medwireNews: Researchers have found that co-infection with HIV accelerates hepatitis C virus (HCV)-related liver damage by nearly 10 years.
And this relationship remained even when levels of HCV RNA, chronic hepatitis B virus (HBV) status, gender, race, body mass index (BMI), and alcohol use were accounted for.
"Co-infected patients may have to be monitored more closely for worsening liver disease, and may require earlier and more aggressive treatment than people without HIV infection," suggested co-author Shruti Mehta (Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA) in a press statement.
The study, published in the Annals of Internal Medicine, included 1176 patients with HCV antibodies from a prospective cohort of current and former intravenous drug users, of whom 34% were co-infected with HIV. Between 2006 and 2011, patients were followed up a median of five times with elastography.
In multivariate analysis, liver fibrosis was significantly associated with age and concurrent HIV infection, report lead researcher David Thomas (Johns Hopkins School of Medicine, Baltimore) and colleagues.
And, by calculating the expected liver fibrosis scores according to patient age, the authors showed that those with concurrent HIV infection had liver fibrosis equal to those without HIV infection who were on average 9.2 years older.
Liver fibrosis was also independently associated with alcohol use, BMI, and chronic HBV infection.
The authors also found that patients with low CD4 cell counts or high HIV RNA levels had worse fibrosis than patients with better laboratory findings, suggesting that antiretroviral therapy (ART) could decrease liver fibrosis severity. However, they did not observe an association between ART use and fibrosis.
The mechanisms through which HIV accelerated liver disease are poorly understood, the authors explain. However, they suggest the association may be moderated through telomere shortening, which has been reported in HIV, HCV infection, and cirrhosis, leading to hepatocyte senescence and reduced cell regenerative capacity.
Thomas and colleagues say that further research is needed into the role of HCV and HIV treatment on the progression of fibrosis. In the meantime, they say that changes in modifiable risks such as weight and alcohol use should be more widely used.
"With aging of the populations with HCV and HIV infections, increasing emphasis should be placed on determining the most effective strategies for reducing modifiable risk factors and incorporating newer antivirals into HCV management of complex, older patients," the authors conclude.