The aetiology of fibrocystic disease of the human breast remains problematical. While oestrogens may cause cystic lesions and epithelial proliferation in the mammary glands of experimental animals and certain
progestogens (
chlormadinone acetate and
medroxyprogesterone acetate) may induce severe myoepithelial
hyperplasia in beagles, the classical
oral contraceptives (oestrogens and
progestogens) reduce the incidence of
fibrocystic breast disease in women. The role of
prolactin in human
breast disease is far from clear despite the fact that in rodents mammary
tumors fail to develop following oestrogen administration in the absence of
prolactin. Because women with gross cystic disease of the breast are at four times greater risk of developing malignant
breast disease, it is felt that the administration of courses of
danazol, an impeded
androgen derived from the
progestin, 17 alpha-ethinyl
testosterone, has proved effective in lessening fibrocystic disease of the breast, frequently obviating the need for breast biopsy. The study of the hormonal content of fluid aspirated from gross
breast cysts should help elucidate the pathophysiology of
breast disease.
Breast cyst fluid is rich in
androgens, particularly
dehydroepiandrosterone sulfate; concentrations of
polypeptide hormones like FSH, LH, TSH, PRL, and
calcitonin are invariably present sometimes in less and at other times in greater amounts than that found in plasma. Of particular interest is the finding of measurable levels of beta-hCG in cyst fluid but not in the serum. The question arises whether the beta-hCG is biologically active or are the assay values merely the expression of radioimmunoassayable components? Preliminary (as yet unpublished) studies reveal excellent bioactivity as measured by
testosterone production in Leydig cell cultures. Time will tell whether elevated levels of bioactive beta-hCG portend neoplastic potential.