The exact relationship between vitamin D deficiency and inflammatory bowel disease (IBD) remains unclear. Researchers evaluated the effect of vitamin D3 administration on inflammatory responses and disease severity in patients with IBD.

Vitamin D3 was administered in patients with either vitamin D deficiency or insufficiency and CRP serum vitamin D levels and PMS were re-examined at 6 months of the administration.

In 88 patients with Crohn's disease (CD), a negative correlation was found between serum vitamin D and CRP. In 178 patients with ulcerative colitis (UC), serum vitamin D showed no association with CRP or PMS.

Serum vitamin D increased from 11.08±3.63 to 22.69±6.11 ng/mL in 29 patients with CD and from 11.45±4.10 to 24.20±6.61 ng/mL in 41 patients with UC who received vitamin D3 treatment (P<0.001 and P<0.001, respectively).

In patients with CD, median ΔCRP was -0.24 in the normalized vitamin D group and -0.11 in the non-normalized group (P=0.308). In patients with UC, median ΔCRP was -0.01 in the normalized vitamin D group and 0.06 in the non-normalized group (P=0.359).

Although a negative correlation was found between serum vitamin D and CRP levels in patients with CD, administration of vitamin D did not improve the CRP level in patients with CD. In patients with UC, serum vitamin D level was unrelated to CRP or PMS.

Vitamin D is ingested through food or is synthesized by the action of UV light on the skin. The UV index is stronger in coastal areas than inland, in the countryside than in the city, and in summer than in winter.

Vitamin D levels

Researchers analyzed the vitamin D levels per season before supplementation and found them to be lowest in winter and highest in autumn, but there was no significant difference between summer and autumn.

Latitude, amount of outdoor activity, skin color, and exposure to sunshine influence vitamin D synthesis. In the winter, fewer UV rays lead to lower vitamin D levels in both the patients and the healthy population.

This study has several limitations. First, there were no CDAI data, as this was a retrospective study using hospital electronic medical records. The CDAI score was irregularly measured and hence could not be used for this study. Second, the sample size was small because there were only a few patients in whom vitamin D and CRP levels and PMS were all measured regularly.

In conclusion, although a negative correlation was found between serum vitamin D and CRP level in patients with CD, administration of vitamin D did not improve the CRP level in such patients. In patients with UC, serum vitamin D level was unrelated to CRP or PMS.