Hillaire S
Réseau ville-hôpital Val-de-Seine, Suresnes, France.
Rev Med Interne. 2000 May;21(5):467-9. doi: 10.1016/s0248-8663(00)88963-8.
Cholestasis is a clinical, biological and histological syndrome that is secondary to the decrease in or disruption of biliary secretion. Clinical or biological cholestasis is common in the course of either infections (parainfectious cholestasis), various cancers (paraneoplastic cholestasis), granulomatosis or in the syndrome accompanying macrophage activation. Cytokine (IL-1, IL-6 and tumor necrosis factor-alpha [TNF-alpha]) synthesis by Kupffer's cells (intrahepatic macrophages) in response to the release of endotoxins occurs in the course of the various clinical syndromes, particularly in the course of sepsis.
Recently, it has been demonstrated that proinflammatory cytokines and endotoxins lead to cholestasis through modulation of the activity of bile acid transporters and other organic anions.
Cholestasis observed in various clinical syndromes in response to either proinflammatory cytokines or endotoxins might be related to a decrease in the flow which is secondary to a decrease in the activity of organic anion transporters.
胆汁淤积是一种临床、生物学和组织学综合征，继发于胆汁分泌减少或中断。临床或生物学胆汁淤积在感染（感染后胆汁淤积）、各种癌症（副肿瘤性胆汁淤积）、肉芽肿病或巨噬细胞活化伴随的综合征过程中很常见。库普弗细胞（肝内巨噬细胞）响应内毒素释放而合成细胞因子（白细胞介素-1、白细胞介素-6和肿瘤坏死因子-α [TNF-α]）发生在各种临床综合征过程中，尤其是在脓毒症过程中。
最近，已证明促炎细胞因子和内毒素通过调节胆汁酸转运蛋白和其他有机阴离子的活性导致胆汁淤积。
在各种临床综合征中因促炎细胞因子或内毒素而观察到的胆汁淤积可能与有机阴离子转运蛋白活性降低继发的胆汁流动减少有关。
