ObjectiveTo discuss the etiological factors and risk factors for peptic ulcer hemorrhage with negative Helicobacter pylori (HP). MethodsA total of 182 patients with peptic ulcer treated in our hospital from January 2010 to December 2012 were chosen in our study. There were 85 cases of hemorrhage among them, with 50 HP positive and 35 HP negative ones. The other 97 patients were without hemorrhage. Etiological factors and correlated risk factors for peptic ulcer hemorrhage with HP negative were analyzed. ResultsHP negative rate of the hemorrhage group was 41.2%, while that rate of the non-hemorrhage group was 14.4%, and the difference was significant (P<0.05). The patients with peptic ulcer hemorrhage with negative HP had correlations with age, sex, wine drinking, taking non-steroidal anti-inflammatory medicine and so on. ConclusionPeptic hemorrhage is easily complicated with peptic ulcer with negative HP, and it is intimately correlated with patients' age, sex, wine drinking history, and taking non-steroidal anti-inflammatory medicine, etc.
ObjectiveTo study the relationship between cholecystectomy and Helicobacter pylori （Hp） infection. MethodsOne hundred and eleven patients with cholecystolithiasis were chosen as the investigation group, while 577 patients with upper digestive tract symptoms without cholecystolithiasis as the control group. All the patients took the 13C breath test to determine whether they were infected by Hp. All the patients with Hp infection continued eradical therapy for Hp infection for one course after cholecystectomy and were followed up on outpatient basis. ResultsThe infection rate in the investigation group was 45.9%, while 27.4% in the control group. During the 3 to 6 months of followup for the patients undergoing eradical therapy for Hp infection, we found no patient complaining of epigastric pain, malaise, belching and nausea. ConclusionThe infection rate of Hp in patients with cholecystolithiasis is high, Hp may be one of the factors causing “postcholecystectomy syndrome”. Eradical therapy for Hp after cholecystectomy will help improve the effects of operation.
Objective To investigate the efficacy of pantoprazole and omeprazole as part of triple therapy in treatment of duodenal ulcer. Methods Seventy-eight patients with duodenal ulcer and HP-positive were randomized to two groups. A random number table was used to generate random sequence. The sequence was not concealed. No blinding was used. Thirty-nine patients received pantoprazole 40 mg + amoxicillin 1.0 g + clarithromycin 0.5 g (PAC group) and 39 patients received omeprazole 20 mg + amoxicillin 1.0 g + clarithromycin 0.5 g (OAC group), twice daily with duration of 7 days. The follow-up time was 4 to 6 weeks. Results At the end of the treatment, 38 patients completed the study, and 1 patient lost to follow-up in the PAC group; thirty-seven patients completed the study, two patients lost to followup in the OAC group. The results of intention-to-treat analysis and per-protocol analysis showed that the HP eradication rates were 87.2%/89.5% in the PAC group and 87.2%/91.9% in the OAC group (P＞0.05); the clinical improvement rates were 79.4%/81.6% in the PAC group and 82.0%/86.5% in the OAC group (P＞0.05). The side effect rates were 10.6% in the PAC group and 8.1% in the OAC group (P＞0.05). No significant difference was found between the two groups (P＞0.05). Conclusions The PAC group is therapeutically effective for eradication of HP and improves symptoms and has an equivalent effect to OAC group for patients with HP-positive duodenal ulcer. Both drugs are well tolerated.
To explain how to treat common gastric diseases like chronic gastritis, peptic ulcer, functional dyspepsia and gastric oesophageal reflux disease (GORD) based on evidence-based medicine. Through this paper, we try to help readers find and use clinical evidence to solve clinical problems.
