Male Breast

11.1 FLORID-PHASE GYNECOMASTIA VS. ATYPICAL DUCTAL HYPERPLASIA IN GYNECOMASTIA

	Florid-Phase Gynecomastia	Atypical Ductal Hyperplasia (ADH) in Gynecomastia
Age	Adolescent boys and men in sixth and seventh decade, newborns (rare)	Late teens and adults
Location	Unilateral or bilateral, central and retroareolar	Central, retroareolar
Presentation	Unilateral or bilateral breast mass(es)	Rarely encountered in breast specimens from males with long-standing gynecomastia
Imaging Findings	Nodular density by mammography; ultrasound shows avascular, hypoechoic, nodular or poorly defined density parallel to the chest wall, without posterior enhancement or shadowing	Nodular density by mammography; on ultrasound, avascular, hypoechoic, nodular or poorly defined density parallel to the chest wall, without posterior enhancement or shadowing
Etiology	Relative or absolute estrogen excess: (1) therapeutic estrogen administration for treatment of prostate cancer; (2) increased endogenous production by tumors (e.g., Leydig cell tumor); (3) increased aromatization of androgens to estrogens (e.g., alcoholic cirrhosis, obesity and aging); (4) altered androgen to estrogen ratio (cirrhosis, renal failure, puberty, aging, anabolic steroids); (5) drugs decreasing androgen action, including illicit drugs; (6) transient exposure of male infants to maternal hormones	Unknown; often associated with gynecomastia, but etiologic factors leading to the specific development of ADH within gynecomastia are not known
Histology	Increased number of ducts within fibrous stroma with periductal edema and myxoid stroma (Fig. 11.1.1) Hyperplasia in ducts with thin, tapering micropapillae composed of cells with scant cytoplasm and pyknotic nuclei (Figs. 11.1.1, 11.1.2, 11.1.3) Epithelial micropapillae composed of cells that appear “stuck” to underlying luminal epithelium, rather than emanating from basement membrane (Figs. 11.1.3 and 11.1.4) Individual cell placement irregular and cell borders indistinct (Fig. 11.1.4) Stroma frequently resembles pseudoangiomatous stromal hyperplasia	Ducts are partially involved by a uniform population of bland cells; partial involvement is essential for diagnosis because lobular units are (usually) not present in male breast tissue (Figs. 11.1.5 and 11.1.6) Cells are evenly placed and secondary spaces are rigid with formation of microrosettes (Figs. 11.1.7 and 11.1.8) Residual, normally polarized epithelium is present at the periphery of a portion of the duct (Fig. 11.1.8)
Special Studies	None	None
Treatment	None, usually resolves; excision if cosmetically disfiguring	Total mastectomy
Clinical implication	None, no association with subsequent cancer risk	Due to rarity, clinical implications are not known; however, mastectomy is curative and the usual approach

Figure 11.1.1 Gynectomastia: Many ducts are expanded by an epithelial proliferation, and are encircled by dense stroma.

Figure 11.1.2 Florid hyperplasia of gynecomastia, showing numerous micropapillae.

Figure 11.1.5 Several ducts are expanded by an epithelial proliferation in ADH.

Figure 11.1.6 Cellular uniformity and rigid secondary spaces are present. Some secondary spaces are slit-like, and a normal cell population is present peripherally in this example of ADH.