madman
Super Moderator
Gynecomastia is a benign enlargement of the male breast. If the etiology of breast enlargement remains unknown, gynecomastia is considered as idiopathic, and its frequency is estimated from 25% to 61%. Studies on the etiology of idiopathic gynecomastia involved examination of the level of the following hormones in blood: human prolactin, thyroxin, cortisol, human chorionic gonadotropin (β‐hCG), leptin, growth hormone and insulin‐like growth factor (IGF) and of receptors for estradiol, androgens, β‐hCG, prolactin, and luteotropin in the tissue of men's mammary glands.The studies showed that these factors may play a role in the pathophysiology of gynecomastia. However, their results are inconsistent. There are also some analyses which pointed out that a microsatellite polymorphism in the CYP19 gene can cause gynecomastia.The aim of this research was to examine the receptor status of estrogen (ER) and progesterone (PR) receptors of breast tissue in men with idiopathic gynecomastia and to verify the hypothesis concerning ER and PR overexpression in idiopathic gynecomastia.
In our study, we examined adult men with pathological condition—idiopathic gynecomastia. In our earlier study concerning the etiology of gynecomastia, we found out that prenatal estrogen and testosterone exposure may be a causative factor of idiopathic breast enlargement.To conclude, the obtained results may indicate that men with idiopathic gynecomastia present primary “overexpression” of ER and PR. This thesis may be supported by the fact that in many cases of idiopathic gynecomastia anti‐ estrogens appear to be effective in an unknown mechanism. Additionally, these findings may pave the way for further researches on effective pharmacotherapy in this condition and explain a mechanism of its efficacy.
In our study, we examined adult men with pathological condition—idiopathic gynecomastia. In our earlier study concerning the etiology of gynecomastia, we found out that prenatal estrogen and testosterone exposure may be a causative factor of idiopathic breast enlargement.To conclude, the obtained results may indicate that men with idiopathic gynecomastia present primary “overexpression” of ER and PR. This thesis may be supported by the fact that in many cases of idiopathic gynecomastia anti‐ estrogens appear to be effective in an unknown mechanism. Additionally, these findings may pave the way for further researches on effective pharmacotherapy in this condition and explain a mechanism of its efficacy.
