How would serum 25(OH)D level change in patients with inflammatory bowel disease depending on intestinal mucosa vitamin D receptor (VDR) and vitamin D1-α hydroxylase (CYP27B1)?
However, VDR and CYP27B1 cannot be used to distinguish UC and CD.
📌 3 Key Takeaways
🎯
Objective & Hypothesis:Background/Aims: To investigate how the serum 25-hydroxyvitamin D (25(OH)D) level change in patients with inflammatory boweldisease (IBD) and investigate the intestinal mucosa vitamin D receptor (VDR) and vitamin D1-α hydroxylase (CYP27B1) expressions.Materials and Methods: A total of 105 patients with IBD were enrolled in the present study, including 49 cases with ulcerative colitis (UC)and 56 cases with Crohn’s disease (CD), compared with 45 healthy controls (CON) during the same period by testing the permeability ofthe intestinal mucosa.
📊
Key Findings & Data:The expressions of VDR and CYP27B1 in the intestinal mucosa were detected, so as the serum endotoxin, tumornecrosis factor (TNF)-α, and 25(OH)D levels.Results: The lactulose and mannitol absorption ratio (LMR) and serum endotoxin and TNF-α levels were significantly higher in the IBDgroup than in the CON group (p 0.05).
💡
Conclusion & Impact:However, VDR and CYP27B1 cannot be used to distinguish UC and CD.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters
Özet
Background/Aims: To investigate how the serum 25-hydroxyvitamin D (25(OH)D) level change in patients with inflammatory boweldisease (IBD) and investigate the intestinal mucosa vitamin D receptor (VDR) and vitamin D1-α hydroxylase (CYP27B1) expressions.Materials and Methods: A total of 105 patients with IBD were enrolled in the present study, including 49 cases with ulcerative colitis (UC)and 56 cases with Crohn’s disease (CD), compared with 45 healthy controls (CON) during the same period by testing the permeability ofthe intestinal mucosa. The expressions of VDR and CYP27B1 in the intestinal mucosa were detected, so as the serum endotoxin, tumornecrosis factor (TNF)-α, and 25(OH)D levels.Results: The lactulose and mannitol absorption ratio (LMR) and serum endotoxin and TNF-α levels were significantly higher in the IBDgroup than in the CON group (p 0.05). CYP27B1 in the IBD and CD groups was significantly up-regulated compared with the CONgroup (p 0.05).Conclusion: Patients with IBD exhibit vitamin D metabolism imbalance, lower serum 25(OH)D, and lower VDR expression, but higherCYP27B1 expression in the colonic mucosa. However, VDR and CYP27B1 cannot be used to distinguish UC and CD.
🔖
Cite This Article
HUANG, J., CHEN, T., LIU, Y., LYU, L., LI, X., YUE, W. (2019). How would serum 25(OH)D level change in patients with inflammatory bowel disease depending on intestinal mucosa vitamin D receptor (VDR) and vitamin D1-α hydroxylase (CYP27B1)?. Turkish Journal of Gastroenterology, Cilt: 30 - Sayı: 2, 132–138. https://ajindex.com/articles/408797
Büsch K, Sonnenberg A, Bansback N. Impact of inflammatory bowel disease on disability. Curr Gastroenterol Rep 2014; 16: 414. [CrossRef ] Malik TA. Inflammatory Bowel Disease: Historical Perspective, Epidemiology, and Risk Factors. Surg Clin North Am 2015; 95: 1105-22. [CrossRef] Fiocchi C. Inflammatory bowel disease pathogenesis: where are we? J Gastroenterol Hepatol 2015; 30(Suppl 1): 12-8. [CrossRef ] Zezos P, Kouklakis G, Saibil F. Inflammatory bowel disease and thromboembolism. World J Gastroenterol 2014; 20: 13863-78. [CrossRef] Algaba A, Guerra I, Marín-Jiménez I, et al. Incidence, management, and course of cancer in patients with inflammatory bowel disease. J Crohns Colitis 2015; 9: 326-33. [CrossRef ] Gallinger ZR, Weizman AV. Colorectal cancer in inflammatory bowel disease: a shift in risk? Expert Rev Anticancer Ther 2014; 14: 847-56. [CrossRef] Burisch J, Jess T, Martinato M, Lakatos PL. The burden of inflammatory bowel disease in Europe. J Crohns Colitis 2013; 7: 322-37. [CrossRef] Taleban S, Colombel JF, Mohler MJ, Fain MJ. Inflammatory bowel disease and the elderly: a review. J Crohns Colitis 2015; 9: 507-15. [CrossRef] Molodecky NA, Soon IS, Rabi DM, et al. Increasing incidence and prevalence of the inflammatory bowel diseases with time, based on systematic review. Gastroenterology 2012; 142: 46-54.e42; quiz e30. Zhang YZ, Li YY. Inflammatory bowel disease: pathogenesis. World J Gastroenterol 2014; 20: 91-9. [CrossRef ] Sheehan D, Moran C, Shanahan F. The microbiota in inflammatory bowel disease. J Gastroenterol 2015; 50: 495-507. [CrossRef ] Holick MF. Vitamin D deficiency. N Engl J Med 2007; 357: 266-81. [CrossRef ] Chałupniak A, Waszczuk K, Hałubek-Głuchowska K, Piasecki T, Gotszalk T, Rybka J. Application of quartz tuning forks for detection of endotoxins and Gram-negative bacterial cells by monitoring of Limulus Amebocyte Lysate coagulation. Biosens Bioelectron 2014; 58: 132-7. [CrossRef ] Lin AV. Indirect ELISA. Methods Mol Biol 2015; 1318: 51-9. [CrossRef] Van Schoor NM, Heymans MW, Lips P. Vitamin D status in relation to physical performance, falls and fractures in the Longitudinal Aging Study Amsterdam: A reanalysis of previous findings using standardized serum 25-hydroxyvitamin D values. J Steroid Biochem Mol Biol 2017; 177: 255-60. [CrossRef ] Palmer MT, Weaver CT. Linking vitamin d deficiency to inflammatory bowel disease. Inflamm Bowel Dis 2013; 19: 2245-56. [CrossRef ] Silvennoinen J. Relationships between vitamin D, parathyroid