Abstract: TH-PO1142
Villous Adenoma: A Rare Cause of Hypokalemia and Metabolic Alkalosis
Session Information
- Fluid, Electrolyte, Acid-Base Disorders
November 02, 2017 | Location: Hall H, Morial Convention Center
Abstract Time: 10:00 AM - 10:00 AM
Category: Fluid, Electrolytes, and Acid-Base
- 704 Fluid, Electrolyte, Acid-Base Disorders
Authors
- Bianchi, Daniel, Loma Linda University School of Medicine, Loma Linda, California, United States
- McMillan, James I., Loma Linda University, Loma Linda, California, United States
Background
The differential diagnosis of hypokalemia and metabolic alkalosis is large and includes fluid loss without HCO3- wasting (vomiting/diuretics), mineralocorticoid excess, and hereditary conditions such as Bartter syndrome. We present an unusual case of hypokalemia and metabolic alkalosis.
Methods
A 58 year-old previously healthy male was admitted to the ICU after 15 days of weakness, muscle cramps, orthostatis and blood streaked stools. He had hyponatremia and acute kidney injury, and was fluid resuscitated. Two months later his physician saw him for rectal pain, diagnosing hemorrhoids, and noted a potassium of 2.4. He was given KCl without work up.
He had two more ICU admissions for severe volume depletion in 4 weeks. Representative labs: serum Na 131, K 2.9, Cl 88, CO2 34, Cr 1.5, aldosterone 78 and plasma renin activity 39.5. He was believed to have Bartter’s syndrome, given amiloride and ibuprofen, and referred to our facility for nephrology consultation. A history of rectal mucoid discharge prompted a suspicion of villous adenoma, confirmed by colonoscopy. The 11 cm distal rectal lesion was resected transrectally. All symptoms resolved.
Conclusion
The mistaken initial diagnosis of Bartter Syndrome was based on the elevated aldosterone, hypokalemia, metabolic alkalosis, and lack of hypertension. However inadequate resuscitation of his fluid and electrolyte loss from the villous adenoma explains the hormonal and electrolyte abnormalities.
Villous adenoma depletion syndrome (McCrittrick Wheelock) is rare, resulting from a mucous secreting villous adenoma in the distal colon causing volume depletion, hypokalemia, and usually metabolic acidosis. Up to 3% of villous adenomas are secretory. Hypersecretion of bicarbonate and electrolytes from abnormal enterocytes is likely the cause.
We describe a rare case of villous adenoma with metabolic alkalosis. Literature review identified 58 cases of villous adenoma depletion syndrome; 7 had metabolic alkalosis. The cause of the metabolic alkalosis variant may be over expression or activation of apical chloride channels in adenoma goblet cells. Increased cAMP or cGMP production in goblet cells could also lead to over activity of CFTR channels causing chloride secretion. Finally, decreased expression of the Downregulated in Adenoma (DRA) gene may decrease expression of Cl/Na exchangers reducing chloride absorption.