Vitamin B6 intake/supplementation, Plasma PLP and inflammatory disease

Introduction: Patients with the inflammatory disease, rheumatoid arthritis, have significantly lower plasma pyridoxal‐5‐phosphate (PLP) levels than controls, despite normal intakes and metabolism of vitamin B6. Because of the theoretical role for PLP in the inflammatory response, we sought to investigate plasma PLP levels in patients with other chronic inflammatory conditions. Methods: We searched pubmed for studies that examined plasma PLP levels in diseases that are known to involve inflammation, using keywords such as plasma PLP, vitamin B6, inflammation, rheumatoid arthritis, inflammatory bowel disease, diabetes, obesity, and cardiovascular disease. Results: All studies that examined plasma PLP levels in patients with rheumatoid arthritis (N=5), inflammatory bowel disease (N=1), and diabetes (N=3) reported that patients had lower levels of plasma PLP than controls despite normal intakes. For CVD, 16 out of 20 studies found patients to have lower plasma PLP levels than controls and/or a higher prevalence of PLP deficiency than in controls. Collectively , these studies find plasma PLP to be inversely correlated with markers of inflammation including: CRP, α‐acid‐glycoprotein, fibrinogen, ICAM, VCAM, IL‐6r, and erythrocyte sedimentation rate. Discussion: The basis for these relationships is presently unclear. Supplementation with B6 is effective in increasing plasma PLP levels, but this does not seem to bring about an improvement in disease outcomes. A possible explanation for this phenomenon is that the observed decrease in plasma PLP is caused by its mobilization and utilization by the inflamed tissue. If so, in those cases where chronic inflammation has adverse effects, PLP supplementation could be harmful. Clearly, further research into the role of PLP in inflammatory disease is a priority.