To our knowledge, this is the first study to investigate
the effect of rhGH in HIV-infected patients both with and without HALS. The lipolytic effect of rhGH appeared to be present in patients with and without HALS. The difference between groups in indices of abdominal fat accumulation was the result of an improvement in the GH group and a deterioration in the placebo group. This was particularly the case for patients suffering from HALS, indicating a deterioration of fat distribution over time in these patients. No such change took place in the patients without HALS. Indices of fat atrophy in the extremities did not show the same tendency. Although fasting plasma glucose increased significantly (0.4 mM) in the GH group compared with the placebo group, it is important to note that indices of beta-cell function (2-h post-challenge glucose level) and insulin resistance (HOMA-IR) did not change in any of the study groups. Screening Library in vivo The frequency of patients with IGT did not change over the course of the study in either the placebo or the GH group, and did not differ between groups at baseline or week 40. In patients who had a mildly impaired glucose tolerance at baseline, fasting glucose
levels did not deteriorate selleck kinase inhibitor more with rhGH treatment. The chosen dose of rhGH can probably be considered safe with respect to glucose metabolism in this group of patients, although the slight increase in plasma glucose indicates that parallel monitoring of glucose metabolism is warranted. Other cardiovascular risk factors, such as lipid levels and blood pressure, did not change during the course of the study. The HIV-infected patients enrolled in the present study are probably representative of the morphological and metabolic problems in the general HIV-infected population by not merely reflecting the group DOK2 of patients with HALS, which could probably benefit the most from rhGH treatment. Thus, we may have underestimated the morphological changes that occur in patients more seriously
affected by fat redistribution. Lo et al.  investigated one-selected group of HIV-infected patients with both relative GH deficiency and HALS, and reported that as many as a third of HIV-infected patients with HALS have a relative GH deficiency. We have previously shown that HIV-infected patients with HALS probably compensate for impairments in GH secretion by increasing the GH sensitivity of GH target tissues . It is unknown whether GH sensitivity in relatively GH-deficient patients is increased, and whether those patients could possibly benefit even more from rhGH treatment. The complex dynamics in the GH/IGF-I axis of HIV-infected patients impedes comparison with data from the present study. However, it is possible that we underestimated the effect of rhGH in patients with HALS and relative GH deficiency. There are several limitations to the present study.