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Background/Aim: In chronic spontaneous urticaria (CSU), Helicobacter pylori (HP) has been discussed as a cause, but it is unknown whether the bacterium itself or concomitant inflammation is causing the urticaria. Our aim was to investigate HP and upper gastrointestinal lesions as signs of inflammation independently of each other in the pathogenesis of CSU. Methods: A total of 36 prospectively enrolled CSU patients from Moscow were investigated by gastroscopy and screened for the presence of HP and/or upper gastrointestinal lesions. Those having a positive result were treated according to the Maastricht III recommended guidelines for eradication therapy, and success was assessed by a follow-up gastroscopy. Simultaneously, the activity of CSU was measured before and after therapy of the gastrointestinal condition. Results: HP was observed in 26 of the 36 patients. Erosions or ulcers were found in 18 of the 36 patients, 14 of whom were also positively tested for HP. There was a significant difference in improvement of urticarial symptoms between those who succeeded in healing the erosions and those who did not succeed (p < 0.01) independent of the presence of HP. No significant difference in symptom relief was observed between those who had successful eradication and those in whom HP eradication failed. Conclusions: Upper gastrointestinal inflammatory disorders can cause CSU and trigger exacerbations independently of HP. This might imply that also in HP-positive patients, urticaria is not based on an immunological reaction against the germ but rather on the underlying inflammation. These findings also strengthen the importance of a gastroenterological workup of patients with CSU.

This cohort study compares the risk of infection with SARS-CoV-2 among health care workers by mask preference and level of patient exposure.

Marginal-zone B cells of the mucosa-associated lymphoid tissue (MALT) are the normal counterpart of the neoplastic cells in MALT lymphoma. In both cases these lymphocytes express surface immunoglobulins, but are negative when stained for B cell associated antigens like CD10 and CD23. Furthermore, the B cell gene rearrangement has been found in Helicobacter pylori associated chronic gastritis and in extranodal type of marginal-zone lymphoma. The aim of this study was to quantify the number of IgM-, CD10-, and CD23-positive lymphocytes in patients with type B gastritis and to compare the results with the antigen profile of mononuclear cells in patients with gastritis not associated with H. pylori. Additionally, the immunoglobulin heavy-chain (IgH) gene rearrangement in H. pylori positive and H. pylori negative gastritis was studied. From 23 patients with a positive urease test and/or histologically proven H. pylori infection and chronic gastritis and from 22 patients with H. pylori negative chronic gastritis mucosa biopsy specimens were taken. Single-cell suspensions were obtained following enzymatic digestion. For immunocytochemistry, an alkaline phosphatase-antialkaline phosphatase method was applied. IgH gene rearrangement in formalin-fixed, paraffin-embedded specimens was determined by polymerase chain reaction in 11 patients with chronic gastritis. An increase in mu-positive plasma cells and B lymphocytes was detected in patients with H. pylori positive gastritis as compared with patients with H. pylori negative gastritis (10.0 vs. 3.9%, p < 0.001, and 4.3 vs. 1.6%, p < 0.01, respectively). In both groups, the proportion of CD10- and CD23-positive lymphocytes was <1%. IgH gene rearrangement was not restricted to type B gastritis; single bands were also present in 3 of 7 patients with H. pylori negative chronic gastritis. Our finding of IgH gene rearrangement in some of the patients with H. pylori negative chronic gastritis indicates that additional factors may be critical for these genotypical changes and for the pathogenesis of gastric MALT lymphoma.

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