Endocrine Abstracts

Introduction: Hyperandrogenism is an uncommon finding in postmenopausal women. Possible sources of the elevated androgen levels include Cushing’s syndrome, Polycystic ovarian syndrome, benign and malignant androgen secreting ovarian tumors, ovarian hyperthecosis, adrenocortical tumours and iatrogenic hirsuitism.

Case: A 65 year-old lady was referred with a raised testosterone level of 2.6 nmol/l [0–1.8 nmol/l]. She experienced weight gain and fatigue for over 6 months. She also had nail changes and hair loss, with increased hair growth on her face and acne that had gradually worsened in the last year. There were no changes to voice or muscle size. She experienced menopause in 2003 and received HRT therapy for a year then stopped it. Clinically she scored 15 on Ferriman Gallway score for hirsutism with no clinical features of Cushing’s syndrome or Acromegaly.

Investigations: Testosterone of 2.7 nmol/l [0–1.8 nmol/l], Androstenedione 3.1 nmol/l [<3.0 nmol/l], LH 42.4 mlU/ml, FSH 104.0 mlU/ml, DHEAS 0.9 umol/L, Oestradiol<90, Prolactin 91 mU/l, 17-hydroxyprogesterone Progesterone <1.6 nmol/l, Insulin growth factor-1: 25.6 nmol/l, overnight dexamethasone suppression test: Cortisol <25, TSH 0.71 mU/l [0.35–5.5 mU/L], T4 13.6 pmol/l [10.0–19.8 pmol/L]. Ultrasound pelvis showed a bulky right ovary. MRI pelvis was unremarkable with no worrying features. DEXA scan showed normal bone density. A CT adrenal scan showed a mildly nodular appearance to the left adrenal gland, however, there were no focal adrenal lesions. GnRH agonist suppression test: GnRH agonist administration resulted in a dramatic decline in testosterone levels with Testosterone level of 0.5 nmol/l, Androstenedione of 2.2 nmol/l, LH 1.4 mlU/ml, FSH 7.8 mlU/ml on the 4th week following the injection. There was dramatic improvement of her symptoms. She has now been referred for oophorectomy.

Discussion: Identification of the source of elevated androgens often creates a clinical challenge. Hyperandrogenism has virilizing physical effects but is also associated with dyslipidaemia, hypertension, insulin resistance, uterine and cardiovascular disease. If the source is identified, surgery (whether oophorectomy or adrenalectomy) is often curative. Medical management with GnRH agonist/analogues or antagonists has been reported in the literature but may have associated side effects.