Antiviral therapy · 2007
Lipodystrophy and metabolic changes in HIV-infected children on non-nucleoside reverse transcriptase inhibitor-based antiretroviral therapy.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Aurpibul Linda, Puthanakit Thanyawee, Lee Benjamin, Mangklabruks Ampica, Sirisanthana Thira, Sirisanthana Virat
Аннотация
BACKGROUND: Highly active antiretroviral therapy (HAART) has recently been implemented in Thailand. Its long-term effects have not been clearly evaluated. The objective of this study was to estimate the prevalence of lipodystrophy (LD) and other metabolic changes in HIV-infected children receiving HAART.
METHODS: Ninety children who began HAART (either nevirapine or efavirenz, together with lamivudine and stavudine) were prospectively followed. LD was assessed by waist-to-hip ratio and LD checklist. Hypercholesterolaemia was defined as total cholesterol > 200 mg/dl and low-density lipoprotein cholesterol > 130 mg/dl. Low levels of high-density lipoprotein cholesterol (HDL-c), hypertriglyceridaemia and hyperglycaemia were defined as HDL-c < 40 mg/dl, triglyceride > 200 mg/dl and plasma glucose > 110 mg/dl, respectively.
RESULTS: The mean age at entry was 7.6 (SD 2.9) years. Fifty-three children received nevirapine- and 37 received efavirenz-based HAART. The prevalence of LD was 9%, 47% and 65% at 48, 96 and 144 weeks after HAART initiation, respectively. Patterns of LD at week 144 were central lipohypertrophy (46%), peripheral lipoatrophy (20%), and combined type (34%). A higher prevalence of LD was found among females (61% versus 39%; P = 0.04) and those with more advanced disease (CDC category B or C) at baseline (73% versus 51%; P = 0.04). There was no difference in prevalence of LD between the two regimens. At 144 weeks, fasting hypertriglyceridaemia was detected in 12%, hypercholesterolaemia in 11%, and increased plasma glucose in 4% of children. Low HDL-cholesterolaemia decreased from 94% at baseline to 12% at week 144 (P < 0.01).
CONCLUSIONS: More than half of the children developed LD at 144 weeks after HAART. Dyslipidaemia occurred in 11-12% of children.
METHODS: Ninety children who began HAART (either nevirapine or efavirenz, together with lamivudine and stavudine) were prospectively followed. LD was assessed by waist-to-hip ratio and LD checklist. Hypercholesterolaemia was defined as total cholesterol > 200 mg/dl and low-density lipoprotein cholesterol > 130 mg/dl. Low levels of high-density lipoprotein cholesterol (HDL-c), hypertriglyceridaemia and hyperglycaemia were defined as HDL-c < 40 mg/dl, triglyceride > 200 mg/dl and plasma glucose > 110 mg/dl, respectively.
RESULTS: The mean age at entry was 7.6 (SD 2.9) years. Fifty-three children received nevirapine- and 37 received efavirenz-based HAART. The prevalence of LD was 9%, 47% and 65% at 48, 96 and 144 weeks after HAART initiation, respectively. Patterns of LD at week 144 were central lipohypertrophy (46%), peripheral lipoatrophy (20%), and combined type (34%). A higher prevalence of LD was found among females (61% versus 39%; P = 0.04) and those with more advanced disease (CDC category B or C) at baseline (73% versus 51%; P = 0.04). There was no difference in prevalence of LD between the two regimens. At 144 weeks, fasting hypertriglyceridaemia was detected in 12%, hypercholesterolaemia in 11%, and increased plasma glucose in 4% of children. Low HDL-cholesterolaemia decreased from 94% at baseline to 12% at week 144 (P < 0.01).
CONCLUSIONS: More than half of the children developed LD at 144 weeks after HAART. Dyslipidaemia occurred in 11-12% of children.