Influence of Vitamin D Deficiency on Inflammatory Markers and Clinical Disease Activity in IBD Patients.

08:00 EDT 11th May 2019 | BioPortfolio

Summary of "Influence of Vitamin D Deficiency on Inflammatory Markers and Clinical Disease Activity in IBD Patients."

Vitamin D has recently been discovered to be a potential immune modulator. Low serum vitamin D levels have been associated with risk of relapse and exacerbation of clinical outcomes in Crohn's disease (CD) and ulcerative colitis (UC). A retrospective, longitudinal study was conducted to determine the association between vitamin D levels and inflammatory markers and clinical disease activity in inflammatory bowel disease (IBD). In addition, circulating 25(OH)D progression was evaluated according to vitamin D supplementation. Participants were separated into three groups according to their vitamin D level: severe deficiency (SD), moderate deficiency (MD) and sufficiency (S). Serum 25(OH)D was inversely correlated with faecal calprotectin (FC) for CD and UC but was only correlated with C-reactive protein (CRP) for UC patients. In the multivariate analysis of FC, CRP and fibrinogen (FBG), we predicted the presence of a patient in the SD group with 80% accuracy. A deficiency of 25(OH)D was associated with increased hospitalisations, flare-ups, the use of steroids and escalating treatment. Supplemental doses of vitamin D were likely to be insufficient to reach adequate serum levels of 25(OH)D. Vitamin D intervention studies are warranted to determine whether giving higher doses of vitamin D in IBD might reduce intestinal inflammation or disease activity.


Journal Details

This article was published in the following journal.

Name: Nutrients
ISSN: 2072-6643


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Medical and Biotech [MESH] Definitions

An autosomal dominant disorder showing decreased levels of plasma protein S antigen or activity, associated with venous thrombosis and pulmonary embolism. PROTEIN S is a vitamin K-dependent plasma protein that inhibits blood clotting by serving as a cofactor for activated PROTEIN C (also a vitamin K-dependent protein), and the clinical manifestations of its deficiency are virtually identical to those of protein C deficiency. Treatment with heparin for acute thrombotic processes is usually followed by maintenance administration of coumarin drugs for the prevention of recurrent thrombosis. (From Harrison's Principles of Internal Medicine, 12th ed, p1511; Wintrobe's Clinical Hematology, 9th ed, p1523)

A nutritional condition produced by a deficiency of VITAMIN E in the diet, characterized by posterior column and spinocerebellar tract abnormalities, areflexia, ophthalmoplegia, and disturbances of gait, proprioception, and vibration. In premature infants vitamin E deficiency is associated with hemolytic anemia, thrombocytosis, edema, intraventricular hemorrhage, and increasing risk of retrolental fibroplasia and bronchopulmonary dysplasia. An apparent inborn error of vitamin E metabolism, named familial isolated vitamin E deficiency, has recently been identified. (Cecil Textbook of Medicine, 19th ed, p1181)

A nutritional condition produced by a deficiency of VITAMIN D in the diet, insufficient production of vitamin D in the skin, inadequate absorption of vitamin D from the diet, or abnormal conversion of vitamin D to its bioactive metabolites. It is manifested clinically as RICKETS in children and OSTEOMALACIA in adults. (From Cecil Textbook of Medicine, 19th ed, p1406)

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A nutritional condition produced by a deficiency of VITAMIN B 12 in the diet, characterized by megaloblastic anemia. Since vitamin B 12 is not present in plants, humans have obtained their supply from animal products, from multivitamin supplements in the form of pills, and as additives to food preparations. A wide variety of neuropsychiatric abnormalities is also seen in vitamin B 12 deficiency and appears to be due to an undefined defect involving myelin synthesis. (From Cecil Textbook of Medicine, 19th ed, p848)

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