Progression of liver fibrosis in HIV/hepatitis C virus‐coinfected individuals on antiretroviral therapy with early stages of liver fibrosis at baseline

Abstract

Objectives The aim of the study was to assess the progression of liver fibrosis in HIV/hepatitis C virus (HCV)‐coinfected patients with no or mild‐to‐moderate fibrosis (stages F0−F2). Methods Liver fibrosis was reassessed by transient elastometry (TE) between January 2009 and November 2011 in HIV/HCV‐coinfected patients with stage F0−F2 fibrosis in a liver biopsy performed between January 1997 and December 2007. Patients with liver stiffness at the end of follow‐up < 7.1 kPa were defined as nonprogressors, and those with values ≥ 9.5 kPa or who died from liver disease were defined as progressors. Cirrhosis was defined as a cut‐off of 14.6 kPa. The follow‐up period was the time between liver biopsy and TE. Cox regression models adjusted for age, gender and liver fibrosis stage at baseline were applied. Results The median follow‐up time was 7.8 years [interquartile range (IQR) 5.5–10 years]. The study population comprised 162 patients [115 (71%) nonprogressors and 47 (29%) progressors; 19 patients (11.7%) had cirrhosis]. The median time from the diagnosis of HCV infection to the end of follow‐up was 20 years (IQR 16.3–23.1 years). Three progressors died from liver disease (1.8%). The variables associated with a lower risk of progression were age ≤ 38 years (hazard ratio (HR) 0.32; 95% confidence interval (CI) 0.16–0.62; P = 0.001], having received interferon (HR 2.18; 95% CI 1.14–4.15; P = 0.017), being hepatitis B virus surface antigen (HBsAg) negative (HR 0.20; 95% CI 0.04–0.92; P = 0.039), and baseline F0−F1 (HR 0.43; 95% CI 0.28–0.86; P = 0.017). Conclusions A high proportion of patients with stage F0−F2 fibrosis progress to advanced liver fibrosis. Advanced liver fibrosis must be included in the list of diseases associated with aging. Our results support the recommendation to offer HCV antiviral therapy to HIV/HCV‐coinfected patients at early stages of liver fibrosis.

Evaluation of hepatic fibrosis in HIV/HCV Co-infected individuals in Yaoundé, Cameroon: Usefulness of APRI score in resource-constrained settings

“…Subjects in the over-60 age group were the most infected with 63.6% of HIV/HCV co-infected subjects and 66.3% of HCV mono-infected subjects. These gures are different from those found in previous studies which found an average age of 48 [45-51] years old (14) and 38 [35-42] years old (15). Given the silent evolution of HCV infection over several years, these results may be explained by the fact that in our context, screening for HCV infection is not systematic among high-risk such as HIV infected patients.…”

HCV co-infection and markers of liver injury and fibrosis among HIV-positive childbearing women in Ukraine: results from a cohort study

“…Overall, 17% of women were HBV co-infected, increasing to 24% among those HCV-seropositive. Hepatitis B has been associated with more rapid liver fibrosis progression among HIV mono-infected and HIV/HCV co-infected individuals [25, 26] but its role in liver fibrosis progression may be complicated by potential interactions of hepatitis B and/or delta virus with HCV to suppress HCV viremia, or vice versa [27, 28]. HBsAg-positive women were less likely to have significant fibrosis than HBsAg-negative women in adjusted analyses, although this did not reach statistical significance ( p  = 0.085).…”

Hepatic fibrosis and factors associated with liver stiffness in HIV mono-infected individuals

“…Long term antiretroviral and non-antiretroviral medications, HIV induced long term inflammation, metabolic complications and direct cytopathic effects may also contribute to the pathogenesis of liver fibrosis (LF) (Rockstroh et al, 2014). An increasing number of papers have been published on fibrosis in HIV/hepatitis virus co-infected patients (Audsley et al, 2016; Brunet et al, 2016; Costiniuk et al, 2016; Fernández-Montero et al, 2013; Gonzalez et al, 2015; Ioannou et al, 2015; Kliemann et al, 2016; Konerman et al, 2014; Kooij et al, 2016; Li Vecchi et al, 2013; Macías et al, 2013a; Macías et al, 2013b; Njei et al, 2016; Sanmartín et al, 2014; Vergara et al, 2007) but only a few studies have appeared on the analysis of data obtained from HIV mono-infected individuals (Akhtar et al, 2008; DallaPiazza et al, 2010; Han et al, 2013; Lui et al, 2016; Rivero-Juárez et al, 2013; Shur et al, 2016). …”