Abstract
A documented case of acinic cell adenocarcinoma of the parotid glands with metastases to the nodes, liver and lung, with ectopic ACTH production, is presented. Our patient had manifestations typical of excessive ectopic ACTH production, characterized by hypokalemic alkalosis and weakness but no hypertension, striae or the typical fat distribution of Cushing's syndrome. The pathologic specimens assured the origin of the tumor to be acinic cell. Assays of blood and of both primary and metastatic tumors demonstrated excessive ACTH. Urinary steroid excretion studies using the double isotope dilution method revealed elevated cortisol and corticosterone levels but normal aldosterone and desoxycorticosterone levels. These results suggest that hypertension occurring with ectopic ACTH-producing tumors may not necessarily be related to the concomitant hypokalemic alkalosis. The findings in this patient suggest that hypokalemia is not necessarily a sequel of increased mineralocorticoid but may be the result of excess production of cortisol and/or corticosterone. A documented case of acinic cell adenocarcinoma of the parotid glands with metastases to the nodes, liver and lung, with ectopic ACTH production, is presented. Our patient had manifestations typical of excessive ectopic ACTH production, characterized by hypokalemic alkalosis and weakness but no hypertension, striae or the typical fat distribution of Cushing's syndrome. The pathologic specimens assured the origin of the tumor to be acinic cell. Assays of blood and of both primary and metastatic tumors demonstrated excessive ACTH. Urinary steroid excretion studies using the double isotope dilution method revealed elevated cortisol and corticosterone levels but normal aldosterone and desoxycorticosterone levels. These results suggest that hypertension occurring with ectopic ACTH-producing tumors may not necessarily be related to the concomitant hypokalemic alkalosis. The findings in this patient suggest that hypokalemia is not necessarily a sequel of increased mineralocorticoid but may be the result of excess production of cortisol and/or corticosterone.
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