Ual or unknown. Mean duration of HAART was 40.6 months. Mean CD4+ cell count was 520.7 cells/mm3. As for HAART, 43 (47.3 ) patients were treated by efavirenz plus two NRTIs and 48 (52.7 ) by lopinavir/ritonavir plus two NRTIs. Patients with efavirenz therapy, than those with lopinavir/ ritonavir-based regimens, had higher serum levels of fasting glucose (106.1 vs. 90.7 mg/dl, P = 0.01) and LDL (124.6 vs. 104.1 mg/dl, P,0.01), HOMA index (2.6 vs. 1.7, P = 0.02), but lower serum levels of uric acid (5.6 vs. 6.2 mg/dl, P = 0.03), and more often had hypercholesterolemia (cholesterol .200 mg/dl; 67.4 vs. 37.5 , P = 0.01) and serum LDL.110 mg/dl (72.1 vs. 41.7 , P = 0.01) (Table 2). For the C1431T HIF-2��-IN-1 polymorphism in PPARc, 47 (51.6 ) patients were the CC genotype, 41 (45.1 ) CT genotype, and 3 (3.3 ) TT genotype. Allele frequency for the C allele was 0.74 and T allele 0.26. The P value of x2 test was 0.09 and such a result was consistent with the Hardy-Weinberg equilibrium. There was no discernible difference in the prevalence of smoking, hazardous drinking, presumed routes of HIV Imazamox infection, HCV co-infection, duration of HIV infection, CD4+ cell counts, or HAART regimen (NNRTI or PI use) between patients with the T allele (CT+TT genotype) and without the T allele (CC genotype)(data not shown). No difference in BMI, waist circumference, systolic and diastolic blood pressure, fasting glucose and insulin, HOMA index, serum cholesterol, LDL, HDL and anti-dyslipidemic therapy was detectable between patients with and without the T allele (Table 3 and data not shown). Patients with the T allele had a trend toward lower rate of hypertriglyceridemia (triglyceride .150 mg/dl; 65.9 vs. 85.1 , P = 0.06; a = 0.05; statistical power = 0.57 in post hoc analysis) and had lower levels of serum uric acid (5.5 vs. 6.3 mg/dl, P = 0.01) than those without the T allele. While the multivariate analysis supported the protective effect of the T allele against development of hypertriglyceridemia (odds ratio [OR] 0.282, 95 confidence interval [CI] 0.087,0.921, P = 0.04) (Table 4), there was no statistical significance under Bonferroni correction for multiple testing. For 46 patients with current anti-retroviral therapy after January 2005, their longitudinal lipid profiles were recorded. Serum triglyceridelevels in patients with the T allele were significantly lower than those without the T allele at several time points after antiretroviral therapy (Figure 1). The effect is of statistical significance in serum triglyceride in patients with the T allele over time using the mixed effect model (P = 0.006, statistical power = 0.79). Although the differences of fasting insulin and HOMA index between patients with and without the T allele did not reach statistical significance, there were trends toward a lower fasting insulin level (7.5 vs.10.3 mg/dl; P = 0.07) and less insulin resistance (HOMA index .3.8; 6.8 vs. 21.7 ; P = 0.09) in those with the T allele. For the Pro12Ala polymorphism in PPARc, 83 (91.2 ) patients belong to the Pro/Pro genotype, and 8 (8.8 ) the Pro/Ala genotype. No patient with the Ala/Ala genotype was identified. Allele frequency for the Pro allele was 0.96 and Ala allele 0.04. The P value of x2 test for the Hardy-Weinberg equilibrium was 0.66. There was no difference in the prevalence of smoking, hazardous drinking, risk factors of HIV infection, HCV co-infection, duration of HIV infection, CD4+ cell counts, or HAART regimen between patients with the Pro/.Ual or unknown. Mean duration of HAART was 40.6 months. Mean CD4+ cell count was 520.7 cells/mm3. As for HAART, 43 (47.3 ) patients were treated by efavirenz plus two NRTIs and 48 (52.7 ) by lopinavir/ritonavir plus two NRTIs. Patients with efavirenz therapy, than those with lopinavir/ ritonavir-based regimens, had higher serum levels of fasting glucose (106.1 vs. 90.7 mg/dl, P = 0.01) and LDL (124.6 vs. 104.1 mg/dl, P,0.01), HOMA index (2.6 vs. 1.7, P = 0.02), but lower serum levels of uric acid (5.6 vs. 6.2 mg/dl, P = 0.03), and more often had hypercholesterolemia (cholesterol .200 mg/dl; 67.4 vs. 37.5 , P = 0.01) and serum LDL.110 mg/dl (72.1 vs. 41.7 , P = 0.01) (Table 2). For the C1431T polymorphism in PPARc, 47 (51.6 ) patients were the CC genotype, 41 (45.1 ) CT genotype, and 3 (3.3 ) TT genotype. Allele frequency for the C allele was 0.74 and T allele 0.26. The P value of x2 test was 0.09 and such a result was consistent with the Hardy-Weinberg equilibrium. There was no discernible difference in the prevalence of smoking, hazardous drinking, presumed routes of HIV infection, HCV co-infection, duration of HIV infection, CD4+ cell counts, or HAART regimen (NNRTI or PI use) between patients with the T allele (CT+TT genotype) and without the T allele (CC genotype)(data not shown). No difference in BMI, waist circumference, systolic and diastolic blood pressure, fasting glucose and insulin, HOMA index, serum cholesterol, LDL, HDL and anti-dyslipidemic therapy was detectable between patients with and without the T allele (Table 3 and data not shown). Patients with the T allele had a trend toward lower rate of hypertriglyceridemia (triglyceride .150 mg/dl; 65.9 vs. 85.1 , P = 0.06; a = 0.05; statistical power = 0.57 in post hoc analysis) and had lower levels of serum uric acid (5.5 vs. 6.3 mg/dl, P = 0.01) than those without the T allele. While the multivariate analysis supported the protective effect of the T allele against development of hypertriglyceridemia (odds ratio [OR] 0.282, 95 confidence interval [CI] 0.087,0.921, P = 0.04) (Table 4), there was no statistical significance under Bonferroni correction for multiple testing. For 46 patients with current anti-retroviral therapy after January 2005, their longitudinal lipid profiles were recorded. Serum triglyceridelevels in patients with the T allele were significantly lower than those without the T allele at several time points after antiretroviral therapy (Figure 1). The effect is of statistical significance in serum triglyceride in patients with the T allele over time using the mixed effect model (P = 0.006, statistical power = 0.79). Although the differences of fasting insulin and HOMA index between patients with and without the T allele did not reach statistical significance, there were trends toward a lower fasting insulin level (7.5 vs.10.3 mg/dl; P = 0.07) and less insulin resistance (HOMA index .3.8; 6.8 vs. 21.7 ; P = 0.09) in those with the T allele. For the Pro12Ala polymorphism in PPARc, 83 (91.2 ) patients belong to the Pro/Pro genotype, and 8 (8.8 ) the Pro/Ala genotype. No patient with the Ala/Ala genotype was identified. Allele frequency for the Pro allele was 0.96 and Ala allele 0.04. The P value of x2 test for the Hardy-Weinberg equilibrium was 0.66. There was no difference in the prevalence of smoking, hazardous drinking, risk factors of HIV infection, HCV co-infection, duration of HIV infection, CD4+ cell counts, or HAART regimen between patients with the Pro/.
