Endocrine Abstracts

Introduction: Adrenal incidentalomas are asymptomatic adrenal masses found accidentally during routine examination, not intended for adrenal pathology evaluation. The functionality of these lesions must be further investigated. Rarely, bilateral adrenal nodular hyperplasia can be detected in a patient with Cushing’s disease. The authors present the case of a patient with possible autonomous cortisol secretion of adrenal origin that eventually emerged as Cushing’s disease.

Clinical case: A 69 years old male, with known history of arterial hypertension, dyslipidaemia and ischemic heart disease, was observed in an Endocrinology outpatient clinic due to adrenal incidentalomas in 2015. Upon investigating axillary adenopathies, thoracoabdominal CT scan revealed adrenal nodules measuring 23 and 15 mm on the right adrenal gland and two 16mm nodules on the left gland. All the nodules had typical adenoma features, except one on the left, which was hyperdense but had a homogeneous contrast distribution. The patient had no clinical features of Cushing’s syndrome. The patient was evaluated for hormone excess: 1mg overnight dexamethasone test not suppressed (3.8 μg/dl) with an overlapping Liddle test; normal urinary 24-hour cortisoluria: 15.0 μg/24h (4.3–176.0) and ACTH <5.0 pg/ml. Urinary normetanephrine and plasmatic catecholamine levels were elevated, but less than twice the normal value. IMIBG scintigraphy was negative. Aldosterone/active renin ratio was normal; thyroid function and fosfocalcic metabolism were also normal. The authors concluded that the patient had a possible autonomous cortisol secretion and opted for a strategy of surveillance – clinical, analytical and imagiological. Two years later, in 2017, the patient presented with syncope and altered mental status and underwent a cerebral CT scan, showing a large expansive lesion on the sphenoidal body, with enlargement of the sella turcica; a second tumoral lesion on the anterior skull base was described, with cystic and solid areas (possibly a pituitary adenoma). There was no hormonal deficit. Cerebral MRI further characterized the lesion on the sphenoidal body extending to the anterior skull base, possibly a meningioma, craniopharyngioma or a pituitary macroadenoma. The patient was admitted for transcranial surgery. Anatomopathological analysis confirmed the diagnosis of a pituitary adenoma, with positive ACTH immunohistochemistry.

Conclusions: In face of a patient with an ACTH producing pituitary adenoma with bilateral adrenal nodules and an investigation directing towards a possible ACTH-independent hypercortisolism, the possibility of a previous bilateral adrenal hyperplasia, which was posteriorly autonomized, is considered. However, it is not possible to exclude concomitant functional adrenal and pituitary nodules.