Objective: To determine the extent and degree of abnormalities of serum lipids, glucose homeostasis and abdominal adipose tissue distribution in protease inhibitor (PI)-treated and PI-naive HIV-infected children.
Design: A cross-sectional study involving HIV-infected children, 3–18 years of age, in a paediatric tertiary care centre.
Main outcome measures: Total, HDL and LDL-cholesterol, triglycerides, glucose, insulin, proinsulin and C-peptide were determined in the fasting state. Insulin resistance was assessed using the homeostatic model assessment–insulin resistance (HOMA–IR). Abdominal adipose tissue distribution was determined by single-slice computed tomography at the umbilical level.
Results: Thirty PI-treated and 20 PI-naive children were evaluated (76% prepubertal). PI-treated children had significantly higher total cholesterol (P = 0.0021), LDL-cholesterol (P = 0.019) and triglycerides (P = 0.0018). Serum glucose, insulin, proinsulin and C-peptide, the insulin : glucose ratio, HOMA–IR and abdominal adipose tissue distribution were similar in the two groups. Clinical and immunological HIV categories, viral load, CD4 cell count and stavudine therapy were not significantly associated with serum lipids, insulin resistance or abdominal adipose tissue distribution. The predictor variable most strongly associated with fasting serum insulin and HOMA–IR was the Tanner stage. Age was the most significant predictor variable of the visceral : subcutaneous adipose tissue ratio.
Conclusion: In this cohort of predominantly prepubertal HIV-infected children, PI therapy was associated with an atherogenic dyslipidemia but not with insulin resistance or abnormal abdominal adipose tissue distribution. The results suggest that children, particularly prepubertal children, are less susceptible than adults to PI-induced changes in glucose homeostasis and abdominal adipose tissue distribution.
From the Divisions of aInfectious Diseases and bEndocrinology and Diabetes, Department of Pediatrics; and the Departments of cRadiology and dPopulation Health Sciences, The Hospital for Sick Children, University of Toronto, Toronto, Canada.
Requests for reprints to: Susan M. King, MD CM, FRCP(C), Associate Professor, Division of Infectious Diseases, Department of Pediatrics, the Hospital for Sick Children, Toronto, Ontario, Canada.
Correspondence to: Ari Bitnun, MD, Division of Infectious Diseases, Department of Pediatrics, the Hospital for Sick Children, Toronto, Ontario, Canada. E-mail: firstname.lastname@example.org
Received: 26 September 2002; revised: 16 January 2003; accepted: 22 January 2003.