ObjectiveTo systematically review the association between Helicobacter pylori (HP) infection and Parkinson's disease (PD). MethodsPubMed, EMbase, The Cochrane Library, CNKI, VIP and WanFang Data databases were electronically searched to collect case-control studies on the association between HP and PD from January 2000 to July 2021. Two reviewers independently screened literature, extracted data, and assessed the risk of bias of included studies. Meta-analysis was then performed using RevMan 5.3 software. ResultsA total of 16 case-control studies involving 2 790 subjects were included. The results of meta-analysis showed that the HP infection rate was higher in PD patients than that in healthy patients (OR=1.87, 95%CI 1.38 to 2.54, P<0.000 1). The results of subgroup analysis showed that the infection rate of HP in PD group in Asia and Africa region was significantly higher than that in control group, but not in Europe region. Breath tests and other detection methods were used to detect HP infection, and the HP infection rate in PD group was significantly higher than that in the healthy control group. However, there was no significant difference in HP infection between the two groups by ELISA. UPDRS Ⅲ score of PD patients with HP infection was significantly higher than that of PD patients without HP infection. ConclusionsCurrent evidence shows that PD patients have a higher HP infection rate than the normal population, and the rates are affected by regions and HP detection methods. In addition, HP infection can aggravate the motor symptoms and motor complications of PD patients. Due to limited quality and quantity of included studies, more high-quality studies are required to verify the above conclusions.
Objective We aimed to evaluate the prevalence of H.pylori infection and the prevalence of cagA+ strains in patients with and without Barrett’s esophagus. Methods A full literature search to February 2008 was conducted in PubMed, MEDLINE and EMbase databases to identify case-control studies or cohort studies evaluating the prevalence of H.pylori in patients with or without Barrett’s esophagus. Summary odds ratios (OR) and 95% confidence interval (CI) were calculated by RevMan 4.2.8. Results Nineteen studies were identified (16 case-controlled studies and 3 cohort studies). In case controlled studies, the prevalence of H.pylori infection significantly decreased in patients with Barrett’s esophagus as compared subjects with normal endoscopic appearance, with a overall OR of 0.56 (95%CI 0.40 to 0.79). The prevalence of H.pylori infection was no statistically significant difference in patients with Barrett’s esophagus as compared to those with gastroesophageal reflux disease, with a overall OR of 0.86 (95% CI 0.74 to 1.00). In cohort studies, the prevalence of H. pylori was no statistically significant difference in patients with Barrett’s esophagus as compared to patients with normal endoscopic appearance or patients with gastroesophageal reflux disease, with a overall OR of 1.12 (95%CI 0.77 to 1.61) and 1.10 (95%CI 0.32 to 3.83). When the analysis was stratified by the status of cagA, the prevalence of cagA positive strains significantly decreased in patients with Barrett’s esophagus as compared both to subjects with normal endoscopic appearance with OR 0.30 and 95% CI 0.12 to 0.74, and to those with gastroesophageal reflux disease (OR 0.55; 95%CI 0.33 to 0.94). Irrespective of the presence of intestinal metaplasia, similar magnitude for the reduction of H.pylori infection was observed for patients with Barrett’s esophagus and those with normal endoscopic appearance. While accompared with the presence of intestinal metaplasia, Barrett’s esophagus was associated with a significantly reduction as compared to the patients with gastroesophageal reflux disease (OR 0.81, 95%CI 0.68 to 0.98). When stratified analyses were performed, a significant reduction of H.pylori infection was observed only in patients with long-segment Barrett’s esophagus (OR 0.54; 95%CI 0.35 to 0.82), but not in those with short-segment Barrett’s esophagus (OR 0.72; 95%CI 0.43 to 1.20). Conclusion This meta-analysis indicated that the prevalence of H.pylori infection, especially the prevalence of cagA positive strains was significantly lower in patients with Barrett’s esophagus than in subjects with normal endoscopic appearance. However, the prevalence of H. pylori infection was no statistical difference in patients with Barrett’s esophagus as compared to those with gastroesophageal reflux disease. Colonization with cagA positive strains may be protective against the formation of Barrett’s esophagus.
