ESPE Abstracts

Hypogonadism, both primary and secondary, are well documented following cancer therapy. Primary ovarian insufficiency (POI) has most often been associated with exposure to alkylating agents (dose response) and radiation (RT) that includes the ovary (dose response). Early onset POI occurs commonly in girls exposed to ovarian RT at doses >10 Gy and following high-dose alkylating agents as is given for stem cell transplant. Late onset POI (ie, premature menopause) may be seen following modest doses of alkylating agents, especially exposure to procarbazine and lower doses of ovarian RT (<10 Gy). Childhood cancer survivors treated with doses of RT > 30 – 40 Gy to the hypothalamic-pituitary axis are at risk for deficits of LH and FSH. Elevated gonadotropins, especially FSH, are the hallmark of POI. It is important to note that levels can fluctuate over time; it is not uncommon for girls treated with chemotherapy alone to demonstrate normalization of gondatropins and spontaneous puberty/menses over time. As there are no long-term data correlating AMH levels in children and adolescents and subsequent ovarian function, measurement of AMH is not useful in making a diagnosis of POI. Gonadotropin deficiency needs to be considered in survivors exposed to high-dose hypothalamic-pituitary radiation who demonstrate delayed or arrested puberty associated with low or normal gonadotropins and low levels of estradiol. Treatment of hypogonadism in cancer survivors is, in general, similar to what is done in the non-cancer population. Special considerations are needed for those who have been exposed to chest RT and are at higher risk of developing breast cancer later in life.