High Vitamin D-Binding Protein Concentration, Low Albumin, and Mode of Remission Predict Relapse in Crohn's Disease.
Inflamm Bowel Dis. 2016 Oct;22(10):2456-64. doi: 10.1097/MIB.0000000000000894.
Ghaly S1, Murray K, Baird A, Martin K, Prosser R, Mill J, Simms LA, Hart PH, Radford-Smith G, Bampton PA, Lawrance IC.
Overview Gut and vitamin D contains the following summary
- Gut problems result in reduced absorption of Vitamin D, Magnesium, etc.
- Celiac disease has a strong genetic component.
- Most, but not all, people with celiac disease have a gene variant.
- An adequate level vitamin D seems to decrease the probability of getting celiac disease.
- Celiac disease causes poor absorption of nutrients such as vitamin D.
- Bringing the blood level of vitamin D back to normal in patients with celiac disease decreases symptoms.
- The prevalence of celiac disease, not just its diagnosis, has increased 4X in the past 30 years, similar to the increase in Vitamin D deficiency.
- Review in Nov 2013 found that Vitamin D helped
- Many intervention clinical trials for vitamin D to prevent or treat Gut problems (93 trials listed as of Jan 2017)
- All items in category gut and vitamin D
Gut category listing contains the following
131 items in GUT category - see also Overview Gut and vitamin D,
- "Ulcerative Colitis" OR UC 689 items March 2019
- "celiac disease" OR CD 1280 items Feb 2018
- "inflammatory bowel disease" OR "inflammatory bowel symptom" 1010 items as of March 2019
- Crohn's 1230 items as of Feb 2019
- Gut-Friendly forms of vitamin D
such as: bio-emulsion, topical, spray, sublingual, inhaled, injection . .
Vitamin D (25(OH)D) deficiency occurs in active Crohn's disease (CD) and may be secondary to reduced sunlight exposure and oral intake. Vitamin D-binding protein (VDBP) levels, however, fluctuate less with season and sunlight. The aim, therefore, was to examine patients with CD in remission and determine any associations between VDBP, serum 25(OH)D, and the calculated free 25(OH)D concentrations with the risk of disease flare.
Subjects were identified from prospectively maintained inflammatory bowel disease databases at 3 teaching hospitals in Australia. Patients were in steroid-free clinical remission at the time of blood draw and were followed for at least 12 months. Total and epimer-25(OH)D3, VDBP concentrations, and genotypes were determined.
A total of 309 patients with CD (46% men) met the inclusion criteria. A disease flare occurred in 100 (32.4%). Serum 25(OH)D3 was deficient (<50 nmol/L) in 36 (12%) and insufficient (50-75 nmol/L) in 107 (35%) patients. Total, free, and epimer-25(OH)D3 serum levels did not predict disease flare.
Higher VDBP concentrations, however, significantly correlated with increased risk of disease flare (hazard ratio 1.2, 95% CI, 1.0-1.5). On multivariate analysis, VDBP concentration, low albumin, and medication-induced remission were significantly more associated with disease flare. VDBP genotypes were significantly associated with 25(OH)D and VDBP concentrations but not disease flare.
Vitamin D deficiency was uncommon in our patients with CD in remission, and serum 25(OH)D3 did not predict disease flare, whereas higher VDBP concentrations were significantly associated with disease flare. Further investigations to explore the possible mechanisms for this association are warranted.
PMID: 27631600 DOI: 10.1097/MIB.0000000000000894