Therefore, a sensitivity analysis was performed by restricting th

Therefore, a sensitivity analysis was performed by restricting the analysis to subjects with initiation CD4 counts Apitolisib chemical structure <100 cells/μL. A relatively brief period of adherence to HAART may produce a 1 log10 copies/mL drop in HIV-1 RNA level. Therefore, a second sensitivity analysis was performed by defining virological response as a ≥2 log10 copies/mL drop in HIV-1 RNA at 6 months after initiation. Because subjects censored for regimen change may have had high hospitalization rates because of drug toxicity, we performed a third sensitivity analysis by excluding subjects

thus censored. The 604 subjects reporting IDU as an HIV risk factor make up a significant portion (44%) of our study cohort. We performed a subgroup analysis of hospitalization rates among these subjects. The analysis was performed on 1385 HAART-naïve patients, almost three-quarters of whom (1010) were responders. Responders tended to be older than nonresponders, with median ages at the time of HAART initiation being 40 and 38 years, respectively (P<0.01; Table 1). Responders were

less likely to be female (34%vs. 40%; P=0.04) and African American (75%vs. 86%; P<0.001). A smaller proportion of responders than nonresponders initiated HAART during 1997–1998 (38%vs. 58%; P<0.001). The median CD4 counts at HAART [interquartile ranges (IQRs)] for patients initiating HAART in 1997–1998, 1999–2002 and 2003–2006 were 156 (41, Selleckchem FK866 331), 133 (30, 266), and 196 (80, 291) cells/μL, respectively. Among subjects with CD4 counts at HAART <50 cells/μL, responders were more likely than nonresponders to be prescribed Mycobacterium avium prophylaxis (92%vs. 78%; P<0.001). Median changes in CD4 count at 6 months (IQRs) were increases of 101 cells/μL (39, 173) for responders and 7 cells/μL (−21, 61) for nonresponders. Eighty-eight per cent of responders and 71% of nonresponders were observed >180 days after HAART initiation and contributed to each post-initiation time period (P<0.001; Fig. 1). Seventy-nine per cent of responders and 61% of nonresponders were observed for 365 days without censoring.

Responders were censored because of regimen change less frequently than nonresponders (13%vs. 34%; P<0.001). There was no significant difference in censoring because of withdrawal/loss to follow-up (7% of responders and 4% of nonresponders; P=0.06) or death (1%vs. 2%; P=0.29). Among the 1385 subjects, there were 23 deaths NADPH-cytochrome-c2 reductase within 365 days following HAART initiation. There were no significant differences in death rates across time periods or for responders vs. nonresponders within time periods. For the 6-month period prior to HAART initiation, 94% of responders and 96% of nonresponders contributed some observation time; 50% of responders and 68% of nonresponders contributed a full 180 days (P<0.001). The all-cause hospitalization rate in virological responders during the first 45 days following HAART initiation was 75.1/100 PY [95% confidence interval (CI) 58.2, 96.8/100 PY; Fig. 1].

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