CLOMIPHENE CITRATE DOES NOT MODIFY THE EXAGGERATED THYROTROPHIN RESPONSE TO THYROTROPHIN-RELEASING HORMONE OCCURRING IN PRIMARY TESTICULAR FAILURE

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Abstract
Patients with primary testicular failure have increased basal TSH levels and an exaggerated TSH response to TRH in the presence of normal circulating levels of thyroid hormones. To evaluate if this TSH profile is an estrogen-related phenomenon, 16 patients with primary testicular failure were challenged with 200 .mu.g TRH prior to and after the administration of clomiphene citrate. The latter was given in a dose of 100 mg/day for 4 wk to 10 patients; 200 mg/day for 4 wk to 3 patients and 100 mg/day for 2 mo. to the final 3 patients. The patients demonstrated increased mean basal TSH levels with an exaggerated TSH response to TRH. Following clomiphene citrate administration, there were no changes in thyroxine, T3 [triiodothyronine] Sephadex or total T3 levels and in basal or stimulated TSH levels. Clomiphene did produce an increase in estradiol, testosterone, basal gonadotropins and luteinizing hormone response to LHRH. Since the estrogen antagonist, clomiphene citrate, had no effect on TSH secretion, it is unlikely that the exaggerated TSH response to TRH is mediated by estrogens.

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