PUTTING IT ALL TOGETHER: A CASE OF PRIMARY HYPOGONADISM. E.J. Favus 1 , R.C. Brooks 2 , R. Granieri 1 ; 1 University of Pittsburgh, Pittsburgh, PA; 2 Pittsburgh VA Healthcare System, Pittsburgh, PA (Tracking ID #73840) LEARNING OBJECTIVES: 1. To recognize the clinical presentation of male hypogonadism. 2. To recognize the differential diagnosis of acquired primary hypogonadism. CASE INFORMATION: A 66 year-old male presented with bilateral gynecomastia, osteoporosis, and erectile dysfunction. Three years ago he was seen by a urologist for erectile dysfunction and hesitency. He was diagnosed with a low testosterone state (laboratory values unavailable), and treated with testosterone. He had improvement of his erectile dysfunction but worsening of his hesitency and was switched to sildenafil. No cause was found for urinary hesitancy, but he was treated with tamsulosin without relief. Two years ago he fell and broke his left fourth metatarsal. Dual x-ray absorptiometry scan revealed a T-score of À2.7, and he was treated with alendronate. He denied a history of glucocorticoid use. One year ago he noticed increased breast tissue bilaterally and a mass in the right breast. A bilateral mammogram was negative and a breast biopsy was negative for malignant cells. His medical history is significant for tinea capitis, treated with 2% ketoconazole shampoo. His medications are sildenafil, alendronate, and ketoconazole shampoo. He has no history of alcohol, tobacco, or drug use. Physical examination reveals a normal thyroid, moderate bilateral gynecomastia without masses, no kyphosis, and normal size and shape of the penis, testicles, and prostate. Laboratory tests show total testosterone 239 ng/dL (241±827ng/dL), free testosterone 5.28 ng/dL (5±21ng/dL), FSH 32.1 mIU/mL (adult male normal range 1.55±9.70 mIU/mL), LH 14.7 mIU.mL (adult male normal range 0±9.0 mIU/mL), prolactin 13.0 ng/mL (adult male normal range 3.7± 17.9 ng/mL), TSH 4.13 uIU/mL (0.35±5.5 uIU/mL), PSA 1.68 ng/mL (0±4ng/mL). Given his low-normal testosterone and his clinical symptoms, he was re-started on testosterone therapy. IMPLICATIONS/DISCUSSION: The clinical presentation of osteoporosis, erectile dysfunction and gynecomastia should provoke a search for a unifying diagnosis of hypogonadism. The medical history of this patient is suggestive of a low testosterone state. His serum testosterone level is in the very low-normal range, and the FSH and LH levels needed to maintain this low-normal testosterone level are three times the upper limit of normal. High levels of FSH and LH exclude the diagnosis of secondary and tertiary hypogonadism. The low-normal level of testosterone has not been enough for this patient to avoid developing clinical disease. Male hypogonadism is defined as a failure of the testes to produce a sufficient amount of testosterone. Hypogonadism can be primary (testicular failure), secondary (pituitary failure), tertiary (hypothalamic failure), or combined primary and secondary. Primary hypogonadism can be either acquired or developmental. Our patient's laboratory values suggest primary hypogonadism. Since he had normal sexual development and fathered two children, he likely has acquired primary hypogonadism. Acquired primary hypogonadism may be the result of amyloidosis, autoimmune destruction, cryptorchidism, leprosy, leukemia, mumps, polyarteritis nodosa, radiation therapy, trauma, surgery (castration), or drugs such as cancer chemotherapy, ethanol, ketoconazole, marijuana, or spironolactone. In this patient, long term administration of ketoconazole shampoo for the treatment of tinea capitis may have resulted in acquired primary hypogonadism.