Endocrine Abstracts

A 49-year-old woman was referred to our hospital for the evaluation of adrenal incidentaloma. She had no past medical history and no family history of notable illness. The patient was 150 cm tall and weighed 60 kg. Her blood pressure was 103/60 mmHg. She had no Cushingoid features. Osteoporosis was absent. Routine laboratory examinations were within the normal ranges including normokalemia. The hormonal examination revealed normal circadian variation in serum cortisol levels (11.7 μg/dl at 0800 h and 3.3 μg/dl at 2300 h) and plasma ACTH level was undetectable (<2.0 pg/ml). Plasma cortisol level was suppressed after the low-dose overnight dexamethasone suppression test but was not suppressed after the high-dose test. The plasma aldosterone concentration (PAC) level was normal (110 pg/ml) and the plasma renin activity (PRA) was suppressed (0.1 ng/ml per h). The captopril test and furosemide-upright test were positive, whereas the saline-loading test was negative. CT scans of the abdomen showed bilateral adrenal tumors. Adrenal scintigraphy revealed bilateral adrenal activity. To determine the laterality of the excessive cortisol or aldosterone secretion, we performed adrenal venous sampling (AVS). Finally, we made a diagnosis of subclinical primary aldosteronism (PA) caused by both adrenal glands and subclinical Cushing’s syndrome (CS) caused by both adrenal tumors. Interestingly, this patient had no risk factors for cardiovascular disease such as hypertension, obesity, diabetes mellitus or dyslipidemia. Thus, we are observing her without medical therapy. Three years after diagnosis, she has not been detected hypertension, hypokalemia, cardiomegaly in echocardiography and atherosclerosis in carotid ultrasonography. One important remaining question is why excessive hormone secretion did not affect the cardiovascular status of this patient. In this regard, several possible mechanisms have been reported including mineralocorticoid resistance. Further study is going to resolve this issue.