Although growth failure is common among HIV-infected children, especially those with more advanced disease, primary endocrinopathies are relatively uncommon. Also, despite the prevalence of encephalopathy among HIV-infected children, hypothalamic-pituitary function is rarely affected. Highly active antiretroviral therapy (HAART) with protease inhibitors (PIs) can cause specific derangements of body composition and metabolism. When true endocrine dysfunction occurs in HIV-infected children, it usually results either from infection or malignancy affecting specific glandular function or from the effects of pharmacological agents on hormone synthesis or action.

Growth failure (failure-to-thrive) and pubertal delay

Growth failure [1–3] occurs in 20–80% of symptomatic HIV-infected children regardless of route of acquisition. In perinatally infected children, failure-to-thrive (FTT) presents as early as 6 months of age. As the infection becomes more advanced, growth failure may progress to a distinct wasting syndrome (analogous to that which occurs in adults).

Proposed mechanisms of growth failure

Mechanisms include the non-specific effects of chronic disease, decreased intake (anorexia, esophagitis, and abdominal pain), and enteropathy (diarrhea, malabsorption, and gut infection)[2]. In addition, affected children manifest hypermetabolism (increased resting expenditure)/ catabolism. Their caloric intake, even if normal or increased for age, may not meet their energy needs. Hormonal aberrations also have been implicated, including deficiencies of growth hormone (GH), sex steroids (during adolescence), and thyroid hormones (see below).