A randomized controlled trial on the effect of vitamin D3 on inflammation and cathelicidin gene expression in ulcerative colitis patients.
Saudi J Gastroenterol
; 22(4): 316-23, 2016.
Article
em En
| MEDLINE
| ID: mdl-27488327
ABSTRACT
BACKGROUND:
Inflammatory bowel disease (IBD) is an intestinal chronic inflammatory condition and includes Crohn's disease (CD) and ulcerative colitis (UC). It has been proposed that Vitamin D supplementation may have a beneficial role in IBD.AIM:
To characterize the effects of Vitamin D on cathelicidin (hCAP/LL37) gene expression, ESR, and serum hs-CRP levels. MATERIALS ANDMETHODS:
Ninety UC patients on remission were randomized to receive 300,000 IU intramuscular Vitamin D or 1 mL normal saline as placebo, respectively. Before and 90 days after intervention, serum levels of 25 (OH)-Vitamin D3, PTH, Calcium, ESR, and hs-CRP were measured. Cathelicidin gene expression was also quantified using qRT-PCR.RESULTS:
Baseline serum 25-OH-Vitamin D3 levels were not different between the two groups and after intervention, increased only in Vitamin D group (P < 0.001). Hs-CRP levels were lower in Vitamin D group after intervention (Before 3.43 ± 3.47 vs 3.86 ± 3.55 mg/L, P = 0.56; after 2.31 ± 2.25 vs 3.90 ± 3.97 mg/L, P= 0.023). ESR decreased significantly in Vitamin D group (Before 12.4 ± 6.1 vs 12.1 ± 5.3 mm/h, P= 0.77; after 6.7 ± 4.5 vs 11.4 ± 5.5 mm/h, P< 0.001). The mean fold change in hCAP18 gene expression in Vitamin D group was significantly higher than placebo group. (Mean ± SD 3.13 ± 2.56 vs 1.09 ± 0.56; median ± interquartile range 2.17 ± 3.81 vs 0.87 ± 0.53, P< 0.001).CONCLUSION:
Decreases in ESR and hs-CRP levels and increase in LL37 gene expression support the hypothesis that Vitamin D supplementation may have a beneficial role in UC patients.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Vitaminas
/
Colite Ulcerativa
/
Colecalciferol
/
Catelicidinas
Tipo de estudo:
Clinical_trials
Limite:
Adult
/
Female
/
Humans
/
Male
/
Middle aged
Idioma:
En
Ano de publicação:
2016
Tipo de documento:
Article