Bierhoff E, Fischer H P, Pfeifer U, Rockstroh J, Spengler U
Pathologisches Institut, Rheinischen Friedrich-Wilhelms-Universität Bonn.
Verh Dtsch Ges Pathol. 1995;79:249-53.
Liver biopsy (n = 35) and autopsy (n = 71) specimens from HIV infected HCV-positive and HCV-negative haemophiliacs and non-haemophiliacs and liver biopsies (n = 33) from HIV-negative HCV-infected haemophiliacs and non-haemophiliacs were studied by histo- and immunohistochemistry to investigate the influence of HIV-coinfection on chronic C hepatitis (> 10 years duration). Almost all HIV-infected patients had a CD4 cell counts < 200/microns3. In biopsies and autopsies HCV-infection lead to stronger portal, periportal and lobular inflammatory changes independent from HIV-infection and haemophilia. However, HIV-infected patients with HCV-coinfection showed much more granulocytic infiltrates, particularly in the small bile ducts. In biopsies and autopsies HCV infection was associated with a stronger (centrilobular) fibrosis, particularly in HIV-positive haemophiliacs, and significantly stronger compared to HCV-negative patients. In the autopsy group half of the HIV-infected and HCV-positive haemophiliacs (n = 20) had developed posthepatitic liver cirrhosis due to C hepatitis, contrasted by two liver cirrhosis in HCV-infected non-haemophiliacs (n = 6) due to chronic B and C hepatitis and chronic alcohol abuse; no liver cirrhosis was observed in HIV-positive HCV-negative non-haemophiliacs (n = 45). Cholestasis and mild granulocytic cholangiolitis was a predominant feature in HIV/HCV-coinfection and similar distributed in haemophiliacs and non-haemophiliacs. The findings are suggestive that HIV-coinfection aggravates the course of a preceding hepatitis C virus infection, by a more granulocytic inflammatory infiltrate, stronger (centrilobular) fibrosis followed by a high incidence of posthepatitic cirrhosis--particularly in multitransfused haemophiliacs--and by cholestatic hepatopathy.
对来自感染HIV的丙型肝炎病毒阳性和阴性的血友病患者及非血友病患者的肝活检标本（n = 35）和尸检标本（n = 71），以及来自未感染HIV的丙型肝炎病毒感染的血友病患者及非血友病患者的肝活检标本（n = 33）进行了组织学和免疫组织化学研究，以调查合并感染HIV对慢性丙型肝炎（病程> 10年）的影响。几乎所有感染HIV的患者CD4细胞计数均<200/立方毫米。在活检和尸检中，丙型肝炎病毒感染导致更强的门静脉、汇管区和小叶炎症变化，这与HIV感染和血友病无关。然而，合并感染丙型肝炎病毒的HIV感染患者显示出更多的粒细胞浸润，特别是在小胆管中。在活检和尸检中，丙型肝炎病毒感染与更强的（小叶中央型）纤维化相关，特别是在HIV阳性的血友病患者中，并且与丙型肝炎病毒阴性患者相比明显更强。在尸检组中，一半感染HIV且丙型肝炎病毒阳性的血友病患者（n = 20）因丙型肝炎发展为肝炎后肝硬化，相比之下，6例丙型肝炎病毒感染的非血友病患者因慢性乙型和丙型肝炎及慢性酒精滥用而出现2例肝硬化；在HIV阳性、丙型肝炎病毒阴性的非血友病患者（n = 45）中未观察到肝硬化。胆汁淤积和轻度粒细胞性胆管炎是HIV/丙型肝炎病毒合并感染的主要特征，在血友病患者和非血友病患者中分布相似。这些发现提示，合并感染HIV会加重先前丙型肝炎病毒感染的病程，表现为更多的粒细胞炎性浸润、更强的（小叶中央型）纤维化，继而肝炎后肝硬化的发生率较高——特别是在多次输血的血友病患者中——以及胆汁淤积性肝病。
