Endocrine Abstracts

A 60-year-old lady was referred with male pattern hair loss and facial hirsutism of 5–7 years duration. She was otherwise well and had two children in their 30s. She was not taking any medication and reported a normal menstrual cycle prior to menopause at the age of 50.

Her androgen profile showed a high testosterone level of 6.1 nmol/l (range <2.5), androstenedione 3.8 nmol/l (0.7–3.8), DHEAS 5.7 μm/l (0.80–4.9), SHBG 33 nmol/l, FAI 17.9% (0.1–2.6). LH was 22 IU/l and FSH 59.6 IU/l consistent with post-menopausal state. Thyroid function was normal.

CT of adrenals showed no evidence of tumour. Pelvic US showed a normal right ovary, left ovary not visualized.

She subsequently underwent laparoscopic bilateral salpingo-oophorectomy. Ovarian histopathology indicated Leydig cell hyperplasia, an uncommon cause of hyperandrogenism in post-menopausal women. Her testosterone level normalized to 1.3 nmol/l 3 months after surgery.

Interestingly her elder sister had also undergone bilateral salpingo-oophorectomy 3 years earlier. She had been found to have a testosterone level of 7.0 with clinical evidence of virilization. Her ovarian histology was unremarkable. In light of family history slides from 2013 were recently re-examined by a Histopathologist. No evidence of Leydig cell hyperplasia was seen but it was suggested that this could be focal and therefore not present in the tissue sampled.

Leydig cell hyperplasia causing hyperandrogenism in women is rare with several case reports only in the literature. This case raises the possibility of a genetic component which has been described in males due to LH receptor mutations but never reported in females to the best of our knowledge. Our patient has not yet had genetic testing. Normal ovarian imaging does not exclude an ovarian source of hyperandrogenism and bilateral oophorectomy is a safe and effective procedure after excluding an adrenal source.