P642 Crossroads of vitamin B6 deficiency and inflammation in inflammatory bowel disease: Preliminary results of a cross-sectional study
Farrag, K.(1,2);Woldeab, J.(3);Stein, J.M.(1,2,4);Aksan, A.(2,5);
(1)DGD Clinics Sachsenhausen, Department of Gastroenterology and Clinical Nutrition, Frankfurt am Main, Germany;(2)Interdisciplinary Crohn-Colitis Centre Rhein-Main, Clinical Research, Frankfurt am Main, Germany;(3)Goethe University Frankfurt, Medical School, Frankfurt am Main, Germany;(4)Goethe University Frankfurt, Institute of Pharmaceutical Chemistry, Frankfurt am Main, Germany;(5)Justus-Liebig University Giessen, Institute of Nutritional Science, Giessen, Germany;
The robust relationship between vitamin B6 and inflammation has become apparent over the last decade. However, the mechanistic nature of this relationship remains unclear. Evidence suggests an inverse relationship between blood levels of B6 and inflammation, but also a potential two-way relationship between the two. Thus, whereas inflammation can deplete serum vitamin B6, vitamin B6 insufficiency can attenuate inflammation. This study aimed to assess vitamin B status in patients with IBD in routine clinical practice and identify possible relationships between vitamin B6 status and clinical disease characteristics.
In a comparative, retrospective cross-sectional study, serum samples of patients with IBD were studied. CBC, albumin and hsCRP were determined and samples assessed for presence/absence of inflammation (serum hsCRP, cut-off <5mg/L). Vitamin B6 status was determined via direct measurement of pyridoxal 5´-phosphate (PLP) by enzymatic assay.
149 patients with IBD (64f/85m; 82CD/67UC; 39.9±14.6y) were included. Of these, 44/149 had inflammation (19f/25m; 22CD/22UC; 41.2±14.9y) and 105/149 no inflammation (45f/60m; 60CD/45UC; 39.3±14.4y). In patients with inflammation, mean serum PLP levels were significantly lower (7.2[1.9-46.0] µg/L) vs. patients without inflammation (9.8[0.1-88.0] µg/L) (p<0.05). Accordingly, vitamin B6 deficiency occurred significantly more frequently in patients with vs. without inflammation (34.1% vs. 19.0%, p<0.05). A higher incidence of vitamin B6 deficiency was seen in patients with CD vs. UC, though without statistical significance (26.8% vs. 19.4%, p>0.05). The frequency of vitamin B6 deficiency did not differ according to disease localisation (p>0.05). Serum PLP levels inversely correlated with the inflammatory markers hsCRP and ESR (r=-0.306, p<0.001 and r=-0.203, p<0.001, respectively). Furthermore, there was a significant positive correlation between blood PLP levels and other selected acute-phase reactants, e.g., TSAT% (r= 0.207, p<0.05). However, no significant correlation was found with ferritin (r=-0.152, p=0.064).
Low serum total vitamin B6 levels were associated with inflammation but not disease type or localisation in patients with IBD. In line with preclinical findings and previous observational studies, vitamin B6 deficiency was more pronounced in patients with inflammation. Our findings suggest vitamin B6 may have a bigger role than thought in IBD; besides its relationship with inflammation, a possible involvement of vitamin B6 deficiency as cause or effect in IBD pathogenesis warrants investigation. Routine assessment and correction of vitamin B6 status may ameliorate IBD and help maintain intestinal integrity.