Alcohol may adversely affect immunologic function and impact adherence to HAART among those HIV infected, resulting in adverse outcomes.
Reported alcohol use within the Department of Defense (DoD) has been higher compared to age-matched civilians, yet no data exists as to alcohol use among HIV seropositive active duty members. We evaluated alcohol use, the impact of at-risk drinking on HAART outcomes and at-risk drinking as an outcome within an HIV positive cohort.
The DoD HIV Natural History Study has been following HIV seropositive DoD beneficiaries since 1986 at six month intervals. Since 2006, self-reported alcohol use was collected; only those with alcohol data were included. At-risk drinking was defined as > 4 drinks in a 24h period or > 14 drinks/wk (men), > 3 drinks or > 7 drinks/wk (women). CD4 and VL analyses were limited to those that initiated HAART (HI) after 2006. Viral failure was defined as 2 consecutive VL > 400 after HI. GEE logistic regression analyses were used.
Of 1891 participants, 728 (38.5%) reported at-risk drinking on their first alcohol questionnaire. At-risk drinkers at baseline were more likely to be Caucasian (47% v 37%), active duty at HIV diagnosis (94% v 87%), younger (27; range 23-33 v 31; range 25-37), and were less likely to have ever been on HAART (19% v 8%); all p < 0.01. At-risk drinkers primarily remained at-risk (67%), while “not-at-risk” drinkers remained “not at risk” (87%) compared to the prior year. Trends remained similar at HI (n=1659); at-risk drinkers had a higher CD4 at HI (350 [range 266-462]) but no differences in log10VL at HI or follow-up were noted.
CD4 was not associated with at-risk drinking. VL failure in the multivariate model was marginally significant (OR 1.2 (1.01-1.45) adjusting for years on HAART, age, and year of HI.
Using at-risk drinking as the outcome, Caucasian (OR 1.4, p<0.005) and younger (OR 0.98/year, p<0.01) at-risk drinkers were significantly more likely to report at-risk drinking at their next visit, adjusting for not at-risk drinking, gender, years on HAART, CD4 and VL.
At-risk drinking was reported in more than a third of our cohort and they often remained at-risk. Although at-risk drinking had no effect on CD4 and a marginal effect on viral failure in our population to date, targeted alcohol interventions among Caucasians and younger age are warranted.
G. E. Macalino,
O. Mesner, None
J. Okulicz, None
M. Bavaro, None
A. Ganesan, None
J. Glasser, None