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The syndrome of ectopic ACTH secretion from an occult carcinoid tumor is a well-recognized entity. There are roughly two types of ectopic ACTH syndrome, one associated with overt malignancy like oat cell carcinoma and the other with oc­ cult neoplasm. Carcinoid tumors are the most common occult source of A CTH .1 In a recent review of 68 cases of ectopic ACTH-secreting tumors, 60% were carcinoid followed by small cell carcinoma of the lung (10%), pan­ creatic neuroendocrine neoplasia, and miscellaneous other tumors.2 Typically, ectopic ACTH is suspected when a patient with a known malignancy is found to have refractory hypokalemia and metabolic alkalosis. Less frequently pa­ tients may present with typical clinical and/or biochemical features of Cushing syndrome before the oncologic diag­ nosis. Somatostatin receptor scintigraphy (SRS) allows us to differentiate between patients with somatostatin recep­ tor positive tumors, which are likely to respond favorably to treatment with somatostatin analogue (octreotide) and those who are SRS negative, for whom chemotherapy may be indicated.3 A reduction in cortisol excess in response to keto­ conazole can be expected in most patients with ectopic Cushing syndrome, and clinical improvement in hypo­ kalemic metabolic alkalosis, diabetes mellitus, and hy­ pertension may occur even in the absence of a complete hormonal response. Ketoconazole is an effective and safe treatment for ectopic Cushing syndrome, but ultimate control of the syndrome is dependent on successful treat­ ment of the underlying malignancy.4

Metastatic hepatic carcinoid associated with ectopic ACTH syndrome, resistant to octreotide and ketoconazole therapy