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Liver Death Rate Twice Higher With HBV Than HCV in Gay HIV+ Men of MACS
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18th Conference on Retroviruses and Opportunistic Infections, February 27-March 2, 2011, Boston
Mark Mascolini
Compared with chronic HCV infection, chronic HBV infection more than doubled the rate of liver-related death in HIV-positive gay men in the Multicenter AIDS Cohort Study (MACS) [1]. Treatment with an antiretroviral active against HBV did not independently lower the liver death rate in this analysis, though MACS researchers noted that the advent of tenofovir coincided with a falling liver death rate.
Both HBV and HCV can instigate end-stage liver disease, liver cancer, and death. Because little is known about the relative risk of liver-related mortality with HBV and HCV in HIV-positive men, MACS investigators planned this comparison of gay men positive for hepatitis B surface antigen or hepatitis C antibody and HCV RNA. The researchers excluded men infected with both HBV and HCV and men with little or no follow-up. They determined cause of death from death certificates.
The analysis included 337 men with chronic HBV and 343 with chronic HCV. In the HBV group, 229 (68%) had HIV, and 242 men with HCV (71%) had HIV. Median age was younger in the HBV group (32 versus 38 years), and a higher proportion with HBV were white (77% versus 44%). Fewer people with HBV than HCV injected drugs (9% versus 57%). Among 63 men who did not drink alcohol, 56 (89%) had HCV and 7 (11%) had HBV. But rates of moderate and heavy drinking were similar in the two groups.
Liver-related mortality was significantly higher with HBV than with HCV (P < 0.05) for the whole study group and for HIV-coinfected men in all three study periods, although differences between groups diminished in the most recent period. Coinfected men had higher death rates than men infected only with HBV or HCV. Also, the MACS team noted that liver-related mortality dropped after 2002 in HBV/HIV-infected men, around the time tenofovir began seeing wide use.
1984-1996 liver-related mortality
All HBV: 10.4%
All HCV: 5.3%
HBV/HIV: 16.2%
HCV/HIV: 8.2%
1997-2002 liver-related mortality
All HBV: 12.9%
All HCV: 7.3%
HBV/HIV: 18.2%
HCV/HIV: 12.1%
2003-2010 liver-related mortality
All HBV: 8.0%
All HCV: 5.2%
HBV/HIV: 7.7%
HCV/HIV: 7.0%
The MACS researchers devised a multivariate model restricted to men with HIV and adjusted for hepatitis status (B versus C), age, race, CD4 count, HBV-active antiretroviral use, and alcohol use. Compared with HCV infection, HBV infection more than doubled the rate of liver-related mortality (incidence rate ratio [IRR] 2.17, 95% confidence interval [CI] 1.0 to 4.6, P = 0.047). Compared with a CD4 below 200, a count of 200 to 350 lowered the liver death rate 60% (IRR 0.4, 95% CI 0.2 to 0.9, P = 0.048) and a count above 350 lowered the rate 93% (IRR 0.07, 95% CI 0.02 to 0.2, P < 0.001). Age over 40 and use of HBV-active antiretrovirals (tenofovir or lamivudine) did not independently affect liver mortality incidence.
All-cause mortality did not differ significantly in any study period by HBV versus HCV status in univariate or multivariate analysis. Nor did all-cause mortality differ significantly by coinfection status in any study period.
The MACS researchers believe their findings support the following measures in HIV-infected people: (1) screening for HBV, (2) immunization to protect HBV-negative people from HBV infection, and (3) treatment of HBV/HIV-coinfected people with regimens including agents active against HBV. US Department of Health and Human Services experts recommend starting antiretroviral therapy in HBV-coinfected people--regardless of CD4 count--when those people also need anti-HBV therapy. In such people they endorse treatment with two agents active against HBV, either tenofovir/emtricitabine or tenofovir/lamivudine.
Reference
1. Falade-Nwulia O, Seaberg E, Rinaldo C, Badri S, Witt M, Thio C. Liver-related mortality risk is greater from chronic HBV than from chronic HCV: MACS 18th Conference on Retroviruses and Opportunistic Infections. February 27-March 2, 2011. Boston. Abstract 968.
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