Primary endocrinopathies in children with HIV infection are relatively uncommon. Hypothalamic–pituitary function is rarely affected. True endocrine dysfunction in HIV infection usually results from infection or malignancy affecting specific glandular function or from the side effects of pharmacological agents on hormone synthesis or action.

Growth failure and pubertal delay

Growth failure [1–3] occurs in 20%–80% of symptomatic HIV-infected children. Among perinatally infected children, it presents as early as 6 months of age. As the HIV infection becomes more advanced, growth failure may progress to a distinct wasting syndrome.

Proposed mechanisms of growth failure

Mechanisms include the non-specific effects of chronic disease, decreased intake, and enteropathy. Affected children manifest hypermetabolism (increased resting energy expenditure)/catabolism. Hormonal aberrations, while rare, can include deficiencies of growth hormone (GH), sex steroids (during adolescence), and thyroid hormones (see below).

GH/insulin-like growth factor-I (IGF-I) axis

GH deficiency occurs less often than might be predicted, based on the prevalence of AIDS encephalopathy in children. Levels of the GH-dependent surrogates, IGF-I and insulin-like growth factor binding protein-3 (IGFBP-3), even without GH deficiency, are typically low secondary to undernutrition. IGFBP-3 proteolysis also can occur. GH/IGF-I resistance has been documented in vitro [4].

Sex steroid deficiency

Delayed puberty appears to be common in children with HIV infection [5]. The mechanism remains unknown, but is most likely related to the effects of chronic disease.