Costa BG, Yoshihara RNY, Spiller AL, Castelhano NS, Santos A, Baima JP, Imbrizi M, De Freitas MB, Magro DO, Sassaki LY. Vitamin D, vitamin D receptor gene polymorphisms, and inflammatory bowel disease outcomes: From molecular mechanisms to clinical application. World J Gastroenterol 2026; 32(15): 115533 [DOI: 10.3748/wjg.v32.i15.115533]
Corresponding Author of This Article
Ligia Yukie Sassaki, MD, PhD, Assistant Professor, Researcher, Department of Internal Medicine, Medical School, São Paulo State University (UNESP), Avenida Professor Montenegro, Distrito de Rubiao Junior, Botucatu 18618-686, São Paulo, Brazil. ligia.sassaki@unesp.br
Research Domain of This Article
Gastroenterology & Hepatology
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Minireviews
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Apr 21, 2026 (publication date) through Apr 15, 2026
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Publication Name
World Journal of Gastroenterology
ISSN
1007-9327
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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
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Costa BG, Yoshihara RNY, Spiller AL, Castelhano NS, Santos A, Baima JP, Imbrizi M, De Freitas MB, Magro DO, Sassaki LY. Vitamin D, vitamin D receptor gene polymorphisms, and inflammatory bowel disease outcomes: From molecular mechanisms to clinical application. World J Gastroenterol 2026; 32(15): 115533 [DOI: 10.3748/wjg.v32.i15.115533]
World J Gastroenterol. Apr 21, 2026; 32(15): 115533 Published online Apr 21, 2026. doi: 10.3748/wjg.v32.i15.115533
Vitamin D, vitamin D receptor gene polymorphisms, and inflammatory bowel disease outcomes: From molecular mechanisms to clinical application
Beatriz Gabriela Costa, Ryan Nunes Yoshio Yoshihara, Amanda Luísa Spiller, Natalia Salvador Castelhano, Andrey Santos, Júlio Pinheiro Baima, Marcello Imbrizi, Maiara Brusco De Freitas, Daniéla Oliveira Magro, Ligia Yukie Sassaki
Beatriz Gabriela Costa, Ryan Nunes Yoshio Yoshihara, Amanda Luísa Spiller, Natalia Salvador Castelhano, Júlio Pinheiro Baima, Ligia Yukie Sassaki, Department of Internal Medicine, Medical School, São Paulo State University (UNESP), Botucatu 18618-686, São Paulo, Brazil
Andrey Santos, Department of Internal Medicine, School of Medical Sciences, University of Campinas (UNICAMP), Campinas 13083-887, São Paulo, Brazil
Marcello Imbrizi, Daniéla Oliveira Magro, Division of Gastroenterology, School of Medical Sciences, University of Campinas (UNICAMP), Campinas 13083-970, São Paulo, Brazil
Maiara Brusco De Freitas, Center for Molecular Prediction of Inflammatory Bowel Disease, Department of Clinical Medicine, Aalborg University, Copenhagen 2450, Denmark
Author contributions: Costa BG, Yoshihara RNY, Spiller AL, Castelhano NS, Santos A, Baima JP, Imbrizi M, De Freitas MB, Magro DO, and Sassaki LY contributed equally to the conception and design of the article, writing, and editing of the manuscript, and review of the literature. All the authors approved the final version of the article to be published.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Corresponding author: Ligia Yukie Sassaki, MD, PhD, Assistant Professor, Researcher, Department of Internal Medicine, Medical School, São Paulo State University (UNESP), Avenida Professor Montenegro, Distrito de Rubiao Junior, Botucatu 18618-686, São Paulo, Brazil. ligia.sassaki@unesp.br
Received: October 20, 2025 Revised: October 30, 2025 Accepted: February 2, 2026 Published online: April 21, 2026 Processing time: 178 Days and 13.2 Hours
Abstract
Inflammatory bowel diseases (IBD), including Crohn’s disease and ulcerative colitis, arise from intricate interactions among genetic, environmental, microbial, and immune factors. Beyond its classical role in calcium and bone metabolism, vitamin D has emerged as a key regulator of the intestinal barrier integrity and immune homeostasis. Vitamin D deficiency is highly prevalent in these disorders, mainly because of malabsorption, dietary restrictions, chronic inflammation, and impaired metabolic activation. Genetic variants of the vitamin D receptor, such as ApaI, TaqI, BsmI, and FokI polymorphisms, may alter receptor function and downstream signaling, influencing disease susceptibility and progression. These polymorphisms have been linked to impaired epithelial barrier function, dysregulated nucleotide-binding oligomerization domain-containing protein 2 signaling, and exaggerated immune activation, central to IBD pathogenesis. Despite growing evidence, clinical assessment and correction of vitamin D deficiency in IBD remain inconsistent, and the influence of vitamin D receptor polymorphisms on therapeutic responses has not been sufficiently characterized. Understanding the interplay between vitamin D status and genetic background could support individualized management strategies. This review underscores the potential of vitamin D supplementation as an adjunctive approach, particularly in patients receiving immunosuppressive or biologic therapies, and emphasizes the need for personalized monitoring to optimize outcomes in IBD.
Core Tip: Vitamin D is essential in the pathogenesis and managing inflammatory bowel diseases. In addition to its classical bone metabolism function, vitamin D modulates intestinal epithelial integrity and immune responses. Genetic polymorphisms in the vitamin D receptor may influence disease activity and treatment outcomes. This minireview emphasizes the need for routine assessment of vitamin D status and consideration of vitamin D receptor genetic variants in personalized therapeutic strategies for inflammatory bowel diseases, especially in patients receiving immunosuppressive or biologic therapies.
