Virginia Commonwealth University Health System, Richmond, USA.
Clin Gastroenterol Hepatol. 2010 Dec;8(12):1070-6. doi: 10.1016/j.cgh.2010.08.004. Epub 2010 Aug 20.
BACKGROUND & AIMS: Fibrosis progression might be accelerated in patients who are coinfected with human immunodeficiency virus (HIV) and HCV (HIV/HCV). However, no studies have directly compared fibrosis progression by paired liver biopsy between patients infected with HIV and HCV versus those infected with only HCV.
Liver biopsy samples were collected from patients with HIV/HCV (n = 306) and those with HCV; biopsies from 59 without a sustained virologic response (SVR) or cirrhosis were matched with those from patients with only HCV (controls) for initial fibrosis stage, demographics, and HCV treatment. For HIV/HCV patients, categorical variables at baseline and the area under the curve of continuous variables per unit time were analyzed for associations with fibrosis progression.
Liver biopsies from HIV/HCV patients had more piecemeal necrosis than controls (P = .001) and increased lobular inflammation (P = .002); HIV/HCV patients also had shorter intervals between liver biopsies (4.7 vs 5.9 years, P < .0001). Between the first and second biopsies, fibrosis remained unchanged or progressed 1 or 2 units in 55%, 18%, and 18% of HIV/HCV patients, respectively, compared with 45%, 30%, and 9% of controls. The fibrosis progression rate was similar between HIV/HCV and control patients (0.12 ± 0.40 vs 0.091 ± 0.29 units/y; P = .72). In paired biopsies from 66 patients, including those with SVR, there were no associations between fibrosis progression and demographics; numbers of CD4+ T cells; levels of aspartate aminotransferase or alanine aminotransferase; use of highly active antiretroviral therapy; response to HCV therapy (no treatment, SVR, or non-response); baseline levels of FIB-4; or histologic features including inflammation, fibrosis, or steatosis.
On the basis of analysis of liver biopsy samples, fibrosis progression was similar between HIV/HCV-infected and HCV-infected patients; no clinical or laboratory parameters predicted disease progression.
人类免疫缺陷病毒(HIV)和丙型肝炎病毒(HCV)合并感染可能会加速纤维化进展。然而,尚无研究直接比较 HIV/HCV 感染患者与单纯 HCV 感染患者的肝活检纤维化进展情况。
收集 HIV/HCV(n=306)感染患者和单纯 HCV 感染患者的肝活检样本,对 59 例未获得持续病毒学应答(SVR)或肝硬化的患者进行配对,根据初始纤维化分期、人口统计学和 HCV 治疗情况与单纯 HCV 感染患者(对照组)的肝活检样本进行配对。对于 HIV/HCV 感染患者,采用分类变量和单位时间内连续变量的曲线下面积来分析纤维化进展的相关性。
与对照组相比,HIV/HCV 感染患者的肝活检标本中碎片状坏死更多(P=0.001),汇管区炎症更重(P=0.002);HIV/HCV 感染患者肝活检的间隔时间也更短(4.7 年 vs 5.9 年,P<0.0001)。在第一次和第二次肝活检之间,55%、18%和 18%的 HIV/HCV 感染患者的纤维化保持不变或进展 1 或 2 个单位,而对照组的比例分别为 45%、30%和 9%。HIV/HCV 感染患者和对照组患者的纤维化进展率相似(0.12±0.40 单位/y vs 0.091±0.29 单位/y;P=0.72)。在 66 例包括 SVR 患者的配对肝活检标本中,纤维化进展与人口统计学特征、CD4+T 细胞数量、天门冬氨酸氨基转移酶或丙氨酸氨基转移酶水平、是否使用高效抗逆转录病毒治疗、HCV 治疗应答(无治疗、SVR、无应答)、基线 FIB-4 水平以及炎症、纤维化或脂肪变性等组织学特征均无相关性。
基于肝活检样本分析,HIV/HCV 感染患者和单纯 HCV 感染患者的纤维化进展情况相似;无临床或实验室参数可预测疾病进展。