏时也被认为存在类似情况。这一机制解释了原幼红细胞和幼红细胞阳性反应率相对较高的现象,而这并不总是伴随着细胞增殖的增加。巨核细胞大小和PCNA染色能力的测定结果显示,微巨核细胞中PC10阳性细胞显著增加。我们对该细胞系的研究结果与以下假设一致:在较高倍体水平时核内复制活性受阻,而在较低倍体阶段的小巨核细胞中,核内有丝分裂明显未失调。