Endocrine Abstracts

Introduction: Primary hyperaldosteronism is the main endocrine cause of secondary hypertension. Its association with an autonomous cortisol secretion is rarely described in the literature. Here we report the case of a patient having a unilateral adrenal adenoma responsible for both mineralocorticoids and glucocorticoids excess.

Observation: A 54-years-old female diagnosed at the age of 26 years with hypertension. She received up to four antihypertensive treatments including thiazide diuretics without prior investigation. At the age of 52 years, she was admitted for angina with normal coronary arteries where a severe hypokalemia was detected and treated with potassium supplementation in addition to the withdrawal of diuretics. The diagnosis of renal artery stenosis was ruled out and the CT scan revealed a 2 cm unilateral left adrenal adenoma. The patient was hospitalized later in our department for hormonal investigation. At admission she presented clinical symptoms of tetany, U wave in electrocardiogram with low serum potassium (2.5 mmol/l). The hypokalemia required up to 20.8 g per day of oral and IV potassium supplementation in order to maintain normokalemia. Renin dosage was low (3.6 mIU/l) despite the use of ACE inhibitor which cannot be stopped due to the severity of hypokalemia and hypertension. Once spironolactone (50 mg per day) was introduced in addition to captopril (150 mg per day) and amlodipine (10 mg per day), blood pressure and potassium was stabilized and the patient didn’t require additional supplementation. 1 mg overnight dexamethasone suppression and 2-day low-dose dexamethasone tests were elevated 20 and 24 ng/ml successively. The patient didn’t have catabolic signs. ACTH level was incompletely suppressed (14.9 pg/ml) and the pituitary imaging was normal. Surgical treatment was chosen due to the glucocorticoids excess in addition to prediabetes and bone demineralization.

Discussion: Connshing syndrome is a challenging disease characterized by overproduction of mineralocorticoids and glucocorticoids from adrenal adenoma. Hypercortisolism, although generally mild, is able to increase the risk of developing diabetes mellitus and osteoporosis. Medical treatment could normalize hypertension and hypokalemia but it has no effect on glucocorticoids excess which requires adrenalectomy to be cured. The long evolution of resistant hypertension in our patient without clinical feature of Cushing syndrome may rise the question whether the overproduction of glucocorticoids is concomitant or not to primary hyperaldosteronism.