icon- folder.gif   Conference Reports for NATAP  
 
  16th CROI
Conference on Retroviruses and Opportunistic Infections Montreal, Canada
February 8-11, 2009
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HIV+ Die More Quickly in FRAM & Low CD4 Predicts Death
 
 
  Factors Associated with Mortality in the Study of Fat Redistribution and Metabolic Change in HIV Infection
 
"Mortality risk was 3 times higher among HIV-infected individuals than controls"

 
Reported by Jules Levin
CROI 2009 Feb 8-12
 
L Modrich1,2, R Scherzer1,2, A Zolopa3, D Rimland4, C Lewis5, R Kronmal6, P Bacchetti1, C Grunfeld1,2, M Shlipak1,2, Phyllis Tien*1,2, and the FRAM Study 1Univ of California, San Francisco, US; 2VAMC, San Francisco, CA, US; 3Stanford Univ, CA, US; 4VAMC, Atlanta, GA, US; 5Univ of Alabama at Birmingham, US; and 6Univ of Washington, Seattle, US
 
Background: Despite the widespread use of HAART in the United States, the mortality rate in HIV-infected individuals remains higher than in the general uninfected population. We compared the mortality risk of HIV-infected and control subjects and evaluated risk factors for mortality in subjects from the Study of Fat Redistribution and Metabolic Change in HIV infection (FRAM).
 
Methods: Vital status was ascertained in 922 HIV-infected men and women receiving clinical care and 278 controls enrolled in FRAM between 2000 and 2002. Analyses that compared mortality of HIV-infected to control subjects excluded HIV-infected individuals with recent opportunistic infection at baseline, and were restricted to the age range of controls (age 33 to 45, n = 468). Multivariable exponential survival regression was used to estimate hazards ratios (HR) for the: association of HIV infection with mortality after adjustment for demographic characteristics (age, sex, and race) and traditional cardiovascular disease (CVD) risk factors (smoking, diabetes, systolic and diastolic blood pressure, total and high-density lipoprotein [HDL] cholesterol), and association of HIV-related factors with mortality among HIV-infected subjects.
 
Results: After 5 years of follow-up, 12% of HIV and 2% of control subjects had died (HR = 6.9, 95%CI 3.0 to 16.1; p <0.0001). After multivariable adjustment, the hazards ratio for death was 3.4 (95%CI 1.3 to 8.5, p = 0.009). The figure shows mortality by time of attempted follow up in HIV-infected subjects stratified by baseline CD4 count and controls. Within HIV-infected subjects, the factors independently associated with death included current smoking (HR = 2.73 vs never smokers, p = 0.0001), increasing age (HR = 1.61 per decade, p = 0.0001), and low baseline CD4 count (HR = 0.65 per CD4 doubling, p <0.0001).

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Conclusions: Mortality risk was 3 times higher among HIV-infected individuals than controls even after adjustment for demographic and traditional CVD risk factors. In addition to low baseline CD4 count, older age, and current smoking were strong and independent predictors of mortality in HIV-infected individuals.