Role Of Pylorus Research Articles

The potential role of Helicobacter pylori in chronic rhinosinusitis with or without nasal polyposis

BackgroundCertain gastrointestinal and extra-intestinal diseases are caused by the gram-negative bacterium Helicobacter pylori (H. pylori). We aimed to determine the potential H. pylori role in chronic rhinosinusitis (CRS) with or without nasal polyposis. This cross-sectional study was conducted on 80 subjects of any age and sex diagnosed with CRS (CRSWNP and CRSSNP) who had failed medical treatment and scheduled for surgery. Patients were further categorised into two equal groups: study group (n = 40) were diagnosed with CRS with or without nasal polyposis (CRSWNP and CRSSNP) who had failed medical treatment and scheduled for surgery, and control group (40 patients) were admitted for septoplasty. All patients had clinical assessment, physical assessment, diagnosis of rhinosinusitis (according to EPOS), based on symptoms, rhinoscopic/endoscopic findings, CT scan findings, questionnaire for gastroesophageal reflux disease (GERD), and questionnaire for laryngopharyngeal reflux (LPR). Samples were collected in the operating room during surgery from both groups and PCR tissue was done.ResultsThe study group patients demonstrated significantly higher history of GERD, LPR, and H. pylori. H. pylori patients had significantly lower ages than those without (P = 0.03). Patients with H. pylori revealed significantly higher GERD history (P < 0.001) and LPR (P = 0.002) than those without H. pylori. History of GERD (P = 0.003), LPR (P = 0.043), and H. pylori presence (P = 0.028) were significant predictors, controlling for the abovementioned variables.ConclusionsWe concluded that a significant correlation was observed between the H. pylori presence in the sinonasal mucosa and nasal polyps and the development of chronic rhinosinusitis with or without nasal polyps.

The role of gastroesophageal reflux disease in the middle ear pathology formation

The extraesophageal reflux effect investigation on the middle ear structures in adults is of considerable interest. The gastroesophageal reflux disease associated otitis media formation mechanism is closely related to such concepts as nasopharyngeal reflux and laryngopharyngeal reflux. It has been established that the pathophysiological mechanism originates in the nasopharynx and further spread to the middle ear structures. The tympanic cavity mucous membrane under the gastric enzymes influence is prone to remodeling, which results in the various chronic inflammation types gradual formation. The study purpose was to analyze medical literature from 1990 to 2024, aimed at studying the middle ear cavity inflammation causes and mechanisms formed by the gastric contents influence. As materials and methods, this article uses publications in such scientific databases as PubMed, eLIBRARY, Science Direct, Research Gate. The analyzed scientific materials provide insight into the relationship between the tympanic cavity inflammation formation and extraesophageal manifestations of GERD, as well as the potential negative H. Pylori impact on the middle ear structures. Conclusions. A detailed understanding of the middle ear cavity inflammation formation by pathophysiological mechanisms of the extraesophageal reflux influence, consisted of various gastrointestinal tract components had been obtained. The potential H. Pylori role in the tympanic cavity mucous membrane alteration remains controversial. This is due to the large number of scientific publications conflicting results in this research field. Major scientific studies confirm that gastroesophageal reflux disease acts as a risk factor for the different types middle ear cavity inflammation formation

Cardiovascular and Neurological Diseases and Association with Helicobacter Pylori Infection-An Overview.

This article investigates the link between Helicobacter pylori (H. pylori) infection and cardiovascular and neurological disorders. Recent research suggests that H. pylori may play a role in cardiovascular diseases like atherosclerosis, myocardial infarction, and stroke, as well as neurological diseases including Alzheimer's disease, multiple sclerosis, and Parkinson's disease. Cardiovascular Diseases: H. pylori induces endothelial dysfunction and chronic inflammation, promoting atherosclerotic plaque formation and other cardiac complications. High infection prevalence in cardiovascular patients implies that systemic inflammation from H. pylori accelerates disease progression. Eradication therapies combined with anti-inflammatory and lipid-lowering treatments may reduce cardiovascular risk. Neurological Diseases: H. pylori may contribute to Alzheimer's, multiple sclerosis, and Parkinson's through systemic inflammation, neuroinflammation, and autoimmune responses. Increased infection prevalence in these patients suggests bacterial involvement in disease pathogenesis. The eradication of H. pylori could reduce neuroinflammation and improve outcomes. Discussions and Future Research: Managing H. pylori infection in clinical practice could impact public health and treatment approaches. Further research is needed to clarify these relationships. Longitudinal and mechanistic studies are essential to fully understand H. pylori's role in these conditions. Conclusions: H. pylori infection is a potential risk factor for various cardiovascular and neurological conditions. Additional research is critical for developing effective prevention and treatment strategies. Targeted therapies, including H. pylori eradication combined with anti-inflammatory treatments, could improve clinical outcomes. These findings highlight the need for an integrated clinical approach to include H. pylori evaluation and treatment.