Objective To provide evidence of the role of helicobacter pylori eradication in the treatment of functional dyspepsia. Methods We searched VIP, CBMdisc, MEDLINE and The Cochrane Library for systematic reviews, meta-analysis, randomized controlled trials and clinical guidelines involving helicobacter pylori and functional dyspepsia, so as to provide the best evidence for clinical practice. Results We included two systematic reviews, one meta-analysis and eleven randomized controlled trials. The evidence identified showed that helicobacter pylori infection was more prevalent in functional dyspepsia than in asymptomatic patients, but the effect of H pylori infection in the pathogenesis of functional dyspepsia remained controversial. H pylori eradication therapy had a relatively weak effect in H pylori positive functional dyspepsia. An economic model suggested that this modest benefit may still be cost-effective, but more studies are needed to assess this. Conclusion According to the current evidence, it can be concluded that helicobacter pylori eradication for the treatment of functional dyspepsia should be individualized.
Objective To evaluate the efficacy and safety of furazolidone-based first-line therapy for Helicobacter pylori infection. Methods The randomized controlled trials (RCTs) of furazolidone-based first-line therapy for Helicobacter pylori infection were identified from Cochrane Library (Issue 1, 2009), PubMed (1992 to January 2009), OVID (1994 to January 2009), Wanfang Data (1994 to January 2009), CNKI (1994 to January 2009), and VIP Data (1994 to January 2009). The quality of included RCTs was assessed, and the meta-analysis was conducted with RevMan5.0 software. Results Among five included RCTs involving 499 patients, four were graded as B in methodology quality and the left one was graded as C. As to the intention-to-treat (ITT) analysis, the Helicobacter pylori eradication rate was 78.3% in furazolidone group and 66.8% in control group (RR=1.18, 95%CI 0.86 to 1.62), while the Per Protocol (PP) analysis, the eradication rate of furazolidone group and control group was 83.1% and 70.9% respectively (RR=1.17, 95%CI 0.88 to 1.57). The incidence rate of mild side-effects was 40.8% in furazolidone group and 39.4% in control group (RR=1.03, 95%CI 0.79 to 1.36), and while that of severe side-effects in furazolidone group and control group was 7.8% and 3.7% respectively (RR=1.86, 95%CI 0.84 to 4.09). Conclusions With similar efficacy and safety as control group has, the furazolidone-based therapy could be recommended as a first-line therapy for Helicobacter pylori infection. The high-quality RCTs with large sample are required to prove the above conclusion for the limitation of quantity and quality of included studies.
Gastric cancer is common as one kind of digestive tract malignant tumor, and Helicobacter pylori (Hp) infection is the most important cause of gastric cancer. With the wide application of quadruple therapy, the incidence of Hp-related gastric cancer has been significantly decreased. In addition to the involvement of gastric microbes in the regulation of normal gastric physiological function, the imbalance of gastric microbes is also involved in the pathogenesis of gastritis and gastric cancer. The imbalance of gastric microbes also plays an important role in the development of gastric cancer after eradication of Hp, and the mechanism has also been preliminary studied. Based on this, this article reviews the research progress of gastric microbes in gastric cancer, in order to further understand the pathogenic mechanism of gastric cancer and provide reference for seeking safer and more effective treatment for gastric cancer.
ObjectiveTo understand the mechanisms of gastric carcinogenesis relevant to Helicobacter pylori (H. pylori)-related cell apoptosis and explore potential causes of gastric cancer development through cell apoptosis. MethodThe literature of recently domestic and international research on the mechanisms of H. pylori-related cell apoptosis in the gastric carcinogenesis was searched and reviewed. ResultsThe H. pylori infection was one of the important risk factors in the occurrence and development of gastric cancer, which was characterized by the imbalance of the interaction between gastric epithelial cells and various cell components in the gastric microenvironment, and which promoted or inhibited the process of apoptosis, and thus interfered with the process of gastric cancer. ConclusionsH. pylori, through the regulation of various cellular components and molecular pathways, increases the sensitivity of gastric epithelial cells to apoptosis, actively participates in the progression of gastric cancer. With the advent of the era of precision medicine, research on the mechanisms of H. pylori-related cell apoptosis in gastric carcinogenesis is transitioning to clinical applications, offering promising new treatment strategies for gastric cancer patients.