Endocrine Abstracts

JOINT2857

Introduction: New-onset moderate-severe post-menopausal hyperandrogenism is associated with significant metabolic disorders that increase the risk of cardiovascular disease and mortality, prompting early diagnosis and treatment.

Case Report: We present the case of a 58-year-old nulliparous woman, menopaused at 55 years, with medical history of autoimmune thyroiditis, mild hypothyroidism, and important cardiometabolic comorbidities (arterial hypertension, heart failure, coronary stent, poorly controlled type 2 diabetes mellitus requiring insulin treatment, hyperlipidemia), that was referred to the Endocrinology Department to evaluate slowly progressive androgenic alopecia and hirsutism developed over the last 8 years, exacerbated 3 years before presentation. Clinical examination revealed a BMI of 38 kg/m² with abdominal fat distribution, blood pressure of 160/100 mmHg, frontotemporal alopecia, increased terminal hair growth, particularly on the face, trunk, forearms and thighs, skin hyperpigmentation, and acanthosis nigricans. Initial biological evaluation showed significantly elevated total testosterone:13.87 nmol/l(reference range 0.10-1.42) and estradiol: 39 pg/ml (postmenopausal<10 ) with FSH and LH at the lower limit of normal values. Serum ACTH, cortisol, DHEAS, TSH, prolactin, and 17-OH-progesterone were within the normal range, while IGF-1 and random GH levels were elevated (IGF1= 308 ng/ml, reference range <225, 24 hours random serum GH between 1 ng/ml and 2.15 ng/ml). After undergoing a long dexamethasone suppression test (5 days, 4x0.5 mg/d), serum cortisol was adequately suppressed (<1.8 mg/dl), DHEAS was suppressed more than 60% but testosterone levels exhibited a paradoxical increase (17.74 nmol/l, N<1.42). Abdominal-pelvic MRI revealed bilateral increased ovarian volume with a 9-mm right ovarian mass and a right adrenal adenoma of 14/9 mm. Alpha-fetoprotein, CA 125, CEA, and CA 19-9 levels were normal. The patient was referred to the Surgery department to undergo bilateral oophorectomy for definitive diagnosis and treatment.

Discussion: Multiple causes of hyperandrogenism may be considered in this case: 1. Adrenal hyperandrogenism/Cushing syndrome – ruled out due to adequate DHEAS and cortisol suppression, 2. Ovarian hyperandrogenism – either hyperthecosis or virilizing ovarian tumor, considering the imaging evidence of enlarged ovaries together with an ovarian mass and high non-suppressible testosterone which make this hypothesis the most likely, 3. Autonomous GH secretion- cannot be ruled out, needing further evaluation after the surgical intervention and optimal control of diabetes mellitus.