Endocrine Abstracts

A 20-year-old female first presented in 2013 with a six-month history of feeling faint, palpitations, weight loss and oligo-amenorrhoea. She was found to have autoimmune thyrotoxicosis with a fT3 15.2, fT4 43.3, TSH <0.05 and TPO antibodies strongly positive. She was subsequently commenced on Carbimazole 20 mg once a day and was biochemically euthyroid within 6 months. Interestingly, however, she continued to lose weight and remained oligo-amenorrhoeic. Her BMI was now 18 (weight 46 kg).

Her initial pelvic ultrasound did not show polycystic ovaries. Serum testosterone was 1.2 mmol/l, LH 0.9U/L, FSH 3.7U/L, oestradiol 161 pmol/l, prolactin 124 mU/L with 9am cortisol and remaining pituitary profile within normal range. MRI pituitary was unremarkable. Her TFTS remained within normal range off the Carbimazole. DEXA scan: T-score −0.2 at lumbar spine, −0.1 at left hip.

She was diagnosed with anorexia nervosa by the eating disorders team. With their support, she gradually gained weight from 46 kg in January 2014 to 54.3 kg in April 2015, 65 kg in September 2015 and now 73 kg in 2016 (BMI 30). However despite normalisation of her weight, spontaneous periods did not resume. Her repeat pelvic ultrasound showed ovaries that were a little bulky with several small peripheral follicles and were thought to be polycystic in appearance with a reverse FSH:LH ratio (FSH 7.1U/L, LH 9.3U/L, oestradiol 255 pmol/L, Prolactin 132 mU/L, TFTs normal) suggestive of PCOS. She has no immediate plans to start a family and is taking an oral contraceptive pill at present, with regular withdrawal bleeds. She has been given lifestyle advice to regain a normal weight.

This case highlights multiple diagnostic and treatment challenges in a young patient with oligo-amenorrhoea. It is proposed that her amenorrhoea may originally have been due to Graves’ disease, was subsequently due to her persistent low body weight (hypothalamic amenorrhoea secondary to anorexia nervosa), and ultimately, after gaining excess weight, due to exacerbation of underlying polycystic ovary syndrome - a clinical conundrum?