Endocrine Abstracts

Introduction: Primary hyperaldosteronism is a known cause for secondary hypertension. In addition to its effect on blood pressure, aldosterone exhibits proinflammatory actions and plays a role in immunomodulation of autoimmunity. Autoimmune hyperthyroidism (Graves’ disease) and primary hyperaldosteronism rarely coexist but underlying mechanisms associating the two are still unclear.

Case report: A 32-year-old female referred to endocrine unit for further evaluation and management of hypertension and hypokalemia. She was on three antihypertensive medications at the time of presentation but had poor blood pressure control. She also had nonspecific body aches and intermittent muscle cramps palpitation and sweating with associated heat intolerance, recent weight loss, for the past 2 months. She did not have any virilizing features. She was not on diuretics or any long-term medications except three antihypertensive medications. None of her family had hypertension, strokes, or sudden deaths at younger age. Examination, pulse: 110 /minute, blood pressure: 140/100 mmHg while on antihypertensive therapy BMI: 23 kg/m2. There was a small diffusely enlarged goiter without any tenderness. Bilateral mild exophthalmos normal eye movements and vision. Investigations:potassium, 2.1 mmol/l (3.5–5) Patient with hypertension, hypokalemia, possibility of primary hyperaldosteronism was considered. Aldosterone: renin ratio (ARR) was measured after correcting the potassium value and adjusting the interfering medications ARR was 198 [ng/dl]/[ng/ml/hr] (n:<20) A contrast enhanced computed tomography (CT) of abdomen showed a right-sided homogenously dense (density of 9.5 Hounsfield Units {HU}) adrenal lesion measuring 2.0 × 1.5 × 0.8 cm Evaluation of the thyroid status revealed evidence of hyperthyroidism: TSH < 0.08 μIU/ml (0.27–4.0), free T4—4.60 ng/dl (0.7–1.9), and free T3—7.36 pg/ml (2–4.4). Ultrasound scan of the thyroid showed diffusely enlarged gland with increased echo pattern and vascularity on Doppler studies, compatible with Graves’ disease Thyrotoxicosis was managed with antithyroid drugs (Carbimazole)30 mg/day titration till she was on 10 mg/day and once patient rendered euthyroid, laparoscopic right adrenalectomy was performed. Antithyroid medications were discontinued after 12 months after which patient achieved remission of Graves’ disease.

Conclusion: Primary hyperaldosteronism (PA) is a leading endocrine cause for secondary hypertension, particularly in resistant hypertension Recent studies have demonstrated role of aldosterone on immunomodulation together with its effects on adaptive immune system, suggesting the possible rare link with development of autoimmune disorders