GYNECOMASTIA
GYNECOMASTIA: Excerpt from Differential Diagnosis in Primary Care
Because gynecomastia is produced by a hormonal disturbance, the many causes of this disorder can be recalled by using the physiologic model of intake, production, transport, regulation, destruction, or excretion.
GYNECOMASTIA
Intake
Obviously if one takes estrogen or other feminizing hormones, gynecomastia may result. Injections of human chorionic gonadotropin (HCG) as are used in the treatment of obesity may cause gynecomastia. Not so obvious is the gynecomastia resulting from ingestion of methyl testosterone and desoxycorticosterone. Taking drugs such as amphetamines, tricyclic antidepressant, methadone and isoniazid may also cause this disorder.
Production
The production of estrogen or estrogenlike substances is increased in testicular tumors such as seminomas, sertoli cell tumors, and adrenal tumors. The production of prolactin or HCG is increased in pituitary tumors and carcinoma of the lung. Several drugs including phenothiazines, marijuana, reserpins, and methyldopa increase prolactin production. Carcinoma of the lung may also increase HCG production. Production of testosterone and other androgens or androgen-producing substances is decreased in Klinefelter syndrome, advancing age, mumps orchitis, hypothalamic lesions, liver disease, and neurologic disorders such as myotonic dystrophy, syringomyelia, and Friedreich ataxia. Testosterone production is also reduced in pseudohermaphroditism and congenital adrenal hyperplasia.
Regulation
The regulation of the ratio of circulating estrogen and androgen may be affected in hyperthyroidism, hypothyroidism, renal failure, and dialysis.
Drugs such as spironolactone, digitalis, griseofulvin, cimetidine, and cannabis antagonize androgens causing gynecomastia.
Transport
Plasma proteins that carry hormones are reduced in starvation and many debilitating states reduce testosterone activity and availability leading to gynecomastia.
Destruction
In liver disease such as hemochromatosis, cirrhosis, carcinoma, and hepatitis there may be increased conversion of testosterone to estrogens. The same mechanism may occur in hyperthyroidism.
Approach to the Diagnosis
It is important to find out if the patient has been taking drugs of any kind. On physical examination, the physician may find bronze skin (a sign of hemochromatosis), a testicular mass, neurologic signs (suggesting Friedreich ataxia, myotonic dystrophy, paraplegia, etc.) or abnormal secondary sex characteristics (suggesting Klinefelter syndrome or pseudohermaphroditism). The laboratory workup should include a thyroid profile, liver profile, serum prolactin, urine drug screen, serum iron and iron binding capacity and serum FSH, LH, testosterone, and estradiol. Referral to an endocrinologist may be wise before ordering these expensive tests.
Other Useful Tests
- Buccal smear for Barr bodies (Klinefelter syndrome)
- Serum cortisol (Cushing syndrome)
- Cortisol suppression test (Cushing syndrome)
- Rapid corticotropin test (congenital adrenal hyperplasia)
- β-HCG (pituitary tumor, neoplasm of lung)
- Neurology consult
Book Source Details
- Book Title: Differential Diagnosis in Primary Care
- Author(s): R. Douglas Collins
- Year of Publication: 2007
- Copyright Details: Differential Diagnosis in Primary Care, Copyright © 2007 Lippincott Williams & Wilkins.
More About Gynecomastia
More Medical Textbooks Online about Gynecomastia
Review other book chapters online related to Gynecomastia:
Medical Books Excerpts
- Gynecomastia
- "Professional Guide to Signs & Symptoms (Fifth Edition)" (2006)
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- Gynecomastia
- "The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter" (2000)
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
» Next page: BREAST DISCHARGE (Differential Diagnosis in Primary Care)
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