P-118 YI De Novo Inflammatory Bowel Disease in Immunosuppressed Pediatric Transplant Recipients

Abstract

BACKGROUND: Post transplantation patients are usually considerably immunosuppressed in order to allow for graft survival. However despite adequate immunosuppression these patients may go on to develop inflammatory bowel disease (IBD). We describe 9 cases of pediatric transplant patients who developed de novo inflammatory bowel disease whilst on immunosuppression. METHODS: The records of all pediatric patients who had been diagnosed with IBD post liver, isolated intestine or multivisceral transplants at our centre were assessed. Data on their symptomatology, endoscopy reports, pathology, serology and radiology reports were collected. Patients who had been diagnosed with IBD prior to transplantation were excluded. RESULTS: Nine patients (3 girls, 6 boys) developed de novo IBD post transplantation. Four of these had undergone liver transplants, 3 liver/intestine, 1 isolated intestine and 1 liver/intestine/bone marrow. Two patients were transplanted for autoimmune hepatitis (AIH): of these 1 also had primary sclerosing cholangitis, 1 for ornithine transcarbamylase (OTC) deficiency, 2 for necrotizing enterocolitis, 1 for intestinal atresia, 2 for gastroschisis and 1 etiology of liver failure was unknown. Only 2 patients had any personal history of autoimmune disease. Six patients (66%) were diagnosed with Crohn's, 2 (22%) with indeterminate and 1 (11%) with ulcerative colitis (UC). The diagnosis of IBD occurred 5-18 years after transplant (mean = 10.1 years). All patients were on Prograf (100%) for immunosuppression at time of diagnosis, 2 were also on MMF (22%), 3 also on Medrol (30%) and 1 was also on MMF and rapamycin (11%). Patients presented with an array of symptoms including diarrhea, abdominal pain, growth failure and anemia; 1 had fistulizing disease. There were 5 of 6 patients (83.3%) who had positive serology, (4 had only positive ASCA, 1 had positive ASCA and ANCA), 3 patients did not have serology drawn. Five patients failed treatment with salicylates and elevated Prograf dosing and required escalation of care to 6MP (1 patient) and infliximab (4 patients, 44%). CONCLUSIONS: The use of Prograf was not protective against development of IBD in these patients and we question whether immunosuppressive therapy may actually play a role in the development of de novo IBD. These patients presented with a full spectrum of IBD but were more likely to develop Crohn's disease than UC. They were more likely to have positive serology than is typically seen in IBD patients. In addition they did not respond well to salicylates or increased Prograf dosing requiring biologics 44% of time suggesting aggressive disease. It is important for clinicians to be aware of possibility of IBD after transplant as the presentation may be confused with rejection or infection and may delay institution of appropriate treatment