Emerging data suggest that vitamin D has a significant role in inflammatory bowel disease (IBD). Prospective data evaluating the association of vitamin D serum status and disease course are lacking. We sought to determine the relationship between vitamin D status and clinical course of IBD over a multiyear time period.
IBD patients with up to 5-year follow-up from a longitudinal IBD natural history registry were included. Patients were categorized according to their mean serum 25-OH vitamin D level. IBD clinical status was approximated with patterns of medication use, health-care utilization, biochemical markers of inflammation (C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR)), pain and clinical disease activity scores, and health-related quality of life.
A total of 965 IBD patients (61.9% Crohn’s disease, 38.1% ulcerative colitis) formed the study population (mean age 44 years, 52.3% female). Among them, 29.9% had low mean vitamin D levels. Over the 5-year study period, subjects with low mean vitamin D required significantly more steroids, biologics, narcotics, computed tomography scans, emergency department visits, hospital admissions, and surgery compared with subjects with normal mean vitamin D levels (P<0.05). Moreover, subjects with low vitamin D levels had worse pain, disease activity scores, and quality of life (P<0.05). Finally, subjects who received vitamin D supplements had a significant reduction in their health-care utilization.
Low vitamin D levels are common in IBD patients and are associated with higher morbidity and disease severity, signifying the potential importance of vitamin D monitoring and treatment.
1Department of Medicine and Division of Gastroenterology, Hepatology and Nutrition, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA
Correspondence: David G. Binion, MD, Department of Medicine and Division of Gastroenterology, Hepatology and Nutrition, University of Pittsburgh Medical Center, Presbyterian Hospital Mezzanine Level C Wing, 200 Lothrop Street, Pittsburgh, Pennsylvania 15213, USA. E-mail: email@example.com
SUPPLEMENTARY MATERIAL accompanies this paper at http://links.lww.com/AJG/A621
Received 02 September 2015; accepted 02 January 2016
Writing assistance: None.
Specific author contributions: Toufic A. Kabbani: enrollment of subjects, acquisition of data, analysis and interpretation of data, and drafting of manuscript. Ioannis E. Koutroubakis: acquisition of data, analysis and interpretation of data, drafting of manuscript, and critical review of manuscript. Robert E. Schoen: critical review of manuscript. Claudia Ramos Rivers: enrollment of subjects and acquisition of data. Nilesh Shah: statistical analysis. Jason Swoger: acquisition of data. Miguel Regueiro: acquisition of data. Arthur Barrie: acquisition of data. Marc Schwartz: acquisition of data. Jana Hashash: acquisition of data. Leonard Baidoo: acquisition of data. Michael Dunn: acquisition of data. David G. Binion: acquisition of data, analysis and interpretation of data, drafting of manuscript, critical review, and final approval of the manuscript.
Financial support: Ioannis Koutroubakis was supported by a sabbatical salary of Medical Faculty University of Crete Greece; Michael Dunn and David G. Binion were supported by a grant W81XWH-11-2-0133 from the US Army Medical Research and Material Command.
Potential competing interests: Ioannis Koutroubakis: consulting/advisory board for Abbvie and MSD; Miguel Regueiro: has served as a consultant for Abbvie, Janssen, Shire, Takeda, and UCB. David Binion: consulting/advisory board for Abbvie, Janssen, FDA Safety Board of UCB Pharma, and grant support from Janssen, Merck, and UCB Pharma. The other authors declare no conflict of interest.