Marbet U A, Shefer S, Leevy C M
Schweiz Med Wochenschr. 1986 Jul 19;116(29):969-70.
The mechanism of intrahepatic cholestasis in active liver disease has not yet been elucidated. Recent investigations in type II drug-induced hepatitis have suggested that lymphocytes produce a cholestatic factor. The authors' studies on lymphocyte cultures of patients with alcoholic hepatitis and acute viral hepatitis suggest that cellular immune phenomena may be of general significance in the pathogenesis of intrahepatic cholestasis. Supernatants of cultured lymphocytes of patients with alcoholic and acute viral hepatitis reduced bile flow and bile acid excretion in a rat model, provided that the lymphocytes had been previously stimulated by the appropriate antigen. An identical cholestatic effect was seen using sera of these patients. The pathogenetic mechanism of this lymphocytic factor is still unknown.
活动性肝病时肝内胆汁淤积的机制尚未阐明。最近对II型药物性肝炎的研究提示,淋巴细胞可产生一种胆汁淤积因子。作者对酒精性肝炎和急性病毒性肝炎患者淋巴细胞培养的研究表明,细胞免疫现象在肝内胆汁淤积的发病机制中可能具有普遍意义。酒精性肝炎和急性病毒性肝炎患者培养淋巴细胞的上清液,在大鼠模型中可使胆汁流量和胆汁酸排泄减少,前提是淋巴细胞此前已受到适当抗原的刺激。使用这些患者的血清也观察到了相同的胆汁淤积效应。这种淋巴细胞因子的发病机制仍然未知。