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Histamine and mucosal mast cells in gluten enteropathy

  • Histamine in Pathological States
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Abstract

Coeliac disease is a malabsorptive disorder caused by intolerance to gluten and is characterized by a remodelling of the intestinal mucosa including villus atrophy, crypt hyperplasia and net increase of mucosal volume. Changes of the number of mucosal mast cells (MMCs) in coeliac mucosa has recently been reported, suggesting that the mast cell activity could have a pathogenetic role in gluten enteropathy. MMCs located solely in the lamina propria are the main repository for small-gut mucosal histamine.

A consecutive prospective study was designed to study the histamine content, MMC numbers, and the relative volume of lamina propria in intestinal biopsies from adult patients suffering from unexplained diarrhea and/or malnutrition. Histamine was measured by a HPLC-method, the number of MMC was counted after long toluidine-blue staining, and the relative volumes of lamina propiria and epithelium were estimated morphometrically. The findings were correlated to the histopathological appearance of the mucosa. As compared to controls the histamine content increased by 80% and MMC numbers by about 60% in the coeliac mucosa. There was also a correlation between MMC numbers and histamine content for both normal and coeliac mucosae (r=0.81). The morphometric estimation of the relative volumes of epithelium and lamina propria revealed that the lamina-propria compartment was increased by approximately 40% in coeliac mucosa.

Taking the changes in compartmental volumes of the remodelled coeliac mucosa into account, our results suggest that the histamine content and MMC population were significantly increased. MMC and MMC-associated histamine may therefore be involved in the pathogenesis of gluten enteropathy.

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Supported by the Swedish Medical Research Council, Project Nos. 2235 and 5942.

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Wingren, U., Hallert, C., Norrby, K. et al. Histamine and mucosal mast cells in gluten enteropathy. Agents and Actions 18, 266–268 (1986). https://doi.org/10.1007/BF01988038

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  • DOI: https://doi.org/10.1007/BF01988038

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