Association between Helicobacter pylori antibodies and otolaryngological diseases

ObjectiveObservational studies have shown that Helicobacter pylori is related to some otolaryngological diseases. However, it is unclear if H. pylori infection causally affects these diseases. To elucidate H. pylori role in 12 common otolaryngological diseases, we conducted two-sample Mendelian randomization analysis. MethodsSingle-nucleotide polymorphisms associated with 7 H. pylori antibodies (IgG, CagA, Catalase, GroEL, OMP, UREA and Vac A) served as instrumental variables. We primarily employed random-effects inverse variance weighting for causal estimation, supplemented by MR Egger, weighted median, simple mode, and weighted mode. Sensitivity analyses, including heterogeneity, pleiotropy, and leave-one-out tests, validated robustness. ResultsMR analysis using inverse variance weighting (random effects) revealed genetically predicted H. pylori CagA antibodies correlated with increased risk of nonsuppurative otitis media (OR = 1.0778, 95% CI 1.0114–1.1487, p-value = 0.021). No causal relationship was observed between H. pylori antibodies and other common otolaryngological diseases. Sensitivity analyses found no pleiotropy or heterogeneity, affirming result reliability. ConclusionThis study suggests that the levels of H. pylori CagA antibodies may contribute to the development of nonsuppurative otitis media. Further studies are needed in the future to elucidate the specific mechanism of H. pylori in this disease. Level of evidenceLevel III.

The role of &lt;i&gt;Helicobacter pylori&lt;/i&gt; in cardiovascular toxicity mechanisms

Despite the long history of the concept where infection plays a significant role in cardiovascular diseases (atherosclerosis in particular), today it is relevant and represented a significant interest.This article discusses H. pylori role in mechanisms of cardiovascular homeostasis disturbance. H. pylori involvement in atherogenic damage of arteries, and/or plaque destabilization is no doubt. This vidence is detailed in this review article.

Eradication of Helicobacter pylori in patients without gastric symptoms suffering from recurrent aphthous stomatitis: A pilot study

Background/Aim. Helicobacter (H.) pylori is a widespread bacterium and its involvement in pathogenesis of gastric diseases is well-known. However, H. pylori role in etiology of other histologically similar conditions, especially recurrent aphthous stomatitis (RAS) is still controversial. Research regarding H. pylori and its association with RAS, as well as the treatment options were always conducted on patients with diagnosed gastric problems. The aim of this study was to determine whether H. pylori is present in the oral cavity of patients suffering from RAS but without any symptoms or medical history of gastric disease. Methods. A total of 15 patients with RAS participated in the study. None of the participants suffered from any gastrointestinal disorders. Two dental plaque samples from each participant were collected. The first was analyzed using rapid urease test and the second one was put in transport medium and sent for cultivation. The sensitivity of H. pylori to antibiotics was established using disk diffusion method of sensitivity testing for every patient individually and adequate therapy was prescribed. Results. Before the treatment the mean annual recurrence rate of RAS was 8.1 ? 2.1, with the average number of lesions being 3.9 ? 1.9. During the 12-month observation period after the eradication therapy, none of the patients reported recurrence of aphthous lesions. The treatment was successful in all cases. Conclusion. This study shows that RAS can be effectively treated by successful eradication of oral H. pylori, and that RAS could be possibly considered as an early warning sign of potential gastric infection by H. pilory.

Comment on "Lack of Association Found between Helicobacter pylori Infection and Diarrhea-Predominant Irritable Bowel Syndrome: A Multicenter Retrospective Study".

