Immunoglobulin G-4 disease represents a unique inflammatory condition that induces tumorous swelling of affected organs, histologically characterized with diffuse lymphoplasmacytic infiltration of affected organ, occasional eosinophils, storiform fibrosis, obliterative phlebitis, infiltration by numerous IgG4-bearing plasma cells, and marked clinically by dramatic response to steroid therapy [53]. Autoimmune pancreatitis (AIP) seems to be the prototype

of an IgG4-related disease, suggesting that gastric H. pylori infection triggers AIP in genetically predisposed individuals through molecular mimicry with plasminogen-binding protein of H. pylori exhibiting homology to ubiquitin-protein ligase E3 component n-recognin 2, an enzyme expressed

in pancreatic acinar cells [54]. However, serum IgG4 levels were elevated in only 53% of patients in the mentioned study, suggesting CYC202 in vitro that the cohort assessed might, in substantial part, represent non-IgG4-related AIP (type II AIP). An interesting study by Bago et al. [55] involved 56 patients with UBT-proven H. pylori infection, and 41.1% of patients harbored the bacterium in oral cavity, as detected by PCR. Three months after the learn more triple eradication therapy (PPI twice daily/amoxicillin/clarithromycin), the eradication rate in stomach was 78.3%, and surprisingly, H. pylori was not detected in any sample from oral cavity. The results of this study are not in agreement with the hypothesis that the oral cavity may represent the reservoir for gastric reinfection. A Polish study Montelukast Sodium by Burduk et al. [56] investigated on the possible H. pylori colonization in chronic rhinosinusitis and benign laryngeal diseases. This prospective, controlled study involved a series of 30 patients with nasal polyps and normal nasal mucosa and 30 patients with benign laryngeal diseases who underwent endoscopic sinus and endolaryngeal surgery. DNA was extracted from fresh tissue samples and subjected to PCR analysis for detection of ureA and cagA

H. pylori gene. Tissue samples were positive for ureA in all the patients involved in the study, and cagA+ was identified in 23.3% of patients with laryngeal disease while no positive result for cagA+ was observed in patients with nasal polyps and concha bullosa. In a review, Bulajic et al. [57] examined the studies conducted in the last 10 years, in regard to possible correlation between Helicobacter spp. and extragastric malignancies of digestive system. The PCR subtype most widely used in evaluated studies was nested PCR, and genes targeted most frequently for amplification were 16S rDNA of Helicobacter spp and ureA or cagA genes of H. pylori. A strong correlation between Helicobacter spp.