Excerpt from: http://patients.uptodate.com/topic.asp?file=r_endo_m/6642
PREVENTION OF DRUG-INDUCED GYNECOMASTIA — The simplest method to prevent gynecomastia is to avoid those drugs that cause gynecomastia… Gynecomastia will occur in almost every male who takes a large dose of spironolactone (100 mg/day), and in over 50 percent of those receiving estrogens or antiandrogens for advanced prostate cancer.
Even drugs within the same class do not all cause gynecomastia to the same extent. Among the calcium channel blockers, as an example, nifedipine has the highest frequency of gynecomastia and diltiazem the lowest [1,2]. Thus, in an older man who is at increased risk of gynecomastia simply on the basis of age, diltiazem would be preferable to nifedipine. Another example is the use of H2-receptor or parietal cell proton-pump blockers; the incidence of gynecomastia is highest with cimetidine and then ranitidine, and is lowest with omeprazole. Thus, omeprazole would be a better choice in an older individual with other risk factors for developing gynecomastia. In addition, among the aldosterone antagonists, the frequency of gynecomastia is highest with spironolactone, but much lower with epleronone, a more selective aldosterone antagonist.
Options for treatment of gynecomastia are presented here. The special case of hormone therapy-associated gynecomastia in men with prostate cancer is discussed separately ().
DETERMINANTS OF THERAPY — A major factor that should influence the initial choice of therapy is the duration of gynecomastia. Histologic studies show that the glandular changes in the breast are the same with all inciting causes, and the extent of glandular proliferation depends upon the intensity and duration of the stimulation. The histologic picture changes over time.
Initially, there is extensive ductal epithelial hyperplasia, proliferation and lengthening of the ducts, an increase in the stromal and periductal connective tissue, and proliferation of periductal inflammatory cells. There is also extensive periductal edema and stromal fibroblastic proliferation. This is the early or florid stage of gynecomastia and generally is present for the first six months after onset (show histology 1A-1B) [4-7].
After twelve or more months, the breast tissue evolves into the late or quiescent stage. At this time, there is a slight increase in the number of ducts, with marked dilatation of the ducts and little or no epithelial cell proliferation. There is also an increase in the amount of stroma, stromal fibrosis and a disappearance of the inflammatory reaction (show histology 1A-1B).
It is unlikely that any medical therapy will result in significant regression in the late fibrotic stage. As a result, medical therapies, if used, should be tried early in the course.