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Gynecomastia due to alcoholic cirrhosis - See a little discussion


A 32 year old male patient with normal secondary sex characteristics, no testicular mass, no hystory of drug ingestion, no other endocrine abnormalities and a normal neurological examination.

Discussion

First of all in the evaluation of gynecomastia in adult men it is important to separate the normal(physiologic) from the abnormal breast tissue.
During puberty gynecomastia is a common finding in men beggining betwen 13 and 15 years of age but it usually regresses by age 20.
Gynecomastia of aging is also common and about 35-45% of aged men have it.
In this case the patient is not in puberty and is too young to be considered in the group of aging gynecomastia. Furthemore in the two situations described above it is very uncommon to find such a volomous gynecomastia.

At this point we have to consider a pathologic gynecomastia which can result from one of three basic mechanisms:
1) Drugs
2) Deficiency in testoterone production or action
3) Increase in estrogen production

1) Drugs

This patient denied any drug intake so we can proced the diagnostic evalution

2) Deficiency in testoterone production or action

Can result basically from two different mechanisms:

a) Congenital defects
- Klinefelter syndrome
- Congenital anorchia
- Defects of testosterone synthesis
- Reifenstein syndrome - testicular feminization

b) Secondary testicular failure
- Trauma
- Orchitis(viral)
- Renal failure
- Castration
- Neurologic disease

Again, this patient cannot be said to have any of the diseases above because of the description of his case.

3) Increase in estrogen production

This case was very simple because in the admission history(which was omitted in the case) this patient refers the intake of large amounts of alcohol during the past 15 years so the physician suspected of alcoholic cirrhosis. A liver biopsy was undertaken and Laennec's Cirrhosis was found which confirmed the diagnosis.

An increase in estrogen production in cirrhosis occurs because of diminished catabolism of androstenedione which increases the extraglandular tissues conversion of androgens to estrogens. The estrogens in excess produces gynecomastia.

Causes of increased estrogen production can be divided in:

a) Increased substrate for extragandular conversion
- Liver disease (this patient)
- Malnutrition
- Hyperthyroidism
- Adrenal disease

b) Estrogen secretion
- True hermaphroditism
- Testicular tumors
- Carcinoma producing beta-hCG

References

Frantz AG, Wilson JD: Endocrine disorders of the breast - Williams's Textbook of Medicine, 8th ed, JD Wilson, DW Foster. Philadelphia, Saunders, 1992, pag 953.


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