Rapid Progression to Decompensated Cirrhosis, Liver Transplant, and Death in HIV-Infected Men After Primary Hepatitis C Virus Infection

Rapid Progression to Decompensated Cirrhosis, Liver Transplant, and Death in HIV-Infected Men After Primary Hepatitis C Virus Infection
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DOI:
10.1093/cid/cis1206
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发表时间:
2013-04-01
影响因子:
11.8
通讯作者:
Fierer, Joshua
Fierer, Joshua
中科院分区:
医学1区
文献类型:
--
作者:
Fierer, Daniel S.;Dieterich, Douglas T.;Fierer, Joshua

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背景资料。我们和其他人已经证明,在感染人类免疫缺陷病毒(HIV)的男性中,原发性丙型肝炎(HCV)感染会导致早发性肝纤维化;然而,对这些HIV感染男性肝脏疾病的长期自然病史知之甚少。我们在纽约跟踪了一组感染了HIV的男性患者,他们都是原发的丙型肝炎病毒感染者。4名初次感染丙型肝炎病毒后未痊愈的男性在初次感染丙型肝炎病毒后17个月至6年内发展为失代偿性肝硬变。3例在初次感染丙型肝炎病毒后8年内死亡,1例在初次感染丙型肝炎病毒后2年行肝移植后存活。四名男性中有三名在初次感染丙型肝炎病毒时患有艾滋病,病情进展最快的是感染丙型肝炎病毒时CD4计数最低的两名男性。肝脏组织病理学与丙型肝炎病毒诱导的损伤最为一致,尽管有些人暴露于其他潜在的肝毒素。4例HIV感染者中,原发丙型肝炎病毒感染导致失代偿性肝硬变,2-8年内死亡。因此,在艾滋病毒感染者中,由原发丙型肝炎病毒感染引起的快速纤维化不能被认为是良性的。持续进展为肝功能衰竭的速度可能与HIV感染引起的潜在免疫损害的程度成正比。需要更多的研究来更好地确定加速肝损伤背后的机制。
Background. We and others have shown that primary hepatitis C (HCV) infection in men infected with human immunodeficiency virus (HIV) causes early-onset liver fibrosis; however, little is known about the long-term natural history of the liver disease in these HIV-infected men.Methods. We followed a cohort of HIV-infected men with primary HCV infection in New York City.Results. Four men who were not cured after their primary HCV infection developed decompensated cirrhosis within 17 months to 6 years after primary HCV infection. Three died within 8 years of primary HCV infection, and 1 survived after liver transplant done 2 years after primary HCV infection. Three of the 4 men had AIDS at the time of primary HCV infection, and the most rapid progression occurred in the 2 men with the lowest CD4 counts at the time of HCV infection. Liver histopathology was most consistent with HCV-induced damage even though some had exposures to other potential hepatotoxins.Conclusions. Primary HCV infection resulted in decompensated cirrhosis and death within 2-8 years in 4 HIV-infected men. The rapid onset of fibrosis due to primary HCV infection in HIV-infected men cannot therefore be considered benign. The rate of continued progression to liver failure may be proportional to the degree of underlying immunocompromise caused by HIV infection. More research is needed to better define the mechanisms behind accelerated liver damage.