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Vitamin B12 deficiency in inflammatory bowel disease: a prospective observational pilot study
Robert Battat1, Uri Kopylov, Joshua Byer
1aDivision of Gastroenterology, Department of Medicine, McGill University Health Centre bDivision of Clinical Epidemiology, Department of Medicine, Research Institute of the McGill University Health Centre cDepartment of Medicine, McGill University dDivision of Gastroenterology, Department of Medicine, Jewish General Hospital, Montreal eMedical Genetics Service, Department of Medicine, Centre Hospitalier Universitaire de Sherbrooke (CHUS), University of Sherbrooke, Sherbrooke fDepartment of Gastroenterology, Sheba Medical Center Tel Hashomer and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
Background And Aim:
Diagnostic and management guidelines for vitamin B12 (cobalamin, Cbl) deficiency in inflammatory bowel disease (IBD) are lacking. True deficiency is defined as Cbl concentrations below reference range combined with elevated methylmalonic acid (MMA) concentrations. Studies analyzing Cbl status in IBD use only Cbl concentrations without confirmatory MMA. This study aims to determine the proportion of IBD patients with Cbl concentrations below reference range and their predisposing clinical and genetic characteristics. We then compared this to the proportion with true deficiency.
Patients And Methods:
In a prospective observational pilot study of adult IBD outpatients, Cbl concentrations, MMA levels, and fucosyltransferase 2 mutations were measured at clinic visits.
Results:
A total of 66 Crohn's disease (CD) and 30 ulcerative colitis (UC) patients were recruited. Mean Cbl concentrations (pmol/l) in CD (253.7) were not significantly lower than UC (320.5, P=0.24). Serum Cbl below reference range (<148) was observed in 7.6 and 10% of CD and UC patients, respectively (P=0.70). True deficiency in CD and UC was 3 and 3.3%, respectively (P=1.0). Patients with ileal resections more than 30 cm had lower mean Cbl concentrations (177, P=0.02) and a trend toward higher proportions with Cbl levels below reference range (40%, P=0.06), but not increased deficiency rates (0%, P=1.0). Disease location, severity, and fucosyltransferase 2 mutations were not associated with altered Cbl status.
Conclusion:
True Cbl deficiency was rare in IBD patients in this study. A disparity in Cbl status exists when confirmatory MMA levels are used compared with Cbl concentrations alone. Asymptomatic IBD patients with low serum Cbl require confirmatory tests to guide management and avoid unnecessary treatment.
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