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Eosinophilic esophagitis and the promise of vitamin D
  1. Albert J Bredenoord
  1. Department of Gastroenterology, Amsterdam UMC Location AMC, Amsterdam, The Netherlands
  1. Correspondence to Dr Albert J Bredenoord, Gastroenterology, Amsterdam UMC Location AMC, Amsterdam 1105 AZ, The Netherlands; a.j.bredenoord{at}

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Vitamin D plays an essential role in the calcium and bone metabolism, but it has become clear that subclinical vitamin D deficiency is a risk factor for several other extraskeletal diseases as well. In this issue of Gut, new evidence is published on the role of vitamin D in the pathophysiology of Th2 inflammation and eosinophilic esophagitis (EoE) in particular.1 Brusilovsky et al show that vitamin D has important interleukin (IL)-13 antagonistic properties and was shown to regulate epithelial barrier and immune functions. Vitamin D supplementation in models of vitamin D deficiency counteracted expression of approximately 70% of genes affected by IL-13, it improved histological markers of epithelial barrier disruption and reduced mucosal permeability and reduced eosinophilic inflammation. Vitamin D supplementation reversed IL-13-induced dysregulation of markers associated with oesophageal remodelling, such as transforming growth factor beta (TGFβ), as well. This is intriguing, as there are clear medical unmet needs in EoE and vitamin D supplementation may offer a potential effective, inexpensive, safe and acceptable solution to patients. What are the odds that vitamin D may become a new therapy for EoE? Much can be learnt from research in other extraskeletal diseases in which low serum vitamin D has been identified as a risk factor.

The metabolism of vitamin D is well known. Under the influence of ultraviolet-B (UV-B) 7-dehydrocholesterol is converted to vitamin D3. Production in the skin is the main source of vitamin D in humans, the intake of vitamin D from a regular diet is minimal. Vitamin D is converted enzymatically in the liver to 25-hydroxyvitamin D, the major circulating form of vitamin D, and then mainly in the kidneys by 1-alpha-hydroxylase to …

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  • Contributors AJB is the sole author of this manuscript.

  • Funding AJB is supported by Vidi grant 91718300 from the Netherlands Organisation for Scientific Research NWO.

  • Competing interests AJB received research funding from Nutricia, Norgine, DrFalkPharma, Thelial and SST, and received speaker and/or consulting fees from Laborie, Medtronic, Dr. Falk Pharma, Alimentiv, Sanofi/Regeneron and AstraZeneca

  • Provenance and peer review Commissioned; internally peer reviewed.

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