Background and Study Aims. The association between Helicobacter pylori (H. pylori) and chronic spontaneous urticaria (CSU) remains controversial. This study explored the role of H. pylori in CSU among different virulent genotypes patients. Patients and Methods. Patients infected by H. pylori were sorted into two groups as group A (with CSU) and group B (without CSU). The tissue materials were taken via endoscopy for polymerase chain reaction study to determine virulence factors. After H. pylori eradication therapy, the eradication rate and response of urticaria were evaluated by using C13-UBT and a three-point scale (complete remission, partial remission, or no improvement). Results. The results were comparable between patients of groups A and B in terms of H. pylori infection rates and eradication rate. Longitudinal follow-up of 23.5 months showed complete remission of urticaria in 63.6% but no improvement in 36.4% of the patients after H. pylori eradication. H. pylori infected patients with different virulence factors such as cytotoxin-associated gene A, vacuolating cytotoxin gene A signal region and middle region have similar remission rates for CSU. Conclusions. Current study suggests that H. pylori may play a role in the development and disease course of CSU but may be irrelevant to different virulent genotypes. 1. Introduction Chronic spontaneous urticaria (CSU), defined as spontaneous occurrence of wheal and/or angioedema lasting for a period of longer than 6 weeks, is a common and often frustrating problem, affecting up to 1 percent of the general population [1, 2]. The causes of CSU are numerous; however, in at least 80–90% of the patients, the etiology is undetermined [2, 3]. Recent data show that about 30% of the affected patients may have functional autoantibodies [4]. On the other hand, Helicobacter pylori (H. pylori) infection is probably the most common chronic bacterial infection in humans, with the prevalence rate in general population estimated to be around 50% in developing countries [5]. It has been generally accepted that H. pylori infection plays an etiologic role in the development of chronic active gastritis, peptic ulcer disease, gastric malignancy, and low-grade gastric mucosa-associated lymphoid tissue lymphoma [5–8]. H. pylori is genetically highly diverse, and several genotypes have been identified to associate with severe gastric mucosal inflammation [9]. Cytotoxin-associated gene A (cagA) and vacuolating cytotoxin gene A (vacA), the two most important virulence factors of H. pylori [9], have been reported to enhance its
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