Spironolactone Induced Gynecomastia

The pathophysiology of gynecomastia after spironolactone administration has been carefully studied in man. As noted above, spironolactone induces gynecomastia (and other antiandrogenic effects) principally by binding to cytosolic

R HORMONE RECEPTOR COMPLEX

{ACTIVE AT NUCLEAR LEVEL)

r SPIRONOLACTONE RECEPTOR COMPLEX

(INACTIVE AT NUCLEAR LEVEL)

FIGURE 2. Active androgens and more specifically 5a-dihydrotestosterone (DHT) interact with the androgen receptor (R) in target tissues to form hormone receptor complexes which activate protein synthesis. Low (50-75 mg) or high (200-400) doses of spironolactone interfere with DHT binding with its receptor to form inactive complexes at the nuclear level. From Tremblay.

androgen receptors. Subsequently, in patients who develop gynecomastia, blood testosterone levels decrease and blood estradiol levels increase. These changes come about by increases in metabolic clearance rate of testosterone as well as an increase in peripheral conversion to estradiol. Consequently, excessive stimulation of breast tissue as a result of an imbalance between estrogen and testosterone in the body leads to increased ductal proliferation and tender breast enlargement in males. Discontinuation of the drug results in slow reversal of this process sometimes requiring several months for complete normalization of breast size.

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