ESPE Abstracts

Introduction: Pubertal gynecomastia (PG), the benign enlargement of breast in adolescents, is a condition whose etiology has not been fully elucidated. Its peak incidence is at mid puberty and decreases thereafter. In many cases breast undergoes full or almost complete regression with advancement of pubertal development, but in others it persists into adulthood. There are still controversies on the precise hormonal imbalance that leads in some adolescents only to glandular proliferation of breast tissue and its lack of regression in others.

Methods: A total of 95 boys with PG were included in the present study. They were divided into three groups according to pubertal stage. Anthropometric measurements and hormonal investigations were collected and compared with a group of 64 healthy controls without PG matched in pubertal stage and anthropometrics.

Results: The hormonal investigations in the group with early pubertal development (Tanner stage 2) proved statistically significant elevation of estradiol (E 2 =125, 34 pmol/l) and decrease in testosterone/estradiol ratio compared to control group (E 2 =79, 53 pmol/l, P=0,023). The same is not found in groups of boys with Tanner stage 3, 4 and 5. Difference of the level of testosterone (T), free T, bioavailable T and Free androgen index (FAI) were not proved between patients and control group at the beginning of puberty, but the level of free androgens due to elevated sex-hormone binding protein (SHBG) were found significantly lower in mid puberty (3-rd and 4-th pubertal stage).

Conclusion: A significantly higher level of estradiol at the very beginning of puberty may be the reason for the development of PG, while in the heyday of puberty the low index of free androgen with a higher SHBG may explain the presence of PG.