Endocrine Abstracts

The association of low body weight due to excessive exercise and/or eating disorders, and hypothalamic amenorrhoea is well documented. Delayed or arrest of puberty may occur if low body weight occurs before or during puberty. Normal menstruation is restored once a healthy body weight is regained. In this case, body weight normalised but ovarian function did not.

A 34-year-old woman attended our thyroid clinic for subclinical hypothyroidism following an episode of thyroiditis four years previously. She had a long history of anorexia nervosa since the age of 13 and subsequently developed osteoporosis secondary to her prolonged oestrogen deficiency. She had never attained menarche. She was given the oral contraceptive pill a few years previously, but stopped it after only a few weeks. Hypogonadotrophic hypogonadism was documented while her body weight was low but her BMI had been within the normal range (>18.5) over the last 18 months. Her gonadotrophins had recovered (FSH 127.7 IU/l, LH 74.5 IU/l); however, menstruation had not occurred and serum oestradiol levels remained low (50 pmol/l). Further tests including chromosomal analysis, 17-OHP, short synacthen test and ovarian antibodies were normal. An MRI pelvis showed a small uterus with thin endometrium and streaks of ovarian tissue in the adnexae. She has been commenced on low dose ethinylestradiol.

Patients with anorexia nervosa frequently present with difficult management problems. Osteoporosis occurs in up to 50% of these patients and may be difficult to treat despite adequate oestrogen replacement. Gonadal dysfunction may persist even after correction of body weight but persistent ovarian failure is very rare. We suggest that this patient’s ovarian atrophy is a direct consequence of her arrested pubertal development following prolonged suppression of gonadotrophic function. Early identification and adequate psychological and nutritional support for these patients is essential to restore normal endocrine function.