Wickramasinghe S N, Illum N, Wimberley P D
Department of Haematology, St Mary's Hospital Medical School, London.
Br J Haematol. 1991 Oct;79(2):322-30. doi: 10.1111/j.1365-2141.1991.tb04541.x.
A hitherto undescribed form of congenital dyserythropoietic anaemia is reported. The patient was severely anaemic and hydropic at birth and is now 8 years old. She has a moderate normochromic normocytic anaemia. HbF level of 50%, reticulocyte count of 5-12% and hyperbilirubinaemia. Bone marrow smears showed intense normoblastic erythroid hyperplasia with morphological evidence of dyserythropoiesis; the most common dysplastic features were basophilic stippling of polychromatic erythroblasts and erythrocytes and marked abnormalities of nuclear shape in polychromatic erythroblasts. Electron microscope studies showed that some polychromatic erythroblasts and several erythrocytes contained inclusions which were rounded, elongated or irregular in outline or were doughnut-shaped. These inclusions consisted of compact masses of tubules and saccules which may represent smooth endoplastic reticulum together with Golgi cisternae. The ultrastructural studies also revealed peculiar membrane-bound cylindrical structures in a rare late erythroblast, and phagocytosed erythroblasts within some macrophages. The technique of combined Feulgen microspectrophotometry and 3H-thymidine autoradiography demonstrated a pile-up of early polychromatic erythroblasts in the G1 and G2 phases of the cell cycle, indicating a prolongation of, or an arrest at, these phases. Furthermore, nearly a quarter of all erythroblasts failed to incorporate 3H-leucine into protein. Thus the anaemia appeared to be due to a combination of disordered erythroblast function, increased ineffectiveness of erythropoiesis and peripheral haemolysis. The primary defect may be an excessive synthesis or impaired degradation of intracytoplasmic membranes.
报告了一种迄今未被描述的先天性红细胞生成异常性贫血。该患者出生时严重贫血且全身水肿,现8岁。她患有中度正色素正细胞性贫血。HbF水平为50%,网织红细胞计数为5 - 12%,并有高胆红素血症。骨髓涂片显示有核红细胞呈强烈的增生,并有红细胞生成异常的形态学证据;最常见的发育异常特征是多染性成红细胞和红细胞的嗜碱性点彩,以及多染性成红细胞的核形状明显异常。电子显微镜研究显示,一些多染性成红细胞和几个红细胞含有内含物,其轮廓呈圆形、细长形或不规则形,或呈环形。这些内含物由紧密排列的小管和囊泡组成,可能代表滑面内质网和高尔基体池。超微结构研究还在一个罕见的晚期成红细胞中发现了特殊的膜结合圆柱形结构,以及一些巨噬细胞内吞噬的成红细胞。联合福尔根显微分光光度法和3H - 胸腺嘧啶核苷放射自显影技术表明,早期多染性成红细胞在细胞周期的G1期和G2期堆积,表明这些阶段延长或停滞。此外,几乎四分之一的成红细胞未能将3H - 亮氨酸掺入蛋白质中。因此,贫血似乎是由于成红细胞功能紊乱、红细胞生成无效性增加和外周溶血共同作用所致。原发性缺陷可能是细胞质膜合成过多或降解受损。