Abstract
(1) Background: Direct-acting antiviral therapy for chronic hepatitis C virus (HCV) infection is associated with high sustained virologic response (SVR) and overcomes negative predictive factors, including steatosis, in patients without human immunodeficiency virus (HIV) coinfection. The impact of steatosis on SVR in patients with HIV–HCV coinfection is unknown. (2) Methods: A retrospective analysis of patients treated with direct-acting antivirals was performed. Demographic, laboratory and direct-acting antiviral regimen data were prospectively collected. Metabolic syndrome and its components—diabetes mellitus, hypertension, dyslipidemia and obesity—were assessed. Hepatic steatosis (≥5%) was defined by liver biopsy or controlled attenuation parameter (CAP) measurement during vibration-controlled transient elastography (VCTE). (3) Results: A total of 151 HIV–HCV-coinfected patients on combined antiretroviral therapy and direct-acting antiviral therapy were included in this analysis. Prevalence of steatosis by liver biopsy (n = 34) or CAP (≥263 db/m) during VCTE (n = 92) was 27% and was independently associated with obesity (OR 3.11; 95% CI 1.43–6.82; p = 0.004) and the metabolic syndrome (OR 1.08; 95% CI 1.01–0.15; p = 0.01). The overall SVR rate (n = 148) was 95% and was not impacted by the presence of steatosis (p = 0.42). (4) Conclusions: Hepatic steatosis is common in HIV–HCV coinfection, correlates with obesity and the metabolic syndrome and does not impact SVR.
Highlights
Hepatic steatosis is common in patients living with human immunodeficiency virus (HIV), including those coinfected with chronic hepatitis C virus (HCV) [1,2]
Coinfection [1] and 40%–86% of those with chronic HCV without HIV [6]. Similar to those without HIV, the development of steatosis in patients with HIV is often secondary to the presence of the metabolic syndrome and its components, HIV-related lipodystrophy, microbial dysbiosis and mitochondrial damage leading to insulin resistance and dyslipidemia [7,8,9]
One hundred and fifty one HIV–HCV-coinfected patients on cART and direct-acting antiviral (DAA) were included in this analysis (Table 1)
Summary
Hepatic steatosis is common in patients living with human immunodeficiency virus (HIV), including those coinfected with chronic hepatitis C virus (HCV) [1,2]. In studies of HIV patients at risk for steatosis (e.g., increased liver enzymes) without HCV using liver histology as reference standard, steatosis was detected in 60%–69% [2,3,4,5] compared to 23%–75% of those with HIV–HCV coinfection [1] and 40%–86% of those with chronic HCV without HIV [6] Similar to those without HIV, the development of steatosis in patients with HIV is often secondary to the presence of the metabolic syndrome and its components (diabetes, obesity, hypertension, and dyslipidemia), HIV-related lipodystrophy, microbial dysbiosis and mitochondrial damage leading to insulin resistance and dyslipidemia [7,8,9]. It is plausible that via increased insulin resistance, the presence of diabetes is associated with steatosis; interestingly, this association was not found in this cohort
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