Hagler L, Pastore R A, Bergin J J, Wrensch M R
Medicine (Baltimore). 1975 Mar;54(2):139-64.
Within recent years the combination of aplastic anemia following viral hepatitis has been reported with increasing frequency suggesting the existence of a causal relationship between the two conditions. Two case histories of aplastic anemia following hepatitis are presented in detail, and the information on 193 such patients reported in the literature through 1972 is summarized. A number of parameters were evaluated and extensive cross correlation carried out in order to define criteria which might have diagnostic, prognostic or therapeutic value. Males were more likely to develop bone marrow failure following hepatitis (p congruent to 0.05), but females were less likely to survive the marrow depression (p smaller than 0.025). No other statistically identifiable criteria were detected. The hematologic changes commonly encountered in hepatitis are reviewed. These and other observations support the concept that subclinical hepatitis may be responsible for a significant percentage of so-called idiopathic aplastic anemia, for which, at present, no etiology can be determined in nearly half the cases. Possible pathogenetic mechanisms are discussed as they might relate to chromosomal abnormalities which were found in one of our patients. It is suggested that occasional fortuitious human infection with animal viruses known to be both hepato- and myelotoxic could relate the hepatitis and aplasia.
近年来，病毒性肝炎后再生障碍性贫血的合并病例报告频率日益增加，提示这两种情况之间存在因果关系。本文详细介绍了两例肝炎后再生障碍性贫血的病例史，并总结了截至1972年文献中报道的193例此类患者的信息。为了确定可能具有诊断、预后或治疗价值的标准，对一些参数进行了评估并进行了广泛的交叉关联分析。男性在肝炎后更易发生骨髓衰竭（p约等于0.05），但女性在骨髓抑制期存活的可能性较小（p小于0.025）。未检测到其他具有统计学意义的可识别标准。本文回顾了肝炎中常见的血液学变化。这些观察结果以及其他观察结果支持以下观点：亚临床型肝炎可能是相当一部分所谓特发性再生障碍性贫血的病因，目前在近半数病例中无法确定其病因。文中讨论了可能的发病机制，这些机制可能与我们其中一位患者发现的染色体异常有关。有人提出，偶尔因偶然感染已知对肝脏和骨髓均有毒性的动物病毒，可能将肝炎与再生障碍联系起来。
