Is bariatric surgery really inefficient in hypothalamic obesity?

to tamoxifen alone. The inhibitory effect of androgens on breast cells appears to occur in a dose-dependant manner. Although confounded by the use of gonadotropin-releasing hormone analogue therapy, histological data derived from mastectomies from female-to-male transsexuals exposed to high-dose androgens have demonstrated reduction in glandular tissue in up to 93% of cases. Our case provides clinical evidence that pathologically high levels of androgens cannot only reduce proliferation, but may inhibit normal breast development, despite appropriate pubertal levels of oestrogen and an apparently mature hypothalamic– pituitary–gonadal axis. Thus, it appears that the elevated androgens were having a direct inhibitory effect on the breast tissue. Moreover, the rapid progression of breast development (15 months to attain Tanner 5 breasts, compared with average progression from Tanner 2–4 over 36 months) provides further evidence that removal of the source of the elevated androgens allowed breast development to proceed. Although androgens have been associated with both endometrial atrophy and proliferation, our case provides evidence that high-dose androgens can inhibit endometrial maturation. While at initial presentation, there was no endometrial stripe on ultrasound, postoperatively, with resolution of the hyperandrogenism, regular menses commenced within 2 months. High androstenedione levels have been shown to be a risk factor for primary amenorrhoea and thinner endometrial lining in girls with polycystic ovarian syndrome, supporting the hypothesis that significantly elevated androgens can inhibit the endometrium. In conclusion, our patient, presenting with discordant biochemical and physical signs of puberty, provides unique insight into the potential inhibitory effects of significantly elevated androgens on breast and endometrial maturation.