In children with HIV infection, growth failure occurs early in the course of infection and significantly involves linear growth with preservation of the weight/height ratio. Though true GH deficiency is not commonly detected in this population, we wondered whether deficiencies of GH or mediators of its activity might contribute to the short stature seen in many of these patients. We performed a cross-sectional study in which we measured clonidine-stimulated GH production (n=8), Insulin-like Growth Factor-1 (n=6), IGF Binding Protein-3(n=12), and Growth Hormone Binding Protein (n=12) levels in 12 children with HIV infection, ranging in age from 4 yrs 2 mo to 11 yrs 9 mo. The mean height z-score was -1.84 and mean weight z-score was -1.16. 7 of the children had short stature (ht z score ≤-1.96), and 6 had more advanced stages of HIV infection (CDC class ≥ B2). 4 children had low GH, one of whom also had low IGF-1, IGFBP3, and GHBP levels. Another child with SS and GH deficiency had normal IGF-1, IGFBP3, and GHBP. The other 2 with low GH had normal IGFBP3 and GHBP, did not have short stature, and may reflect false negative responses to clonidine rather than true GH deficiency. One child with extreme SS had normal GH, IGF-1, IGFBP3, and GHBP, but was on chronic steroid therapy. These data suggest that GH deficiency is not the primary cause of SS. The normal levels of GHBP suggest that there is not a deficiency of GH receptor and the finding of normal IGF-1 in 5/6 children also suggests that a qualitative defect in GH receptor is not present in children with HIV infection, whether or not they also have SS and/or more advanced disease.
