Rapid progression of liver fibrosis in HIV-positive gay men recently infected with hepatitis C

A US study has found that many HIV-positive gay men recently infected with hepatitis C virus have rapidly developed moderate-to-severe liver fibrosis. The study is published in the September 1^st edition of the Journal of Infectious Diseases.

Most of the men became infected with hepatitis C through unprotected sex and the infection was only diagnosed because the patients had abnormal liver function tests. The study investigators suggest that HIV-positive gay men should be regularly screened for infection with hepatitis C, warning that “the implications of missing the diagnosis of acute hepatitis C virus infection in these patients are grave.”

A weak immune system accelerates the progression of liver fibrosis in patients infected with hepatitis C virus, and there is evidence of very rapid progression of liver disease in patients who acquire hepatitis C virus infection when their immune system is already impaired.

There have been several outbreaks of sexually transmitted hepatitis C amongst HIV-positive gay men in Europe and the United States. Investigators in New York were concerned that these patients may have an increased risk of experiencing rapid progression of liver fibrosis.

A total of eleven individuals with recent hepatitis C infection were identified by the researchers. In all these patients the infection was only diagnosed because liver function tests performed as part of the patients routine HIV care identified increased transaminase levels. All but one individual reported unprotected anal sex and three patients reported injecting drug use.

Antiretroviral therapy was being taken by ten of the patients, the duration of treatment lasting between eleven months and 16 years. None of the patients had any other risk factors for liver disease.

Liver biopsies showed that nine patients had moderate-to-severe fibrosis (stage 2 on a scale 0 – 4). One patient had stage 1 fibrosis, and the remaining patient had no evidence of hardening of the liver.

All the biopsies showed other evidence of hepatitis C-associated liver damage, including inflammation of the portal vein, and inflammation involving cell death in the lobes of the liver.

In contrast to the rapid progression of liver fibrosis seen in these patients, the investigators note that other studies involving HIV-negative patients with recent hepatitis C infection have found no evidence of fibrosis.

The investigators highlight that current US guidelines for the care of HIV-positive gay men do not recommend regular routine hepatitis C screening. Increases in ALT (alanine aminotransferase) levels that may accompany acute hepatitis C infection can, the investigators write, be short-lived and therefore easy to miss with many cases of hepatitis C infection in HIV-positive gay men remaining undiagnosed as a result. The investigators believe “more intensive screening of HIV-infected men who have sex with men is warranted”. They also call for further research to identify the mechanisms leading to liver damage in HIV-positive patients recently infected with hepatitis C.