Background:  Lipodystrophy syndrome was first described in HIV-infected children nearly 10 years ago. As emergence, evolution, and management of lipodystrophy syndrome in children is still not clearly understood, we have established an active surveillance cohort study in three European countries (Italy, Belgium, and Poland) to explore these issues.

Methods:  In the initial surveillance round, clinicians from the 14 participating sites completed a screening questionnaire for all HIV-infected children/adolescents in their care over a 3- to 4-month period. The point prevalence of fat redistribution and dyslipidemia is estimated. Follow-up evaluation will take place every 6 months.

Results:  Among 435 children and adolescents enrolled, 403 (93%) were vertically infected, 226 were female, median age was 13.6 years (IQR 9.8 to 17.3); 30% were at Tanner stage I and 38% at stage V; 339 (78%) were white and 65 (15%) were of black African origin; 32 (7.5%) were hepatitis C virus (HCV) co-infected. Most (412, 95%) were currently on HAART, 270 (62%) had viral suppression; median CD4 percentage was 33% (IQR 25 to 39), and 69% were currently asymptomatic. A total of 203 (46.7%, 95%CI 41.9 to 51.5) children had ≥1 clinically determined sign of fat redistribution (graded as mild, moderate, or severe):  64 (15%) had fat accumulation alone, mostly in the trunk with 19 presenting with severe fat accumulation; 71 (16%) had lipoatrophy alone, mostly in the legs, with severe lipoatrophy in 26, mostly in the face; 68 children (16%) had a combined type (lipoatrophy and lipohypertrophy), with 12 having severe features. Dyslipidemia (fasting hypercholesterolemia or hypertriglyceridemia defined according to age- and sex-adjusted thresholds) was present in 128 (29%, 95%CI 25.2 to 34.0) children, with 19 having hypercholesterolemia only, 79 hypertriglyceridemia only, and 30 both hypercholesterolemia and hypertriglyceridemia. Median total cholesterol among hypercholesterolemia cases was 226 mg/dL and median triglycerides among hypertriglyceridemia cases was 202 mg/dL. Both dyslipidemia and body fat alterations occurred in 70 children (16%, 95%CI 12.8 to 19.9), with a significant association between these factors overall (c² = 5.29, p = 0.021). Finally, 6 children (1.4%) had impaired glucose tolerance.

Conclusions:  Lipodystrophy syndrome is a relevant syndrome in HIV-infected children. Here, body fat changes affected nearly half, and dyslipidemia around one-third of the patients, with 1 in 6 having both abnormalities, which were significantly associated. This ongoing study will allow description of risk factors in a large study population and evaluation of lipodystrophy syndrome progression and management.