OBJECTIVE: Understanding mortality differences among HIV-infected patients can focus efforts to improve survival. DESIGN: We evaluated death rates, causes, and associated factors among treated patients in the HIV Outpatient Study (HOPS), a large, prospective, multicenter observational cohort of HIV-infected persons seen at a diverse set of US sites of care. METHODS: Among 3754 HOPS participants seen during 1996-2007 with at least 6 months of follow-up after initiating HAART and receiving HAART at least 75% of time under observation ('substantially treated'), we calculated hazard ratios for death using proportional hazards regression models. We also examined death causes and comorbidities among decedents. RESULTS: Substantially treated participants, followed a median 4.7 years (interquartile range, 2.2-8.5), experienced 331 deaths. In multivariable analyses, higher mortality was associated with an index CD4 cell count less than 200 cells/μl [adjusted hazard ratio (aHR), 2.86; 95% confidence interval (CI) 1.95-4.21], older age (aHR, 1.50 per 10 years; 95% CI 1.33-1.70), log(10)HIV RNA (aHR, 1.67 per log(10); 95% CI 1.51-1.85), but not race/ethnicity (aHR, 0.99 for blacks vs. whites, P = 0.92). Mortality was increased among publicly insured (PUB) vs. privately insured participants (PRV) when index CD4 cell count was at least 200 cells/μl (aHR, 2.03; 95% CI 1.32-3.14) but not when index CD4 cell count was less than 200 cells/μl (aHR, 1.3, P = 0.13). By death cause, PUB had significantly more cardiovascular events and hepatic disorders than PRV. Comorbidities more frequent among PUB vs. PRV decedents included cardiovascular disease, renal impairment, and chronic hepatitis. CONCLUSION: Among HAART-treated participants with CD4 cell counts at least 200 cells/μl, PUB experienced higher death rates than PRV. Non-AIDS death and disease causes predominated among publicly insured decedents, suggesting that treatable comorbidities contributed to survival disparities.
OBJECTIVE: Understanding mortality differences among HIV-infectedpatients can focus efforts to improve survival. DESIGN: We evaluated death rates, causes, and associated factors among treated patients in the HIV Outpatient Study (HOPS), a large, prospective, multicenter observational cohort of HIV-infectedpersons seen at a diverse set of US sites of care. METHODS: Among 3754 HOPSparticipants seen during 1996-2007 with at least 6 months of follow-up after initiating HAART and receiving HAART at least 75% of time under observation ('substantially treated'), we calculated hazard ratios for death using proportional hazards regression models. We also examined death causes and comorbidities among decedents. RESULTS: Substantially treated participants, followed a median 4.7 years (interquartile range, 2.2-8.5), experienced 331 deaths. In multivariable analyses, higher mortality was associated with an index CD4 cell count less than 200 cells/μl [adjusted hazard ratio (aHR), 2.86; 95% confidence interval (CI) 1.95-4.21], older age (aHR, 1.50 per 10 years; 95% CI 1.33-1.70), log(10)HIV RNA (aHR, 1.67 per log(10); 95% CI 1.51-1.85), but not race/ethnicity (aHR, 0.99 for blacks vs. whites, P = 0.92). Mortality was increased among publicly insured (PUB) vs. privately insured participants (PRV) when index CD4 cell count was at least 200 cells/μl (aHR, 2.03; 95% CI 1.32-3.14) but not when index CD4 cell count was less than 200 cells/μl (aHR, 1.3, P = 0.13). By death cause, PUB had significantly more cardiovascular events and hepatic disorders than PRV. Comorbidities more frequent among PUB vs. PRV decedents included cardiovascular disease, renal impairment, and chronic hepatitis. CONCLUSION: Among HAART-treated participants with CD4 cell counts at least 200 cells/μl, PUB experienced higher death rates than PRV. Non-AIDS death and disease causes predominated among publicly insured decedents, suggesting that treatable comorbidities contributed to survival disparities.
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