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Mast cells and IgE‐containing cells in gastric mucosa of Helicobacter pylori infected and non‐infected patients with chronic urticaria
Author(s) -
Liutu M,
Kalimo K,
Kalimo H,
Uksila J,
Leino R
Publication year - 2004
Publication title -
journal of the european academy of dermatology and venereology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.655
H-Index - 107
eISSN - 1468-3083
pISSN - 0926-9959
DOI - 10.1111/j.1468-3083.2004.00701.x
Subject(s) - helicobacter pylori , immunoglobulin e , medicine , gastritis , biopsy , immunology , spirillaceae , disease , gastric mucosa , gastroenterology , stomach , antibody
Background Several studies have indicated that antibiotic therapy aimed at eradication of Helicobacter pylori has effects on symptoms of chronic urticaria (CU) patients. However, the possible connections and pathomechanism by which H. pylori might be linked to CU have remained largely unknown. The IgE‐mediated pathway might be a possible link between H. pylori infection and CU. We therefore clarified the role of H. pylori as an inducer of IgE response. Materials and methods Gastroscopy was performed and mucosal biopsy specimens were taken to evaluate the histology, as well as the presence of H. pylori bacteria, mast cells and IgE‐containing cells in the antral mucosa, in 21 CU patients. Controls ( n = 48) included 19 patients with lichen planus, nine patients with atopic dermatitis and 20 patients with no skin or allergic disease. Results The mean densities of IgE‐containing cells were significantly higher in H. pylori‐ infected patients and in patients with skin disease compared to non‐ H. pylori ‐infected patients with no skin or allergic disease. No significant difference was found in the number of IgE‐containing cells between H. pylori ‐infected and non‐infected patients with CU. There was no significant difference in the mean densities of mast cells in the different patient groups. Conclusions Our findings suggest that H. pylori gastritis leads to increased IgE production. However, we could not show a significant difference in IgE staining between H. pylori ‐infected and non‐infected patients with CU.