Moore D C, Schlaepfer L V, Paunier L, Sizonenko P C
J Clin Endocrinol Metab. 1984 Mar;58(3):492-9. doi: 10.1210/jcem-58-3-492.
The plasma profiles of 8 hormones were followed over the course of prepuberty and puberty in 30 adolescent males who developed gynecomastia and 24 who did not. Throughout puberty, ratios of delta 4-androstenedione to estrone (E1) and estradiol (E2) were significantly lower in the gynecomastia group than in the control group. Similarly, ratios of dehydroepiandrosterone-sulfate to E1 and E2 were significantly lower in the gynecomastia group. In contrast, ratios of plasma testosterone to E1 and E2 as well as plasma progesterone and PRL concentrations, were similar in both groups. Because of the adrenal origin of dehydroepiandrosterone and its sulfate, and of peripheral conversion of adrenal androgens to E1 and to E2, it appears that either decreased adrenal production of androgens and/or increased conversion of dehydroepiandrosterone-sulfate and delta 4-androstenedione to estrogens cause transient gynecomastia in adolescent boys.
对30名患男性乳房发育症的青春期男性和24名未患男性乳房发育症的青春期男性，在青春期前和青春期期间跟踪检测了8种激素的血浆水平。在整个青春期，男性乳房发育症组的δ4-雄烯二酮与雌酮（E1）和雌二醇（E2）的比值显著低于对照组。同样，男性乳房发育症组硫酸脱氢表雄酮与E1和E2的比值也显著较低。相比之下，两组的血浆睾酮与E1和E2的比值以及血浆孕酮和催乳素浓度相似。由于脱氢表雄酮及其硫酸盐来自肾上腺，且肾上腺雄激素可在外周转化为E1和E2，因此似乎肾上腺雄激素分泌减少和/或硫酸脱氢表雄酮和δ4-雄烯二酮向雌激素的转化增加导致了青春期男孩出现短暂性男性乳房发育症。
