The effects of gonadotropin treatment on the immunological features of male patients with idiopathic hypogonadotropic hypogonadism

There is a significant line of evidence for a role of androgens in the modu lation of the immune system. However, little is known about immunological f eatures of male patients with idiopathic hypogonadotropic hypogonadism (IHH ) and the potential effects of gonadotropin treatment. Thus, the objective of this study was to evaluate the levels of selected soluble immune paramet ers [IgA, IgG, IgM, C3c, C4, interleukin-2 (IL-2), and IL-4], the CD4(+)/CD 8(+) ratio, and counts of total lymphocyte and some subpopulation of lympho cytes (CD3(+), CD4(+), CD8(+), and CD19(+) cells) before and after gonadotr opin treatment in men with IHH. Twenty-nine IHH patients and 19 age-matched healthy controls were included in the study. The patients were treated wit h human menopausal gonadotropin/hCG for 6 months. The pretreatment levels of serum Igs, C3c, IL-2, and IL-4 in the patients w ere significantly higher than those in the controls (P < 0.001 for all). Af ter treatment, all Igs (P < 0.001), C3c (P < 0.01), and IL-2 and IL-4 level s (P < 0.005) were decreased significantly compared to pretreatment levels. Pretreatment lymphocyte counts (P < 0.05); the percentages of CD3(+) cells (P < 0.001), CD4(+) cells (P < 0.001), and CD19(+) cells (P < 0.001); and the CD4(+)/CD8(+) ratio in the patient group were significantly higher (P < 0.05) than those in the controls. After treatment, the lymphocyte count (P < 0.001); CD3(+) (P < 0.01), CD4(+) (P < 0.001), and CD19(+) (P < 0.005) c ells; and the CD4(+)/CD8(+) ratio (P < 0.001) were decreased, but CD8(+) ce lls were increased significantly (P < 0.001). In summary, lack of testosterone action results in the enhancement of cellu lar and humoral immunity. The results of this study allowed us to conclude that testosterone deficiency affects both cell-mediated and humoral immunit y, and these may be modulated with gonadotropin therapy in male patients wi th IHH.