Hypovitaminosis D as Predisposing Factor for Atrophic Type A Gastritis: a Case–Control Study and Review of the Literature on the Interaction of Vitamin D with the Immune System

Hypovitaminosis D as Predisposing Factor for Atrophic Type A Gastritis: a Case–Control Study and Review of the Literature on the Interaction of Vitamin D with the Immune System

  • نوع فایل : کتاب
  • زبان : انگلیسی
  • مؤلف : Antonio Antico & Renato Tozzoli & Davide Giavarina & Elio Tonutti & Nicola Bizzaro
  • چاپ و سال / کشور: 2011

Description

1,25-Dihydroxyvitamin D displays immunoregulatory and anti-inflammatory properties, and the cells involved in innate and adaptive immune response express the vitamin D receptor and can both produce and respond to this hormone. This article aims at describing the complex immune regulatory role of vitamin D and depicting whether a correlation exists between atrophic type A gastritis and hypovitaminosis. We studied 62 autoimmune gastritis (AIG) patients and compared them to 54 lymphocytic gastritis patients, 21 Helicobacter pylori gastritis patients and 212 healthy subjects. We also statistically analyzed vitamin D concentration in 36,384 outpatients referred to our clinical laboratories. 25- Hydroxyvitamin D levels, the measurable metabolite used to determine vitamin D status in plasma, were measured by a chemiluminescent method. Average level of 25-OHD in AIG subjects was 9.8±5.6 ng/mL (95% confidence interval (CI) 8.4–11.2), 11.1±8.4 (CI 7.5–14.7) in H. pylori gastritis patients, 22.2±13.5 (CI 18.6–25.8) in nonspecific lymphocytic gastritis patients, 21.3±12.2 (CI 19.7–22.9) in healthy subjects, and 21.8±13.1 (CI 21.7–21.9) in the 36,384 outpatients. Vitamin D levels in AIG patients were significantly lower than in patients with nonspecific gastritis or in the general population, supporting the hypothesis that hypovitaminosis D might be a risk factor for the development of autoimmune diseases. The low vitamin D concentration in H. pylori gastritis patients might act as predisposing factor for a more severe Th1-type aggression to the stomach epithelium.
Clinic Rev Allerg Immunol# Springer Science+Business Media, LLC 2011
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