We have read with great interest the paper written by Feng Xiong et al. “Lack of Association Found between Helicobacter pylori Infection and Diarrhea-Predominant Irritable Bowel Syndrome: A Multicenter Retrospective Study” [1]. From the beginning, possible association between H. pylori infection and diarrhea-predominant irritable bowel syndrome (IBS-D) was a challenging topic among clinicians [2]. In this paper, authors concluded that no significant correlation between H. pylori infection and IBS-D was reported. Moreover, IBS-D patients may not benefit from H. pylori eradication. Apart from being an interesting study, there is a short list of critical points to draw a better conclusion within such multicenter studies worldwide. (1) Sample size is mainly lacking in this study. Relatively high rate of treatment efficacy observed in H. pylori infected group can be bound to the low number of investigated individuals. (2) Lack of long-term follow-up in this study is leading to incorrect conclusion regarding relieving bloating symptoms. Moreover, insufficient study design for treatment of the bacterium was another pitfall causing not strong conclusion. According to the current findings, authors concluded that IBS-D patients do not benefit from H. pylori eradication. As a note, determination of successful H. pylori eradication is not clearly described and validated in this study. Also, we need a long-term follow-up (at least 6 months) to confirm primary conclusion drawn by the authors. (3) With regard to the current findings, to be honest, it seems that we have a lack of better evidence rather than lack of association. In conclusion, we agree with Xiong et al., if proven in further studies, about the underlying mechanisms determining H. pylori role in IBS. Finally, the understanding of the H. pylori-host interaction in IBS subjects may open the insight into the development of new therapeutic interventions to manage H. pylori associated extra-digestive disease.

Multifactorial etiology of gastric cancer.

The prevalence of gastric cancer is associated with several factors including geographical location, diet, and genetic background of the host. However, it is evident that infection with Helicobacter pylori (H. pylori) is crucial for the development of the disease. Virulence of the bacteria is also important in modulating the risk of the disease. After infection, H. pylori gains access to the gastric mucosa and triggers the production of cytokines that promote recruitment of inflammatory cells, probably involved in tissue damage. Once the infection is established, a cascade of inflammatory steps associated with changes in the gastric epithelia that may lead to cancer is triggered. H. pylori-induced gastritis and H. pylori-associated gastric cancer have been the focus of extensive research aiming to discover the underlying mechanisms of gastric tissue damage. This research has led to the association of host genetic components with the risk of the disease. Among these is the presence of single nucleotide polymorphisms (SNPs) in several genes, including cytokine genes, which are able to differentially modulate the production of inflammatory cytokines and then modulate the risk of gastric cancer. Interestingly, the frequency of some of these SNPs is different among populations and may serve as a predictive factor for gastric cancer risk within that specific population. However, the role played by other genetic modifications should not be minimized. Methylation of gene promoters has been recognized as a major mechanism of gene expression regulation without changing the primary structure of the DNA. Most DNA methylation occurs in cytosine residues in CpG dinucleotide, but it can also be found in other DNA bases. DNA methyltransferases add methyl groups to the CpG dinucleotide, and when this methylation level is too high, the gene expression is turned off. In H. pylori infection as well as in gastric cancer, hypermethylation of promoters of genes involved in cell cycle control, metabolism of essential nutrients, and production of inflammatory mediators, among others, has been described. Interestingly, DNA changes like SNPs or mutations can create CpG sites in sequences where transcription factors normally sit, affecting transcription.In this chapter, we review the literature about the role of SNPs and methylation on H. pylori infection and gastric cancer, with big emphasis to the H. pylori role in the development of the disease due to the strong association between both.

H. pylori's Role in Glucose Tolerance Under Investigation

H. pylori's Role in Glucose Tolerance Under Investigation

Infectious Diseases: A Treatise of Infectious Processes

Four years have passed since the last edition of Infectious Diseases was published. Knowledge in the field has expanded rapidly. The relationship between roseola (exanthem subitum) and human herpesvirus 6 has been established, and Helicobacter pylori 's role in peptic ulcer disease has been widely accepted. The use of antiretroviral agents to treat human immunodeficiency virus (HIV) infection is being clarified with each passing year. New hepatitis viruses are being discovered. Newspaper headlines draw the world's attention to outbreaks of viral infection in central Africa and the southwest United States. The need for frequent revisions of infectious disease textbooks is obvious. With this fifth edition, senior editor Hoeprich has enlisted the help of an additional editor (Dr Jordan had joined as coeditor of the fourth edition) and nearly 200 highly respected contributors. This edition has grown in page size, if not in total number of pages, and added several chapters.