Semen Zheleznov1, Galina Urzhumtseva2, Natalia Petrova2, Zhanna Sarsaniia1, Nikolai Didkovskii1, Tamara Dörr3, Torsten Zuberbier3. 1. Laboratory of Clinical Immunology, Scientific Research Institute of Physical-Chemical Medicine, Moscow, Russian Federation. 2. Department of Endoscopy, Moscow City Clinical Hospital No. 7, Moscow, Russian Federation. 3. Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Dermatology and Allergy, Allergy Center Charité, Berlin, Germany.
Abstract
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.
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.