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Hepatic steatosis worsens faster in HIV mono-infection than HIV/HCV

Hepatic steatosis progressed faster and was more often associated with liber fibrosis progression among patients with HIV mono-infection compared with patients with HIV/hepatitis C coinfection, according to recently published data from an ongoing cohort study.

“We have initiated the LIVEr disease in HIV (LIVEHIV) Cohort ... to characterize the epidemiology, dynamics and the effect on liver fibrosis of [hepatic steatosis] in HIV-infected adults undergoing a routine screening program with [transient elastography] and associated [controlled attenuation parameter (CAP)],” the researchers wrote.

The LIVEHIV Cohort study, established in September 2013, comprises 1,173 patients as of September 2016. After initial exclusion criteria, the researchers analyzed the data of 726 patients with at least one transient elastography for cofactors of hepatic steatosis and liver fibrosis. Additionally, 313 of the 726 had more than one transient elastography and were analyzed for incidence and predictors of hepatic steatosis and liver fibrosis.

There were 105 patients with HIV/HCV coinfection with HCV RNA and 30 with HCV genotype 3. Overall, 208 patients abstained from alcohol consumption, 359 had low alcohol intake and 159 had moderate alcohol intake. Most patients were on antiretroviral therapy (92%).

Among the 726 with at least one transient elastography, 264 had any grade of hepatic steatosis and 212 had liver fibrosis. There were no significant differences in prevalence of hepatic steatosis grade or severe hepatic steatosis between the patients with HIV mono-infection and patients with HIV/HCV coinfection.

Independent cofactors of significant liver fibrosis included higher BMI (OR = 1.03; 95% CI, 0.99-1.06), HCV coinfection (OR = 8.01; 95% CI, 5.46-11.76), longer time since HIV diagnosis per 10 years (OR = 1.89; 95% CI, 1.52-2.36), detectable HIV viral load (OR = 0.98; 95% CI, 0.68-1.42), higher alanine aminotransferase (OR = 1.32; 95% CI, 1.23-1.41) and higher triglycerides (OR = 1.24; 95% CI, 1.1-1.41).

Regarding the 313 patients with more than one transient elastography, researchers excluded from analysis 81 for having hepatic steatosis at baseline. Among the remaining 232, 97 had hepatic steatosis progression with an incidence rate of 29.7 per 100 person years (95% CI, 24.2-36.5). There was also a higher rate of hepatic steatosis progression among patients with HIV mono-infection (37.8 per 100 person-years; 95% CI 29.2-49) compared with patients with HIV/HCV coinfection (21.9 per 100 person-years; 95% CI 15.6-30.7).

After excluding from analysis those with cirrhosis at baseline, 274 patients with more than one transient elastography remained. Of those, 53 had fibrosis progression with an incidence rate of 12.7 per 100 person-years (95% CI, 9.5-17.1). Patients with HIV mono-infection had higher rates of fibrosis progression if they had any grade of hepatic steatosis (20.4 per 100 person-years; 95% CI, 13.2-31.6) compared with patients without hepatic steatosis (5.8 per 100 person-years; 95% CI 2.6-13).

Data showed an association between fibrosis progression and both longer time since HIV diagnosis (HR = 1.52; 95% CI, 1.29-1.78) and any grade of hepatic steatosis at baseline (HR = 3.9; 95% CI, 1.62-9.37) in patients with HIV mono-infection. In patients with HIV/HCV coinfection, fibrosis progression was associated with detectable HCV RNA (HR = 11.3; 95% CI, 2.51-50.8) and higher ALT (HR = 1.01; 95% CI, 1-1.01).

“[These data underscore] the importance of following the evolution of a liver disease over time that fosters evaluation of incidence, dynamics and predictors, rather than relying on a snapshot to characterize its epidemiology,” the researchers concluded. – by Talitha Bennett

Disclosures: Pembroke reports no relevant financial disclosures. Please see the full study for the other researchers’ relevant financial disclosures.