Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2014) 35 P238 | DOI: 10.1530/endoabs.35.P238

ECE2014 Poster Presentations Clinical case reports Pituitary/Adrenal (50 abstracts)

A rare cause of primary hyperaldosteronism unilateral adrenal hyperplasia: case report

Kamile Gul 1 , Murat Sahin 1 , Ayten Oguz 1 , Fatih Yuzbasioglu 2 , Hamide Sayar 3 & Orcun Altunoren 4

1Department of Endocrinology and Metabolic Diseases, Kahramanmaras Sutcu Imam University School of Medicine, Kahramanmaras, Turkey; 2Department of General Surgery, Kahramanmaras Sutcu Imam University School of Medicine, Kahramanmaras, Turkey; 3Department of Pathology, Kahramanmaras Sutcu Imam University School of Medicine, Kahramanmaras, Turkey; 4Necip Fazil State Hospital, Nephrology, Kahramanmaras, Turkey.

Introduction: Most common two causes of primary hyperaldosateronism are bilateral idiopathic hyperplasia and aldosteron secreting adenoma but unilateral adrenal hyperplasia is a rare cause. We presented a primary hyperaldosteronism case that caused by unilateral adrenal hyperplasia.

Case: A 56-year-old male admitted to endocrinology policlinic with complaints of polydipsia, polyuria, fatigue and muscle wasting. He had hypertension for 4 years. In physical examination blood pressure, pulse was 175/100 mmHg and 92 beat/ min, respectively, Laboratory tests revealed hypernatremia (sodium 147 meq/l), hypokalemia (2.2 meq/l), increased creatinine kinase levels (1095 U/l), and metabolic alkalosis (pH 7.49, bicarbonate 35.9 mmol/l). After potassium correction plasma renin concentration (PRC), plasma aldosterone concentration(PAC), and PAC/PRC rate were 2.1 ng/l (5.3–99 ng/l), 401.5 pq/ml (38–313 pq/ml) and 200 pg/ml per ng per l (<50) respectively. In hormonal tests; TSH was 1.5 μIU/ml, cortisol was 14 μg/dl, urine catecholamine products were normal and dexamethasone suppression test was normal. Saline infusion test confirmed the diagnosis of primary hyperaldosteronism. Surrenal MR revealed a 18×16 mm adenoma in lateral limb of left adrenal gland. Spiranolactone treatment started and left surrenalectomy was performed. Pathologic evaluation detected adrenal hyperplasia that includes macronodular adrenal hyperplasia areas. The patient’s potassium and blood pressure were normal postoperatively.

Discussion: Primary aldosteronism is characterized by hypertension and hypokalemia and caused by increased aldosterone production from adrenal cortex. Our patient had nephrogenic diabetes insipidus and muscle wasting due to hypokalemia. Hypokalemia is observed in 50% of aldosteron producing adenomas and 17% of hyperplasia. Unilateral hyperplasia mimics aldosteron producing adenomas clinically and radiologically. Our patients was male, he had hypokalemia and hypertension and this findings are appropriate with unilateral hyperplasia cases in literature. We presented this case because of Unilateral adrenal hyperplasia is a rare cause of primary hyperaldosteronism and presented with different findings.

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