In order to study the mechanism of gonadal dysfunction in patients with abnormal thyroid function, the pituitary luteinizing hormone (LH) response to 200 mug of luteinizing hormone-releasing hormone (LH-RH) was investigated in 20 untreated and 18 treated hyperthyroid patients and in 21 untreated and 8 treated hypothyroid patients in addition to 29 matched control subjects. Serum LH levels were measured by double-antibody radioimmunoassay technique with HLH kit Daiichi. In untreated hyperthyroid men, the slightly elevated mean basal level and the exaggerated mean response to LH-RH of LH were observed, and in treated hyperthyroid men, both values were found to be similar to those of matched control men. Furthermore, in these patients, the maximal increments and the net increments of responses to LH-RH of LH were correlated with serum thyroxine levels and Thyopac-3 values. In most untreated and treated hyperthyroid premenopausal women with and without menstrual disturbances, the basal levels and the responses to LH-RH of LH were similar to those of matched control premenopausal women. In untreated hyperthyroid postmenopausal women, the mean basal level of LH was elevated, although the mean LH response to LH-RH was similar to that of matched control postmenopausal women, and in treated hyperthyroid postmenopausal women, the mean basal level and the mean response to LH-RH of LH were similar to those of matched control postmenopausal women. Furthermore, in these patients, the basal levels were correlated with serum thyroxine levels. In untreated and treated hypothyroid men, the mean basal level and the mean response to LH-RH of LH were similar to those of untreated and treated hyperthyroid postmenopausal women. In most untreated and treated hypothyroid premenopausal women with and without menstrual disturbances, the basal levels were observed to be inconsistent, and the LH responses to LH-RH were similar to those of matched control premenopausal women. In untreated and treated hypothyroid postmenopausal women, the mean basal level and the mean response to LH-RH of LH were similar to those of matched control postmenopausal women. These data indicate that the ability of the pituitary to secrete LH in patients with abnormal thyroid function was augmented in hyper- and hypothyroid men, and augmented in hyper-, but normal in hypothyroid postmenopausal women. Therefore, it is concluded that the cause of gonadal dysfunction at least in the premenopausal women with abnormal thyroid function lies not inside but outside the pituitary gland.