P448 How good are we at detecting and managing folate deficiency in inflammatory bowel disease?
S. Subramaniam*1, K. Besherdas2
1University College London Hospitals NHS Foundation Trust, Department of Gastroenterology, London, United Kingdom, 2Barnet & Chase Farm Hospitals, Royal Free London NHS Foundation Trust, Department of Gastroenterology, London, United Kingdom
Colorectal cancer (CRC) is the third most prevalent malignancy in the world and is the second leading cause of cancer death worldwide. Epidemiologic and clinical studies indicate that dietary folate intake and blood folate levels are inversely associated with colorectal cancer risk. Folate is involved in the biological methylation and maintenance of intracellular DNA synthesis, therefore, folate deficiency could potentially lead to cancer through disruption of these events. Patients with inflammatory bowel disease (IBD) have a higher risk of developing micronutrient deficiencies including folate in addition to a higher risk of developing CRC, and folate deficiency may synergistically add to this risk of CRC in these patients. Causes of folate deficiency in IBD include inadequate dietary intake, malabsorption and medication interactions. The aim of our study was to ascertain if folate was measured in our IBD patients and whether folate deficiency was corrected.
A single centre, retrospective analysis of IBD patients from a large district general NHS trust in North London was performed. Patients on methotrexate already receiving folic acid were excluded from the study. The data on demographics, diagnosis, treatment, folate levels and supplements from IBD patients were obtained from the local IBD database and electronic patient records.Folate deficiency was defined as a folate level of <3.1ug/ml.
333 patients with IBD were identified in the database. 8 patients were excluded from the analysis (4 patients on methotrexate and 4 with insufficient data). Of the 325 remaining patients, 159 were classified as Crohn's disease (CD), 153 as UC and 13 as IBD unclassified (IBD-U). Folate was checked in 222/325 (68.3%) of IBD patients. Folate deficiency was observed in 27/222 (12.2%) patients: 13/112 (11.6%) CD patients, 12/100 (12.0%) UC patients and 2/10 (20.0%) IBD-U patients. Of the 13 CD patients, 11 (84.6%) have ileal or ileocolonic disease. Folic acid was given to 15/27 (55.6%) patients with a folate deficiency. Only 7 out of these 15 patients had their folate levels rechecked and in all these cases an adequate treatment response with correction of folate levels was achieved.
In this study, almost a third (31.7%) of patients with IBD did not have their folate measured. Folate deficiency was not corrected in 45% of IBD patients in whom it was identified. This may suggest a missed opportunity to reduce the CRC risk in these patients with IBD who do not undergo folate measurement or correction if deficient. We recommend routine measurements of folate in all IBD patients under follow up and supplementing those who are deficient to further reduce the risk of CRC in this group.