Abstract
The possible mechanisms involved in the development of transient gynecomastia during male puberty were investigated by studying 24 h profiles of circulating androstenedione (Ao) and testosterone (T) and their estrogen pairs estrone (E1) and estradiol (E2), in 8 boys with simple delayed puberty, 11 boys with pubertal gynecomastia (3 of whom were re-tested after its spontaneous resolution) and 2 normal adult men. No differences were observed between the 24 h T and Ao profiles of pubertal boys with or without gynecomastia; the initial T rise was nocturnal, associated with sleep. Late in puberty daytime T levels also rise. A small rise in 24 h Ao was seen, but this was not closely related to the stage of puberty. The major new finding was that E2 and to a lesser extent E1 levels are high relative to T for prolonged periods of the afternoon and evening (when T levels are lowest) in male puberty. A frequent finding, seen only in boys with gynecomastia and one who later developed it, was of elevated and markedly fluctuating levels of plasma E2, and an absolute increase in the area under the 24 h E2 profile and between the E2 and T profiles. These fell towards normal in 3 boys who were re-tested after resolution of gynecomastia. In a minority of subjects T and E2 were quite closely correlated, suggesting that in them rapid aromatization of T was occurring within or outside the testis. Normal male puberty is associated with relative estrogen dominance particularly in the daytime. In boys with gynecomastia there is an addition often an absolute elevation of E2 with or without E1, while 24 h T levels are submaximal. Normal men probably require sustained adult circulating T levels to prevent their estrogens from stimulating breast development.