SAT-040 - Ectopic ACTH Production Causing Hypertension and Hypokalemia in A Patient with Two Discrete Stage IV Cancers

Background: Stage IV cancer patients foregoing palliative treatment in favor of surveillance often present to the hospital with new complaints of non-specific symptoms. Although initial work-up and treatment may initially relieve these vague symptoms, persistent electrolyte abnormalities may clue us into additional underlying causes of disease.

Clinical

Case: We report the case of a 66-year-old man with a medical history of stage IV low-grade B-cell Non-Hodgkin lymphoma undergoing surveillance with interval liver and lung lesions, type 2 diabetes, and hypertension who presented due to mild shortness of breath, abdominal pain, fatigue, and weakness after presenting 6 days earlier to a different institution for high glucose and high blood pressure. Upon arrival, he was hypertensive with hyperglycemia, 2+ ketonuria, anion gap 14 mEq/L (n=8-16 mEq/L), and bicarbonate 24 mEq/L (n=22-29 mEq/L) with normal kidney function. Chest x-ray showed known adenopathy from prior CT thorax, and CT abdomen showed no acute process, but an interval increase in size of widespread metastatic disease throughout the liver that had yet to be biopsied. The patient’s potassium remained persistently low throughout his hospitalization, despite daily repletion and the initiation of eplerenone. This hypokalemia, in combination with persistent hypertension and progressive metabolic alkalosis, warranted further workup. Initial work-up of hyperaldosteronism was unremarkable [aldosterone levels (3.3 ng/dL, n=3-30 ng/dL) and ARR (5.5, n < 30)]. Workup of Cushing’s syndrome displayed an elevated late-night serum cortisol level (96.2 nmol/l, n < 50 nmol/l) and 1mg dexamethasone suppression test cortisol (104 nmol/l, n < 50 nmol/l), suggesting that Cushing’s Syndrome is the more likely cause of these symptoms. Workup of secondary causes showed elevated 8 mg dexamethasone suppression test cortisol (103 nmol/l, n >= 50% drop in cortisol) and extremely elevated ACTH (3,179 pg/mL, n=7.2-63.3 pg/mL), which suggested ectopic ACTH secretion as the cause of this patient’s symptoms. A liver biopsy uncovered metastatic non-small cell carcinoma with neuroendocrine features likely responsible for ectopic ACTH production. Given the presence of known lung lesions, the most likely primary source is the lung.

Conclusion: This case highlights the importance of not only interval imaging but also interval basic metabolic panels to look for paraneoplastic syndromes that may be causing symptoms in patients who choose to forgo treatment for Stage IV cancer. While it is easy to attribute new lesions to metastatic progression of the known malignancy, without biopsy confirmation, we cannot exclude the possibility of a new primary malignancy that has also metastasized, and we cannot guide treatment as effectively.

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