Proximal Colonic Secretory Villous Adenoma Causing Diarrhea and Depletion Syndrome: 878

Purpose: An 80-year-old Caucasian woman with hypertension and diverticulosis presented with exacerbation of chronic diarrhea, described as progressive, watery, nonbloody, and voluminous (>1 liter/day). The diarrhea persisted while fasting and sleeping, but was worse with oral intake. She denied pain, fever, nausea, vomiting, dietary changes, recent travel, or any new medications. Colonoscopy performed 5 months prior for similar symptoms showed a 12 mm ascending colon tubulovillous adenoma, which was incompletely resected. Random biopsies revealed a “mild nonspecific chronic colitis.” Loperamide was used for presumed microscopic colitis, with partial improvement. Results: The patient was lethargic, but afebrile with normal vital signs. Physical exam was otherwise unremarkable. Laboratory testing was remarkable for hypokalemia (2.7 mmol/L), acute kidney injury (Cr=1.7 mg/dL), metabolic acidosis, and hypoalbuminemia (2.5 g/dL). Leukocytosis was absent. Metabolic and infectious studies were unremarkable. Fecal calprotectin, fat, and elastase, as well as stool osmotic gap, were normal. Gastrin and VIP levels were within normal limits. Abdominal films and duodenal biopsies were unremarkable. Colonoscopy revealed a 3 cm x 2 cm ascending colon polypoid lesion; biopsies identified it as a villous adenoma. Terminal ileum and random colon biopsies were normal. Endoscopic mucosal resection was performed, completely removing the lesion. Pathology revealed focal areas of villi with abundant, clear mucin-filled goblet cells, suggestive of secretory villous adenoma. On follow-up, this patient had complete resolution of her diarrhea and depletion syndrome, off loperamide. Discussion: Secretory villous adenomas of the colon may cause a depletion syndrome characterized by dehydration, prerenal azotemia, hypokalemia, metabolic acidosis, obtundation, and rarely, death. Histologically the villous epithelia are enriched with abundant, atypical, hypersecretory, clear mucin-filled goblet cells, in contrast to non-secretory villous adenomas. The mechanism of diarrhea may be due to abnormal mucin and/or prostaglandin production. Definitive management is endoscopic or surgical resection. Prostaglandin inhibitors have also been described as temporizing treatment. Cases published to date describe secretory villous adenomas located only in the rectum and sigmoid colon. Conclusion: We report a first case of proximal colonic secretory villous adenoma with depletion syndrome that resolved with endoscopic mucosal resection. This diagnosis should be considered in the differential of subacute or chronic watery diarrhea. It also underscores the importance of thorough right-sided colonoscopic inspection, for all indications.