A111 SEVERE FAT MALABSORPTION IN A PATIENT POST ILEAL POUCH ANAL ANASTAMOSIS: A RARE PRESENTATION OF MICROSCOPIC ENTERITIS

Abstract

Abstract Background Microscopic enteritis (ME) is a rare enteropathy characterized by malabsorptive diarrhea and lymphocytic infiltration +/- collagen deposition in the subepithelial layer of the small bowel. Its etiology is unclear. Aims To elucidate a rare cause of fat malabsorption and vitamin deficiency in a patient with ulcerative colitis and an ileoanal pouch. Methods A 74 yo male with a prior IPAA was referred to Internal Medicine in August 2018 for a 36 kg weight loss over 18 months and >16 bowel movements (BM) per day (baseline 6, no history of pouchitis). Celiac serology and infectious workup were negative. Medical management and nutritional supplements did not result in weight gain or improvement of diarrhea. He was admitted in June 2019 with ongoing weight loss, AKI, and signs of fat-soluble vitamin deficiency. A 72-hour fecal fat analysis showed an average fecal weight of 2100 g/d (ref <250 g/d), and excretion of 70% of daily fat intake (ref <7%). His fecal elastase (FE) was 147 µg/g, consistent with moderate pancreatic insufficiency (PI) with mild atrophy on CT. EGD and pouch endoscopy were macroscopically normal, with histological findings of intraepithelial lymphocytosis and mild villous blunting in the duodenum and afferent limb. CT enterography excluded small bowel abnormalities. He was started on pancreatic enzyme replacement and discharged. He returned with worsening diarrhea and AKI. He was treated with supportive care and sent home. In the ensuing 3 weeks, he had up to 24 BM per day and 4 kg of weight loss. He returned in August 2019 with AKI, lack of PO intake and worsened nutritional status. Re-examination of duodenal biopsies from June 2019 revealed an added finding of focal subepithelial collagen thickening. Budesonide was started. Results On budesonide, his symptoms improved within days. BMs decreased to baseline, and his ability to sustain PO intake improved. At his 4-week follow-up visit, BMs were stable with a 6 kg weight gain and no ensuing laboratory abnormalities. Conclusions ME is a rare enteropathy that presents with malabsorption. Fat-soluble vitamin deficiencies can develop with widespread physiological disruption of the mucosal surface. This patient was a diagnostic challenge. His steatorrhea and reduced FE levels led clinicians down a diagnostic pathway of PI. FE is the most common test used in the diagnosis of PI. Levels <200 µg/g are abnormal. Specificity is highest in chronic pancreatitis; however, this decreases in the presence of mucosal atrophy (i.e. IBD and diffuse small bowel disease). Thus, FE could not delineate the cause of steatorrhea in our patient. We can surmise that he likely has diffuse disease that was underestimated on duodenal biopsy. This is supported by his response to budesonide. This case highlights the heterogeneity of clinical presentations of ME. Awareness can reduce patient morbidity. Funding Agencies None