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 23 November 2017

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News

HCV infection in HIV patients does not increase risk of death or developing AIDS

Infection with hepatitis C virus (HCV) does not appear to increase the risk of death or developing AIDS for HIV patients, nor decrease the response to effective antiretroviral treatment, according to an article to be published in the next issue of the Journal of the American Medical Association.

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Mark S. Sulkowski, of Johns Hopkins University School of Medicine, Baltimore, Maryland, USA, and colleagues conducted a study to assess the effect of HCV infection on clinical and immunologic progression of HIV infection and immunologic response to highly active antiretroviral therapy (HAART).

Co-author Richard E. Chaisson, presented the findings of the research at a JAMA media briefing at the International AIDS Conference in Barcelona, Spain.

According to background information in the article, there are conflicting reports regarding the effect of HCV on the progression of HIV disease.

HIV infection appears to increase the likelihood that HCV infection will become chronic, and, in most studies, increase the risk of progressive HCV-related liver disease.

Due to shared routes of transmission such as by contaminated needles, an estimated 15-30% of HIV-infected persons are coinfected with HCV in the United States and Europe.

The study included 1955 patients enrolled between 1995 and 2001 at the Johns Hopkins Hospital HIV Clinic.

The patients had at least one return visit to the clinic and were free of AIDS at enrolment.

45% of the patients had HCV and HIV coinfection.
Journal of the American Medical Association

It was found that 45% of patients had HCV infection. Median length of follow-up was 2.2 years for HCV-infected and 2.0 years for HCV-uninfected patients.

The authors found, "After adjustment for the administration of HAART and its effectiveness, we did not detect an increased risk of development of AIDS-defining illness, death, or CD4 cell count decline to below 200/µl among HCV-infected compared with HCV-uninfected patients.

"In addition, among patients prescribed HAART, we found no evidence that HCV infection alters the virological or immunologic response to potent antiretroviral therapy."

Comparing HCV-infected patients with HCV-uninfected patients, there were no significant differences for acquiring an AIDS-defining illness (26% vs 24%, respectively) or risk of death (18% vs 16%).

Among patients treated with HAART, HCV status was not associated with HIV suppression or CD4 cell response. However, fewer HCV-infected patients received HAART (54%) compared with HCV-uninfected patients (67%).

"Further research is still needed to understand the effect of HCV infection on HIV disease and immune reconstitution in response to HAART.

"However, these findings emphasize the importance of the consideration of effective antiretroviral therapy for HCV-infected and HCV-uninfected persons at immediate risk for the development of AIDS," the authors conclude.

In an accompanying editorial, Stephen J. Rossi and colleagues of the Department of Veterans Affairs Medical Center, and the University of California, San Francisco, comment on the study.

"How should these studies guide clinicians in the management of patients with HCV/HIV coinfection?

"It is likely that many patients with HIV and HCV coinfection will be unable to be treated effectively with current HCV regimens," the authors continue.

"The HCV therapy should be initiated in patients who are expected to tolerate treatment, either before HIV therapy if the latter can be delayed, or during HIV therapy, to delay progression of liver disease.

"Optimal HCV/HIV management will require educating clinicians about the potential for drug interactions between HCV and HIV therapies, continued education of patients about the importance of adherence to prescribed regimens, and for both, education about the importance of alcohol cessation," the authors write.

"Certainly, the patient with coinfection highlights the importance of developing improved HCV regimens that avoid the toxicities of current interferon-based therapies."

JAMA 2002; 288:199-206, 241-3
08 July 2002

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