icon-    folder.gif   Conference Reports for NATAP  
 
  Conference on Retroviruses
and Opportunistic Infections (CROI)
February 22-25, 2016, Boston MA
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Avoiding HCV, HBV, Alcohol Abuse Could Avert
Up to One Third of ESLD Cases With HIV
 
 
  Conference on Retroviruses and Opportunistic Infections (CROI), February 22-25, 2016, Boston
 
Mark Mascolini
 
Avoiding HCV infection or heavy drinking could avert one third of end-stage liver disease (ESLD) cases in people with HIV, according to a 34,000-person analysis of the NA-ACCORD cohort [1]. Never having a CD4 count below 200 would prevent 25% of ESLD cases and avoiding HBV infection would avert 16%.
 
Both HIV-related variables and traditional risk factors probably contribute to the heightened risk of ESLD in people with HIV, the NA-ACCORD researchers noted. To get a better understanding of what drives ESLD incidence in people with HIV, they conducted this prospective analysis. Their primary aim was to estimate the population-attributable fraction of ESLD, that is, the proportion of ESLD cases that could be avoided if all participants were not exposed to a particular risk factor.
 
NA-ACCORD embraces several cohorts in the United States and Canada. This analysis focused on 11 cohorts with validated ESLD diagnoses from January 2000 through December 2009. Modifiable risk factors analyzed were HCV infection, HBV infection, cigarette smoking, CD4 count below 200, viral load at or above 400, clinical AIDS diagnosis, and at-risk alcohol use (3 or more drinks a day or 7 or more per week for women and 4 or more drinks per day or 14 or more per week for men). The HIV-related variables were time-varying. The investigators adjusted analyses for all of these modifiable risk factors and for age, sex, and race.
 
The analysis included 34,044 HIV-positive adults with a median follow-up of 3.1 years. In that time ESLD got diagnosed in 387 people. The researchers had alcohol use data available for 12,158 participants (36%), including 176 with incident ESLD. In the total population, risk factor prevalence in people with versus without ESLD was 51% versus 19% for HCV, 28% versus 10% for HBV, 75% versus 59% for smoking, 36% versus 26% for CD4 count below 200, 56% versus 57% for viral load above 400, and 26% versus 21% for an AIDS diagnosis. In the subgroup with alcohol data, prevalence with versus without ESLD was 58% versus 29% for HCV, 23% versus 10% for HBV, 81% versus 75% for smoking, 35% versus 28% for CD4 count below 200, 60% versus 61% for viral load above 400, and 22% versus 25% for clinical AIDS.
 
The overall adjusted analysis identified five factors that independently predicted ESLD: HCV (3.6-fold higher risk), HBV (3.1-fold higher), CD4s below 200 (4.0-fold higher), viral load above 400 (1.8-fold higher), and a clinical AIDS diagnosis (1.4-fold higher). Alcohol was not considered in the overall analysis. In the at-risk alcohol subgroup, independent predictors of ESLD were HCV (3.0-fold higher risk), HBV (2.0-fold higher), at-risk alcohol versus never drinking (1.7-fold higher), CD4s below 200 (4.3-fold higher), and viral load above 400 (1.7-fold higher).
 
In the population-attributable fraction analysis, the NA-ACCORD team calculated that 33% of ESLD cases could be averted by not having HCV, 16% by not having HBV, 25% by avoiding a CD4 count below 200, and 9% by avoiding a clinical AIDS diagnosis. In the subgroup of people with alcohol data, 33% of ESLD cases could be prevented by avoiding at-risk alcohol use (never drinking), 35% by not having HCV, 10% by not having HBV, and 25% by avoiding a CD4 count below 200.
 
The investigators proposed that ESLD risk can be cut through (1) HCV prevention and eradication, (2) HBV prevention and treatment, (3) alcohol prevention and treatment, and (4) early antiretroviral therapy to keep the CD4 count high and prevent AIDS illnesses. The analysis did not attempt to determine whether at-risk alcohol drinking raised ESLD risk compared with moderate drinking.
 
Reference
 
1. Althoff KN, Justice AC, Eron JJ, et al. Hepatitis B and C, alcohol, and CD4 drive end-stage liver disease in HIV+ adults. Conference on Retroviruses and Opportunistic Infections (CROI), February 22-25, 2016, Boston. Abstract 150.