topically active agents such as break-capsule budesonide and mesalamines. In addition, the medications were reviewed and among them, the use of immunomodulators had significant association with abnormal neo-terminal ileum histology, which may reflect the need for immuno- modulators in patients with small bowel disease, particu- larly in those with CD of the pouch. The significant correlation between acute inflammation in the duodenum and chronic pouchitis may imply the value of having post-operative EGD evaluation. In patients with chronic antibiotic-refractory pouchitis, secondary etiologi- cal factors should be sought out. One of the factors is autoimmune-related mechanism. Pouchitis has been tradi- tionally believed to result from bacterial stasis in the pouch reservoir. The presence of acute duodenal inflammation on histology suggests that in a subset of patients with chronic pouchitis, other parts of GI track may also be involved. This would provide clues for additional etiopathogenetic pathways of pouchitis. There were limitations to our study. It was a historical cohort study from a tertiary care center. There might have been referral and selection biases, because of the nature of practice of our Subspecialty Pouchitis clinic with a majority of the patients having a variety of pouch disorders. Since multiple adverse pouch complications were measured, the study might have been underpowered with type II error. EGD was performed for a variety of indications at different time points from the IPAA surgery with suspicion for upper GI diseases. It would be desirable to design a larger, prospective study to evaluate the predictive role of pre- and post-operative EGD in consecutive patients. In conclusion, EGD with duodenal biopsy may yield additional diagnostic information in patients with IPAA.