Endocrine Abstracts (2017) 50 EP016 | DOI: 10.1530/endoabs.50.EP016

'Connshing syndrome' as a cause of hypertension: case report

Antonia Lefter, Cristina Căpăt´ână, Diana Deciu, Şerban Radian & Cătălina Poiană


Department of Endocrinology, Carol Davila University of Medicine and Pharmacy, C.I. Parhon National Institute of Endocrinology, Bucharest, Romania.


Introduction: An association between primary hyperaldosteronism and autonomous cortisol secretion, tentatively termed ‘Connshing’ syndrome, is becoming increasingly recognized.

Aim: To present a case of primary hyperaldosteronism associated with ACTH-independent subclinical Cushing’s.

Methods: Clinical examination, biochemical testing and imaging studies.

Results: A 49-year old hypertensive (max 210 mmHg), obese (BMI=35 kg/m2), normoglycemic female patient without clinical signs of Cushing’s was screened for secondary hypertension, revealing normokalemia (4.1 mEq/L), an increased plasma aldosterone to renin (PAC/PRC) ratio and unsuppressed PAC during the saline loading test (PAC nadir=10.2 ng/dL, N<10). Cortisolemia was unsuppressed following 1 mg dexamethasone (DEX) overnight (4.66 ug/dL, N<1.8), 2×2 mg DEX (5.74 ug/dL) and 2×8 mg DEX (9.79 ug/dL). 24 hr urinary free cortisol (UFC) levels were normal, but did not suppress with DEX. Contrast-enhanced CT revealed bilateral diffuse adrenal hyperplasia, without identifiable nodules; adrenal sampling was not available. A pituitary microincidentaloma, initially found on a head CT scan was not confirmed by pituitary MRI. The patient’s hypertension was controlled with the addition of spironolactone. Regular follow-up is being performed to prevent development of clinical Cushing’s.

Conclusion: Subclinical Cushing’s is possibly underdiagnosed in primary aldosteronism patients, depending on subject selection and tests used for screening of hypercortisolism.

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