A 62 year old lady presented to the clinic with hirsutism, virilisation and temporal balding. Her past medical history included type 2 diabetes, hypothyroidism, ischaemic heart disease and peripheral vascular disease. Her body mass index was 30 kilograms per metre squared and she had mild cliteromegaly. Her serum testosterone was 3.6 nanomols per litre.
She had a high dose dexamethasone suppression test and CRH test to exclude Cushings Syndrome or Disease, a synacthen test for 17 Hydroxyprogesterone was normal, as were 24-hour urine steroid metabolites. Her serum testosterone was 2.8 nanomols per litre after low dose dexamethasone suppression test therefore HCG stimulation followed by leuprorelin suppression was performed to assess ovarian testosterone production. Serum testosterone fell to 0.6 nanomols per litre. Ultrasound showed the ovaries to be bulky with abnormal parenchymal pattern and CT scan showed normal adrenals
Bilateral oophrectomy was performed. Histology showed ovarian stromal hyperplasia with no evidence of malignancy. Post operatively her serum testosterone fell to 0.6 nanomols per litre with clinical improvement.
The post-menopausal ovary is an androgen producing gland, producing 40% of the total body testosterone and is composed mainly of stromal cells. There is no correlation between ovarian size and stromal hyperplasia which sometimes appear in normal sized ovaries. There is a positive correlation with degree of hyperplasia and androgen levels, both androstendione and testosterone, increasing body weight and some evidence for correlation with cortisol levels.
Virilisation is usually most readily attributable to a testosterone producing tumour. Bilateral ovarian enlargement can conceal small stromal-Leydig cell tumours although this is rare. Stromal hyperplasia is associated with virilisation, obesity and diabetes mellitus and is most often encountered in post-menopausal women.
22 - 24 Mar 2004
British Endocrine Societies