C. SETH LANDEFELD, M.D.; MORRIS SCHAMBELAN, M.D.; SELNA L. KAPLAN, M.D., Ph.D.; STEPHEN H. EMBURY, M.D.
Grant support: in part by grant HL 20985, and in part by General Resource Center grant RR00083, Division of Research Resources, National Institutes of Health.
▸Requests for reprints should be addressed to Stephen H. Embury, M.D.; Building 100, Room 263, San Francisco General Hospital, 1001 Potrero Avenue; San Francisco, CA 94110.
LANDEFELD CS, SCHAMBELAN M, KAPLAN SL, EMBURY SH. Clomiphene-Responsive Hypogonadism in Sickle Cell Anemia. Ann Intern Med. 1983;99:480-483. doi: 10.7326/0003-4819-99-4-480
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Published: Ann Intern Med. 1983;99(4):480-483.
Two 19-year-old men with sickle cell anemia and hypogonadism had hypothalamic dysfunction that responded to oral clomiphene therapy. The patients had no nutritional deficiencies or anatomic lesions known to result in the hypogonadism associated with sickle cell anemia. Their sickle cell disease was characterized by infrequent crises, severe hemolytic anemia, urinary iron loss, and iron deficiency. Partial hypothalamic hypogonadism was shown by low levels of testosterone, low to low-normal levels of luteinizing hormone and follicle-stimulating hormone, and a nearly normal rise in gonadotropin levels in response to exogenous gonadotropin releasing hormone. Treatment with oral clomiphene raised luteinizing hormone, follicle-stimulating hormone, and testosterone levels to normal, and induced puberty in both patients. Treatment was discontinued in one patient because of the onset of priapism, but was continued for 10 months without side effects in the other. Severe hypogonadism in patients with sickle cell anemia should be thoroughly evaluated and clomiphene therapy considered in patients with hypothalamic dysfunction.
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Hematology/Oncology, Red Cell Disorders.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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