Adrenal cortex adenoma

No decrease in survival. Increased frequency of adrenal cortex adenomas in females 25% vs. 1.3% in controls... 

No decrease in survival 20% of females developed adrenal cortical adenomas and 10% had neoplastic nodules in the adrenal cortex vs. 0% in controls... 

Metyrapone is commonly used in tests of adrenal function. The blood levels of 11-deoxycortisol and the urinary excretion of 17-hydroxycorticoids are measured before and after administration of the compound. Normally, there is a twofold or greater increase in the urinary 17-hydroxycorticoid excretion. A dose of 300-500 mg every 4 hours for six doses is often used, and urine collections are made on the day before and the day after treatment. In patients with Cushing s syndrome, a normal response to metyrapone indicates that the cortisol excess is not the result of a cortisol-secreting adrenal carcinoma or adenoma, since secretion by such tumors produces suppression of ACTH and atrophy of normal adrenal cortex. 

The remaining 18% of Cushing s syndrome cases are ACTH-independent and are almost equally divided between adrenal adenomas and adrenal carcinomas, with rare cases caused by micronodular or macronodular hyperplasia." The majority of adrenal cortex tumors are benign adenomas. Adrenal carcinoma is found more often in children than in adults with Cushing s syndrome. 

Primary aldosteronism implies that the physiologic abnormality is within the adrenal cortex. The most common causes include a solitary adrenal adenoma (60%) or idiopathic adrenocortical hyperplasia (35% bilateral and 5% unilateral). Other rare causes include adrenal cortex carcinoma, primary adrenocortical hyperplasia, renin-responsive adrenocortical adenoma, and genetic mutations, such as in glucocorticoid-suppressible hyperaldosteronism. " " ... 

Synaptophysin Neuroendocrine tumors pituitary adenomas, medullary thyroid carcinoma, pheochromocytoma, islet cell tumors, small cell carcinoma, carcinoid and neuroendocrine Medulloblastoma, retinoblastoma, neurocytoma, ependymoma, neuroblastoma, adrenocortical tumors. Merkel cell tumors Neuronal and neuroendocrine cells, carotid body cells, adrenal cortex and medulla... 

In patients with primary aldosteronism, the aldosterone levels in the blood and the amount of aldosterone excreted in the urine are markedly increased. Primary aldosteronism may or may not be associated with the development of a tumor of the adrenal cortex. When a tumor exists, it is usually small and weighs less than 6 g. Chemical analysis of the adrenal indicates that the cortex is rich in aldosterone, probably as a result of hypersecretion. Eighty-five per cent of the patients have a single or multiple adenoma of the adrenal cortex. Bilateral hyperplasia of the adrenals is found in 10% of the patients. 

This is the secretion of excess aldosterone, due in most cases to a benign aldosterone-secreting adenoma of the adrenal cortex. Excess aldosterone causes sodium retention at the expense of potassium, and hypokalaemia develops. 

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