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Endocrine Abstracts (2006) 11 P145

ECE2006 Poster Presentations Clinical case reports (128 abstracts)

Postmenopausal androgen excess: a clinical perspective

SA Ritchie 1 , A Collier 2 , M McIntyre 3 & JMC Connell 1

1Western Infirmary, Glasgow, United Kingdom; 2Ayr Hospital, Ayr, United Kingdom; 3Royal Alexandra Hospital, Paisley, United Kingdom.

We present two cases of postmenopausal, gonadotrophin-dependent androgen excess.

Case 1: A 59-year-old postmenopausal female presented with a 4-year history of hirsuitism and male pattern balding. Past medical history included Type II diabetes, hypertension, and polycystic ovarian syndrome. Investigations revealed androgen excess (testosterone 8.9 nmol/l [ref range<2.5], free androgen index 31.8 [ref 0-7], androstenedione 13.7 nmol/l [ref<6.8], DHAS normal). Ovarian and adrenal imaging was normal. Venous sampling was inconclusive and she was referred to our unit for further investigation. Repeat MRI showed bilateral ovarian enlargement.

Case 2: A 59-year-old women with previous hysterectomy presented with 1 year of hirsuitism, voice deepening and male pattern alopecia. Investigations revealed androgen excess (Testo6.7, A’dione 40.3, FAI 21.6), failing to suppress with low-dose dexamethasone. Adrenal and Ovarian imaging was normal. A 4-week trial of GnRH analogue (Buserilin 300 mcg tid) suppressed circulating androgens in both cases, consistent with gonadotrophin-dependent hyperandrogenism. Both patients proceeded to bilateral oophorectomy. Pathology in case 1 showed diffuse stromal hyperplasia, in case 2 pathology was reported as normal. In both cases hirsuitism has regressed postoperatively and serum androgens have normalised. We present 2 cases of severe postmenopausal androgen excess where gonadotrophin suppression led to a clear fall in androgen production, confirming the ovary as the site of androgen production. Stromal cells may contribute to postmenopausal androgen production through a gonadotrophin-driven mechanism, although this hypothesis remains the subject of debate. Case 1 had a history of PCOS and it is unclear whether the pathological findings represent longstanding changes associated with PCOS, a marked cellular proliferation in the peri/postmenopausal period or a combination of both features. Case 2 probably represents less severe stromal hyperplasia. Gonadotrophin suppression offers a useful diagnostic test in patient evaluation with postmenopausal hyperandrogenism.

Volume 11

8th European Congress of Endocrinology incorporating the British Endocrine Societies

European Society of Endocrinology 
British Endocrine Societies 

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