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再生障碍性贫血(aplastic anemia,AA)是由于T淋巴细胞功能亢进攻击造血干/祖细胞而导致的造血功能衰竭症[1]。胎肝在人胚第6周即开始造血,至第4~5个月达到高峰,并被骨髓造血逐渐替代,因此肝脏细胞与造血细胞存在一定交叉抗原,而临床上也常发现肝炎相关性AA,主要由血清学阴性的肝炎所致,基本发生在肝炎后肝功能恢复期,偶有报道是继发于甲、乙或丙型肝炎病毒感染后。临床中,多数情况下是AA合并或者并发慢性
Aplastic anemia (AA) is a disorder of hematopoietic failure caused by attack of hematopoietic stem / progenitor cells by hyperthyroidism of T lymphocytes [1]. The fetal liver begins to hematopoietic in the sixth week of human embryo, reaches the peak in the fourth to the fifth month and is gradually replaced by the bone marrow hematopoietic. Therefore, the liver cells and the hematopoietic cells have some cross-antigens, but hepatitis-related AA , Mainly due to seronegative hepatitis, basically occurs in the recovery of liver function after hepatitis, occasionally reported secondary to hepatitis A, B or hepatitis C virus infection. Clinically, in most cases is AA merger or complicated by chronic