Clinical use of androgenic steroids at a major medical center: who prescribes androgens and how well do they do it?

To assess prescribing practices for androgens at Wilford Hall USAF Medical Center, the authors analyzed prescriptions for all patients receiving therapy during a 12-month period (n = 201) and reviewed the available outpatient records not maintained elsewhere (n = 105). The most commonly prescribed androgens were testosterone enanthate (144/201; 56.7%), and danazol (52/201; 25.9%). Review of the available outpatient medical records of 73 male patients using testosterone enanthate showed a mean age of 59.5 years, mean frequency of injection of 20 days, mean duration of therapy of 3.5 years, and mean dose of 226 mg. Therapy was initiated by a urologist (34/73; 46.6%), an endocrinologist (33/73; 45.2%), or an internist (6.73; 8.2%). Indications for therapy based on pretreatment laboratory and historical data included hypergonadotropic hypogonadism (24/73; 32.9%), hypogonadotropic hypogonadism (23/73; 31.5%), unspecified hypogonadism (7/73; 9.6%), and empiric treatment of elderly men with erectile dysfunction without evidence of hypogonadism (9/73; 26%). Pretreatment prostate examinations as well as measurement of serum testosterone (66/73; 90.4%) and serum gonadotropins (52/73; 71.2%) were often not performed. The authors conclude that records of patients treated with androgens show: 1) Doses are appropriate; 2) Empiric treatment of erectile dysfunction in elderly men is common despite the associated risks; 3) Laboratory and physical evaluation before treatment is often incomplete; 4) There was no evidence of androgenic substance abuse in patients studied.

McCune-Albright syndrome: how many endocrinopathies can one patient have?

In this one patient with McCune-Albright syndrome are seen a multitude of endocrinopathies--more than in any case previously described. Only fibrous dysplasia with café-au-lait spots and/or endocrine hyperfunction are required for the diagnosis of the syndrome. Our patient has polyostotic fibrous dysplasia, café-au-lait spots, and at least four primary endocrinopathies. She had shown precocious puberty (with an ovarian follicular cyst later requiring resection), hyperthyroidism due to toxic nodular thyroid disease, primary hyperparathyroidism, and hyperprolactinemia (with associated hypogonadotropic hypogonadism and premature menopause). With this many organs involved in the same patient, it is hard to imagine that a genetic defect will not soon be identified as the unifying cause of the entire syndrome.

Partial 3 beta-hydroxysteroid dehydrogenase deficiency presenting as new-onset gynecomastia in a eugonadal adult male.

The postpubertal clinical presentation of 3 beta-hydroxysteroid dehydrogenase deficiency (3B-HSD deficiency) is less well-defined for adult males than for adult females, who often present with hirsutism. We describe a male with normal puberty who presented with new-onset gynecomastia at age 24. Common causes of gynecomastia were excluded. Dehydroepiandrosterone-sulfate (DHEA-S), estradiol, estrone, and 24-hour urinary 17-ketosteroid levels were elevated. A feminizing tumor was considered; biochemical tumor markers, chest x-ray, ultrasound of testes, and abdominal computed tomography (CT) scan were negative. Dexamethasone-suppression testing showed normal suppression of 24-hour urinary adrenal steroids. Cosyntropin-stimulation testing showed normal cortisol, 11-deoxycortisol, 17-OH progesterone (17-OHP), and aldosterone levels, but significant elevations of pregnenolone (preg), 17-OH preg, progesterone, DHEA, and androstenedione (A) levels. The sperm count was high and gonadotropin-releasing hormone (GnRH)-stimulation testing showed a normal increase in testosterone (T) level, suggesting that the defect did not involve the testes. It is concluded that this patient's gynecomastia is due to 3B-HSD deficiency with an associated alteration in sex hormone ratios. To our knowledge, this is the first well-described adult male with normal gonadal function presenting with postpubertal gynecomastia due to 3B-HSD deficiency. This defect may be a frequently unrecognized cause of gynecomastia.