Dc. Mynarcik et al., Insulin-like growth factor system in patients with HIV infection: Effect of exogenous growth hormone administration, J ACQ IMM D, 22(1), 1999, pp. 49-55
The purpose of this study was to characterize changes in the levels of insu
lin-like growth factor-I (IGF-I) and IGF binding proteins (BP) 1, 2, and 3
in HIV-infected adults throughout the course of their disease, and to asses
s the responsiveness of the IGF system components to growth hormone (GH) ad
ministration (6 mg/day) for 2 weeks. Healthy control study subjects (n = 10
) were compared with patients who were either HIV-positive (n = 9), had AID
S without weight loss (n = 13), or had AIDS with >10% weight loss (n = 6),
all of whom had been free of acute illness for at least 3 months. Under bas
al conditions, fasting serum concentrations of epinephrine, norepinephrine,
cortisol, glucagon, insulin, IGF-I, and IGFBP-3 were not significantly dif
ferent among the four groups. The serum concentrations of IGFBP-1 and IGFBP
-2 were significantly higher in AIDS patients with wasting than in the othe
r three groups (p < .05). In addition, there was a statistically significan
t positive correlation between the levels of IGFBP-1 (p = .004) and IGFBP-2
(p = .03) and the stage of disease. Following GH administration, the serum
concentrations of insulin and IGF-I were increased in all groups (p < .05)
. In addition, the increases in insulin levels correlated with stage of dis
ease (p = .004). The responses of the IGFBPs were more variable. GH adminis
tration significantly increased the levels of IGFBP-3 in all groups except
the patients with AIDS wasting, whereas the levels of IGFBP-1 were signific
antly decreased in controls and AIDS patients. These results demonstrate th
at there is a continuum of both elevations in the IGFBPs and altered metabo
lic responsiveness in patients infected with HIV that increases with the se
verity of the disease. These data also demonstrate that AIDS patients, who
are free from secondary infection, respond to administration of GH by signi
ficantly increasing hepatic IGF-I production.