Introduction: Inflammatory bowel diseases (IBD), along with other immune-mediated disorders are considered as idiopathic disease entities with no clearly identified etiology. However, they can be triggered by medications, immunotherapy and manipulation of gut microbiome. Other triggers like proctocolectomy have not been well described. Case Presentation: A 29-year-old male with a history of ulcerative colitis (UC) had medically refractory disease to corticosteroids and infliximab, and underwent proctocolectomy with ileal pouch-anal anastomosis. Subsequently, he developed chronic persistent diarrhea and was diagnosed with celiac disease based on endoscopically obtained small bowel and celiac serology. HLA-DQA1 and HLA-DQB1 genotypes however, were negative. He was found to have elevated liver aminotransferases, positive anti-neutrophilic antibody and fatty infiltration on liver biopsy suggesting autoimmune hepatitis. After colectomy he developed multiple autoimmune conditions (Table 1). Some of them included; Hashimoto’s thyroiditis, type-1 diabetes and immune-mediated autonomic ganglionopathy. Subsequently he developed bilateral pulmonary embolism and was diagnosed with anti-phospholipid antibody syndrome. He also had an episode of bowel obstruction due to adhesions. He had chronic pouchitis and enteritis, suggesting autoimmune pouchitis which was unresponsive to multiple antibiotics. He was partially responsive to vedolizumab and then placed on total parenteral nutrition with resolution of diarrhea. Discussion: Several genetic markers have been studied among individuals suffering from IBD and some of these genetic loci are shared with other autoimmune conditions. We theorize that UC is just one part of a wide spectrum of autoimmunogenic complex of IBD. If the diseased organ is removed, then the disease morphs into a new phenotypic expression in the form of acquired autoimmune conditions.
