Symptom Finder - Gynecomastia
GYNECOMASTIA
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.
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 antidepressants, methadone, and isoniazid may also cause this disorder.
Production: The production of estrogen or estrogen-like 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, reserpines, 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.
Transport: Plasma proteins that carry hormones are reduced in starvation, and many debilitating states reduce testosterone activity and availability leading to gynecomastia.
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. Benign gynecomastia is a common condition in adolescent boys.
Destruction: In liver diseases such as hemochromatosis, cirrhosis, carcinoma, and hepatitis there may be increased conversion of testosterone to estrogen. The same mechanism may occur in hyperthyroidism.
Approach to the Diagnosis
It is important to find out if the patient has been taking alcohol or drugs of any kind. On physical examination, the physician may find bronze skin (a sign of hemochromatosis), a testicular mass, neurologic signs (suggesting, e.g., Friedreich ataxia, myotonic dystrophy, paraplegia), 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
1. Buccal smear for Barr bodies (Klinefelter syndrome)
2. Serum cortisol (Cushing syndrome)
3. Cortisol suppression test (Cushing syndrome)
4. Rapid corticotropin test (congenital adrenal hyperplasia)
5. β-HCG (pituitary tumor, neoplasm of lung)
6. Neurology consult
7. Chest x-ray (Carcinoma of the lung)
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.
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 antidepressants, methadone, and isoniazid may also cause this disorder.
Production: The production of estrogen or estrogen-like 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, reserpines, 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.
Transport: Plasma proteins that carry hormones are reduced in starvation, and many debilitating states reduce testosterone activity and availability leading to gynecomastia.
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. Benign gynecomastia is a common condition in adolescent boys.
Destruction: In liver diseases such as hemochromatosis, cirrhosis, carcinoma, and hepatitis there may be increased conversion of testosterone to estrogen. The same mechanism may occur in hyperthyroidism.
Approach to the Diagnosis
It is important to find out if the patient has been taking alcohol or drugs of any kind. On physical examination, the physician may find bronze skin (a sign of hemochromatosis), a testicular mass, neurologic signs (suggesting, e.g., Friedreich ataxia, myotonic dystrophy, paraplegia), 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
1. Buccal smear for Barr bodies (Klinefelter syndrome)
2. Serum cortisol (Cushing syndrome)
3. Cortisol suppression test (Cushing syndrome)
4. Rapid corticotropin test (congenital adrenal hyperplasia)
5. β-HCG (pituitary tumor, neoplasm of lung)
6. Neurology consult
7. Chest x-ray (Carcinoma of the lung)
