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Impotence

As many as one third of patients with impotence have a definable endocrine abnormality. Most of these disorders involve the hypothalamic-pituitary-testicular (HPT) axis. Gonadotrophin releasing hormone (GnRH) stimulates synthesis and release of follicle stimulating hormone (FSH) and luteinizing hormone (LH). The main effect of FSH is on spermatogenesis. LH stimulates the synthesis of testosterone, which in turn suppresses LH secretion.

Measurement of early morning serum FSH, LH, and testosterone provides sufficient information for the classification of most patients with impairment of the HPT axis. Primary testicular failure is associated with increased FSH and LH and low or low-normal testosterone. Testicular failure secondary to hypothalamic or pituitary lesions is associated with low serum FSH, LH, and testosterone levels. Chronic systemic diseases such as renal failure, cirrhosis, and malnutrition are often associated with low levels of testosterone and normal levels of FSH and LH. Disorders of the HPT axis account for 75% of the endocrine causes of impotence.

The remaining 25% of cases of endocrine impotence are usually related to hypthyroidism and/or hyperprolactinemia. Prolactin excess is associated with prolactin secreting tumors of the pituitary; with many drugs including aldomet, cimetidine, estrogens, opiates, and tricyclic antidepressants; and with primary hypothyroidism where the excess thyrotropin releasing hormone stimulates both TSH and prolactin secretion. Prolactin inhibits FSH and LH release with the subsequent failure of testosterone production. Measurement of serum TSH and prolactin, in addition to FSH, LH, and testosterone, will identify these patients.

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