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Single Versus Repeated Dose Human Chorionic Gonadotropin Stimulation in the Differential Diagnosis of Hypogonadotropic Hypogonadism^*

Children's Hospital, University Helsinki Finland

Address requests for reprints to: Leo Dunkel, M.D., Children'sHospital, SF-00290 Helsinki, Finland.

The responses of serum testosterone (T), 17hydroxyprogesterone, and 17β-estradiol (E2) to four im injections of hCG (5000 IU/1.7 m²) given on days 0, 4, 7, and 10 were studied in 10 prepubertal and 10 pubertal boys with hypogonadotropic hypogonadism (groups O and P, respectively). Serum was obtained before each injection and on day 14. The results were compared with those of controls, 16 prepubertal boys with incomplete testicular descent and 6 pubertal boys with constitutional delay of puberty. Serum T levels increased significantly in groups 0 and P to 2.0 and 4.6 nmol/liter, respectively, after the first injection, then progressively to 5.8 and 11.2 nmol/liter. Basal T levels of group O did not differ from those of the controls, but were subnormal for group P (P < 0.001). Stimulated T levels were subnormal in both groups (P < 0.01 and P < 0.001), but repeated doses increased the difference from the control value only in group P. A difference in E₂ response between patients and controls appeared in puberty; only the pubertal control boys had substantial increases in E₂ (P < 0.001). Our results show that the optimal protocol for a diagnostic hCG test in prepubertal boys is a single dose of hCG, with determination of T levels 4 days later. In puberty, if the basal T levels are inconclusive, repeated doses of hCG should be given with determination of both T and E₂. These findings also suggest that the full inhibitory effect of E₂ on T synthesis results from a pubertal maturation process, possibly induced by endogenous gonadotropins, which cannot be induced by two weeks of hCG stimulation in prepubertal boys or those with hypogonadotropic hypogonadism.

^* Portions of this work were presented at the 23rd Annual Meeting of the European Society for Paediatric Endocrinology, Heidelberg, West Germany, September 1984. This work was supported by the Sigrid Juselius Foundation; the Foundation for Pediatric Research, Finland; and the Paulo Foundation.

Received June 5, 1984.

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