Endocrine Abstracts

Background: Primary hyperaldosteronism or Conn’s syndrome is one of the adrenocortical causes of hypertension, alongside hyperdeoxycorticosteronism, apparent mineralocorticoid excess and Cushing syndrome. The two types of hypertension-inducing adrenocortical syndromes (Conn’s and Cushing) are extremely rare to be decribed in the same patient. We describe a case of a patient with clinical and biochemical evidence of Conn’s syndrome due to a left adrenal adenoma, who developed, 5 years after left adrenalectomy, a potential contralateral cortisol secreting adrenal adenoma.

Case presentation: A 50 year old woman that initially presented in our clinic with severe hypertension, palpitations and headaches had undergone a CT scan 2 years prior which showed an adrenal adenoma, but no other further investigations were performed. The clinical examinantion showed severe obesity (BMI = 41 kg/m²) and uncontrolled hypertension on 4 hypotensors. Laboratory tests: potassium level = 3.3 mmol/l, plasma aldosterone concentration (PAC) = 188 pg/ml, plasma renin (PR) = 2.6 pg/ml, with a ratio of PAC to PR of 72 (≥ 20). The patient underwent laparoscopic left adrenalectomy in 2015, the histopathological examination showing reticular and glomerular hyperplasia. Post-surgery there was a slight decrease of the blood pressure and normalisation of aldosterone and renin levels with normal basal cortisol. Two years later, in 2017, at the annual evaluation, the patient underwent another CT scan, which revealed an adenoma of 1.02 cm/ 2.01 cm on the right adrenal gland. In January 2020, at the re-evaluation, the patient described frontal headaches and also had higher blood pressure since the last visit. We discovered that the right adrenal mass had similar dimensions, but the ACTH levels decreased and the basal cortisol levels were higher (plasma cortisol at 0800 h = 24.5 µg/dl). The overnight 1-mg dexamethasone suppression test (DST) was performed, which showed a level of cortisol just under the cut-off point, but close to the upper threshold of the test (1.78 µg/dl vs 1.8 µg/dl). Considering the possibility of the right adrenal mass to determine an ACTH-independent hypercortisolism, the next follow-up will be after 6 months when the 2×2 mg DST will be performed and also the 24-hour urinary free cortisol or late-night salivary cortisol will be assessed.

Conslusions: This case emphasizes the importance of long term follow-up of each patient with endocrine-related hypertension from the clinical point of view (palpitations, headaches, higher blood pressure, muscle weakness, etc.) and also from the hormonal point of view – for aldosteron, renin but mainly cortisol level.