Epidemiology

Hepatic decompensation more likely with HIV and HCV coinfection

Last Updated: 2014-03-17 17:32:16 -0400 (Reuters Health)

By Will Boggs MD

NEW YORK (Reuters Health) - Hepatic decompensation rates are higher in patients coinfected with hepatitis C virus (HCV) and HIV, even when they are receiving antiretroviral therapy (ART), according to a retrospective study.

"Given the increased rate of hepatic decompensation among coinfected patients and since new direct-acting antiviral hepatitis C therapies are now available, which show rates of virologic cure that are comparable to those of HCV-monoinfected patients, clinicians should ensure HIV/HCV patients are on ART and should strongly consider treating chronic hepatitis C in coinfected persons," Dr. Vincent Lo Re III from the University of Pennsylvania and the Philadelphia VA Medical Center told Reuters Health by email.

Ten to 30% of HIV patients are coinfected with HCV, and their disease course is accelerated, with more rapid progression of liver fibrosis, compared with HCV-monoinfected patients.

Few studies have evaluated the incidence and determinants of hepatic decompensation among patients coinfected with HIV and HCV during the ART era, however.

Dr. Lo Re and colleagues used data from the Veterans Aging Cohort Study Virtual Cohort to compare the incidence of hepatic decompensation between 4280 ART-treated patients coinfected with HIV and HCV and 6079 HCV-monoinfected patients and evaluated the determinants of decompensation among the coinfected patients.

Significantly more coinfected patients than monoinfected patients experienced hepatic decompensation (6.3% vs 5.0%; p=0.004). Similar proportions of both groups presented with ascites and spontaneous bacterial peritonitis, but variceal hemorrhage was less common among coinfected patients (26.1% vs 55.1%; p<0.001).

After adjustment for various factors, coinfected patients receiving ART were 83% more likely than monoinfected patients to have decompensation.

The 10-year cumulative incidence of decompensation was 7.4% among coinfected patients, compared with only 4.8% among monoinfected patients (p<0.001).

Rates of decompensation were elevated even in patients who maintained HIV RNA counts below 1000 copies/mL, but rates did not appear elevated for patients who maintained HIV RNA counts below 400 copies/mL. Decompensation rates were highest for coinfected patients with a pre-ART CD4 count less than 200 million cells/L, according to the March 18th Annals of Internal Medicine report.

Hepatocellular carcinoma developed in similar proportions of coinfected (1.7%) and monoinfected (1.6%) patients, though rates were 60% higher for coinfected patients after adjustment for other risk factors. Median survival after HCC diagnosis tended to be shorter for coinfected patients than for monoinfected patients (8.7 vs 14.2 months; p=0.22).

More patients died in the coinfected group (32.9% vs 15.4%), with HIV/AIDS representing the most commonly recorded cause of death in the coinfected group.

The only risk factors for decompensation among coinfected patients were baseline advanced hepatic fibrosis, baseline hemoglobin level below 100 g/L, and nonblack race.

"Our finding that antiretroviral-treated coinfected patients with controlled HIV had lower rates of hepatic decompensation compared to those who did not achieve HIV suppression suggests that suppression of HIV RNA with antiretroviral therapy is an important factor in slowing progression of HCV-related liver fibrosis," Dr. Lo Re said. "All HIV/hepatitis C coinfected patients should receive antiretroviral therapy."

"The increased rate of hepatic decompensation among coinfected patients should prompt earlier consideration for initiating HCV therapy to try to reduce the risk of liver complications," Dr. Lo Re reiterated.

SOURCE: http://bit.ly/1edpamP

Ann Intern Med 2014.