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Abstract: TH-PO360

Ectopic Adrenocorticotropic Hormone (ACTH) Syndrome Presenting with Hypokalemia in a Patient with Prostate Cancer

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

  • 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

  • Rehmani, Muhammed N., The University of Texas Health Science Center at Houston John P and Katherine G McGovern Medical School, Houston, Texas, United States
  • Mandayam, Sreedhar A., The University of Texas MD Anderson Cancer Center, Houston, Texas, United States
Introduction

Cushing’s syndrome is a disorder resulting from excess cortisol levels in the body. Most common clinical manifestations are hypertension, weight gain, excess abdominal fat and hirsutism. We present the case of a patient who presented with refractory hypokalemia and was found to have Cushing’s syndrome from ectopic ACTH production despite no clinical signs. Ectopic ACTH syndrome (EAS) is most commonly seen in neuroendocrine tumors however it is rarely also seen in those with primary prostate cancer.

Case Description

A 61-year-old-male with metastatic castrate-resistant prostate cancer and hypertension was admitted for severe hypokalemia. Nephrology was consulted for persistent hypokalemia, with serum potassium levels between 2-3 mmol/L despite multiple enteral and parenteral replacements. His blood work was remarkable for serum sodium of 149 mmol/L, serum pH of 7.66 and serum bicarbonate of 30 mmol/L suggestive of metabolic alkalosis. Of note, he had routine labs one month prior, including electrolytes, which were normal. Further work up revealed elevated serum cortisol and ACTH levels. Dexamethasone suppression test was performed which showed ectopic ACTH production. He underwent extensive imaging, but no source of ectopic ACTH production could be identified. He was therefore diagnosed with EAS secondary to prostate cancer and started on daily metyrapone. Due to poor prognosis, he was discharged to hospice.

Discussion

Cushing’s syndrome is rare, and diagnosis is frequently delayed due to non-specific symptoms. Our patient had normal labs one month ago and had no clinical manifestations commonly seen in Cushing’s syndrome. Prompt workup of refractory hypokalemia led to a timely diagnosis. Had this patient remained outpatient, diagnosis could have been delayed potentially leading to complications from hypokalemia. This patient also had prostate cancer which does not commonly cause ectopic ACTH production. However, there are growing number of cases in patients with castrate-resistant prostate cancer with treatment related neuroendocrine differentiation as a cause of EAS. Key take-away from this case is that it is important for clinicians to have a high index of suspicion for atypical presentations such as electrolyte disturbances as a presenting sign for underlying Cushing’s syndrome.