Endocrine testicular functions in leprosy.

Pituitary testicular functions were evaluated in leprosy. Forty-three men with leprosy were studied by basal estimations of plasma LH, FSH, Prolactin, Testosterone, 17-beta estradiol, metoclopramide stimulated prolactin responses and hCG stimulated testosterone responses. Fifteen young healthy men with proven fertility were studied as control subjects. The hormone estimations were related to the histologic changes observed in the testicular biopsies of leprous hypogonadism. In lepromatous leprosy (n:18) the basal plasma gonadotropin levels were significantly increased (FSH 29.5 +/- 2.3 mlU/ml; LH 21.5 +/- 1.9 mlU/ml, mean +/- SE). The plasma gonadotropins were in the normal range in tuberculoid leprosy. In borderline leprosy, the basal mean plasma FSH was normal, whereas LH levels were significantly increased (22.5 +/- 1.2 mlU/ml). The basal plasma testosterone levels were significantly decreased in lepromatous leprosy (1.6 +/- 0.12 ng/ml), tuberculoid leprosy (4.2 +/- 1.7 ng/ml) and borderline leprosy (1.8 +/- 0.18 ng/ml). The basal plasma 17-beta estradiol levels were significantly elevated in all the three types of leprosy. The basal plasma prolactin levels in plasma were significantly increased in lepromatous and tuberculoid leprosy. During hCG stimulation tests, the peak plasma testosterone responses were significantly reduced in both lepromatous leprosy and tuberculoid leprosy subjects. The blunted testosterone responses during hCG stimulation tests in leprosy correlated with the high basal 17-beta estradiol levels (r = 0.58; P less than 0.05). These results strongly suggest that hypogonadism in leprosy results from primary testicular failure. The significant elevation of plasma 17-beta estradiol levels in lepromatous, tuberculoid and borderline leprosy could play a role in hypogonadism of leprosy.