I have it noted that there is abnormal leydig cell function -> decrease in testosterone (testicle atrophy, specifically loss of sertoli cells) which leads to an increase in gonadotropins (fsh and lh) due to loss of negative feedback. The increase of fsh causes an increased synthesis of aromatase in leydig cells, the increased LH causes the testosterone release to be converted to estradiol via the increased aromatase--> increased estrogen.