GYNECOMASTIA

Abstract

Gyneco-mastia is the condition of unilateral or bilateral enlargement [long dash]W.H. Spankus of the [male] breast occurring as a result of hyperplasia of duct epithelium and periductal stroma. During World War II, the condition assumed the aspect of an occupational disability because of the mechanical irritation of the enlarged gland and psychic embarrassment resulting from communal living conditions. The etiology is not well understood. The general consensus is that the enlargement of the gland is a result of an altered endocrine status within the individual. Trauma is not a consistent factor. Various authors (Glass, Bergman, Heller, Nelson) have found a reduction in the urinary androgen excretion in the condition with a lowering of the androgen: estrogen ratio. Gynecomastia has been described (Klinefelter, Reifenstein, Albright, Heller, Nelson) as part of a syndrome in [male][male] consisting of breast enlargement, aspermatogenesis, small testes, increased excretion of FSH (follicle stimulating hormone) and frequently low normal to subnormal urinary excretion of 17-ketosteroids. This enlargement of the [male] breast has also followed natural or artificial elevations of the adrenal cortical steroids, estrogen, or androgen levels in the body. The changes in this condition may be similar to those found in chronic cystic mastitis in the [female] ; on occasions the changes resemble the normal pubertal [female] breast, at other times fibrous tissue predominates. In the differential diagnosis of cf breast enlargements, infectious processes, increased subcutaneous tissue and neoplasms must be considered. Surgical excision has been the most satisfactory method of treatment, but good results have been obtained in some cases with testosterone propionate given intramusc. Two cases of gynecomastia are reported. Both patients showed increased urinary excretion of FSH by the method used (uterine wt. increase in virginal 21-day old 9 white mice). Case 1 had an oligospermia but normal urinary excretion of 17-ketosteroids. Case 2 was a eunuchoid type individual with azospermia, atrophic testes, and decreased excretion of 17 -ketosteroids.