Puberty seems to be the time when HIV-infected children taking potent antiretroviral therapy are more likely to develop lipodystrophy and metabolic complications, especially in children with a severe underlying HIV infection. Once developed, lipodystrophy and metabolic changes seem to be extremely stable with time.

No abstract

Leptin replacement is able to reverse metabolic complications in the majority of children with Berardinelli-Seip congenital lipoatrophy and with insulin resistance or dyslipidemia before the development of overt diabetes.

We identified a group of children at risk for intramuscular insulin injections and that may deserve specific injection technique and advice.

No abstract

No abstract

BACKGROUND:The HIV-associated lipodystrophic syndrome (HIV-LDS) combines redistribution of fat mass with insulin resistance and hyperlipidemia. We have previously reported that HIV-LDS prevails in children in a comparable pattern as in adults. The metabolic activity itself of the lipodystrophic adipose tissue in HIV infection has been poorly studied. AIM AND METHODS: To assess in situ the insulin sensitivity of the lipohypertrophic subcutaneous abdominal adipose tissue using the microdialysis technique in HIV-infected children. Insulin sensitivity, assessed by the inhibition of glycerol release, was measured in the abdominal subcutaneous adipose tissue during a standard oral glucose tolerance test (OGTT) in six HIV-infected children under multi-therapy with abdominal lipohypertrophy (supra-iliac skinfold thickness > 97th percentile) (HIV=LHþ), in six obese children (obese group) and in eight HIV-infected children without lipodystrophy (HIV=LH7). RESULTS: Glucose tolerance was normal in all subjects. Mean insulin areas under the curve (IAUC) were significantly higher in the obese and HIV=LHþ groups than in HIV=LH7 (8769 AE 5429, 8161 AE 4552 and 3618 AE 2222 mU min l 71 , respectively; P ¼ 0.04 for the three groups comparison by the Kruskal -Wallis test), reflecting insulin resistance in the two former groups independent of a significant difference in percentage fat mass (37.2 AE 4.7, 22.8 AE 10.9 and 20.7 AE 7.1%, respectively; P ¼ 0.006). The crude inhibition of glycerol release, expressed as the relative change in dialysate glycerol concentration between baseline and 120 min, was not statistically different between the three groups (14% in obese, 738 AE 14% in HIV=LHþ and 751 AE 17% in HIV=LH7 groups; P ¼ 0.3). The inhibition of glycerol release with respect to the circulating insulin level (expressed by IAUC) was similar in HIV=LHþ and obese groups (76 AE 5 Â 10 73 and 77 AE 5 Â 10 73 l mU 71 min 71 , respectively, P ¼ 0.4 for two-groups comparison by the U-Mann -Whitney test) and four-fold less than in the HIV=LH7 group (724 AE 25 Â 10 73 l mU 71 min 71 ; P ¼ 0.02). CONCLUSION: These data argue in favor of insulin resistance in the adipose tissue of lipohypertrophies associated with HIV infection.