A Case of Ectopic ACTH Syndrome Associated with Small Cell Lung Cancer Presented with Hypokalemia.

Hong Jun Yang; Hea Jung Sung; Ji Eun Kim; Hyo Jin Lee; Jin Min Park; Chan Kwon Park; Eun Suk Roh; Jae Hyung Cho; Seung Hyun Ko; Ki Ho Song; Yu Bai Ahn

doi:10.3803/jkes.2007.22.5.359

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Case Report A Case of Ectopic ACTH Syndrome Associated with Small Cell Lung Cancer Presented with Hypokalemia.: Hong Jun Yang, Hea Jung Sung, Ji Eun Kim, Hyo Jin Lee, Jin Min Park, Chan Kwon Park, Eun Suk Roh, Jae Hyung Cho, Seung Hyun Ko, Ki Ho Song, Yu Bai Ahn; Endocrinology and Metabolism 2007;22(5):359-364
DOI: https://doi.org/10.3803/jkes.2007.22.5.359
Published online: October 1, 2007

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Department of Internal Medicine, College of Medicine, The Catholic University of Korea.

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Abstract

We report a case of a 73-year-old female patient who was diagnosed with ectopic ACTH syndrome caused by small cell lung cancer. We initially presumed that the patient was in a state of mineralocorticoid excess, because she had hypertension and hypokalemic alkalosis. This was however excluded because her plasma renin activity was not suppressed and her plasma aldosterone/plasma renin activity ratio was below 25. Moreover, her 24 hour urine free cortisol level was elevated and her serum cortisol levels after a low dose dexamethasone suppression test, were not suppressed. Furthermore, her basal plasma ACTH and serum cortisol levels increased and her serum cortisol level after a high dose dexamethasone suppression test was not suppressed. We performed studies to identify the source of ectopic ACTH syndrome and found a 3 cm-sized mass in the patient's right lower lobe of her lung, which was eventually diagnosed as small cell lung cancer following a bronchoscopic biopsy. In conclusion, Cushing's syndrome, and in particular ectopic ACTH syndrome, must be considered in the differential diagnosis of mineralocorticoid-induced hypertension. The excessive cortisol saturates the 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) activity, which in turn, inactivates the conversion of cortisol to cortisone in the renal tubules. Moreover, excessive cortisol causes binding to the mineralocorticoid receptors, causing mineralocorticoid hypertension, characterized by severe hypercortisolism.

Keywords: Ectopic ACTH syndrome;hypokalemia;small cell lung cancer;

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