Pylori Eradication Treatment Research Articles

The effect of Helicobacter pylori infection on the decline of lung function in a health screening population.

Although Helicobacter pylori (H. pylori) infection has long been associated with many extragastric diseases, its long-term effects on declining lung function and the development of chronic obstructive pulmonary disease (COPD) remains controversial. We conducted a retrospective study in a health screening population (Gene-Environment of Interaction and Phenotype Cohort at Seoul National University Gangnam Health Center in Korea) recruited from 2004 to 2015. The annual decline rates of lung function and the risk for COPD were compared to the seropositivity for H. pylori. We also assessed the impact of the H. pylori eradication treatment on lung function. Among 3,619 subjects, 1,849 subjects (51.1%) tested positive for H. pylori-specific IgG. In the first year, 95 (2.6%) patients were diagnosed with COPD. however, there was no difference in seropositivity for H. pylori in patients with COPD compared to non-COPD subjects (P=0.756). There was no significant difference in the incidence of COPD between the seronegative (2.2%) and the seropositive group (2.0%; P=0.728) even during the follow-up period. The decline rates of the mean FVC and FEV1 were not different between the seronegative and seropositive group (35.38 vs. 34.34 mL/year for FVC, P=0.389; 39.23 vs. 37.49 mL/year for FEV1, P=0.086). The eradication treatment for H. pylori did not affect the decline rates of mean FVC and FEV1. Infection or eradication treatment of H. pylori was not associated with the decline of lung function or COPD progression in this general population health screening. As a result, H. pylori may not be a significant contributor to deteriorating lung function.

Efficacy of second-line regimens for Helicobacter pylori eradication treatment: a systemic review and network meta-analysis

BackgroundCurrent guidelines recommend bismuth-containing quadruple therapy (BQT) and quinolone-containing therapy after failure of first-line Helicobacter pylori eradication therapy. However, the optimum regimen of second-line eradication therapy remains elusive. We conducted...

H. pylori Eradication Treatment Causes Alterations in the Gut Microbiota and Blood Lipid Levels.

Background: The gut microbiome plays an important role in the lipid metabolism. Antibiotic treatment causes changes in the intestinal microbiota. Our objective was to explore the relationship between changes in the intestinal microbiota and the level of plasma high density lipoprotein cholesterol (HDL) and low density lipoprotein cholesterol (LDL).Methods: Prospective case-control study with Helicobacter pylori-positive patients undergoing eradication therapy with omeprazole, clarithromycin, and amoxicillin. Stool and blood samples were obtained from 20 controls (H. pylori negative) and 40 patients before and 2 months after antibiotic treatment. Gut microbiota was determined through 16S rRNA amplicon sequencing (Illumina MiSeq).Results: Eradication treatment for H. pylori increased the HDL levels, and caused changes in gut microbiota profiles. An unfavorable lipid profiles (high LDL and low HDL levels) was associated with a low microbial richness and an increase of the Bacteroidetes phylum. Prevotella copri, Lachonobacterium, and Delsufovibrio were positively associated with HDL while Rikenellaceae was negatively associated with HDL after completing antibiotic treatment.Conclusions: Helicobacter pylori eradication treatment could improve lipid metabolism in relation with an increase in the HDL. Changes in the abundance of specific bacteria, such as P. copri, Lachonobacterium, Delsufovibrio, and Rikenellaceae could be associated with change in the plasma HDL levels.

Regression of a Large Hyperplastic Polyp after Helicobacter pylori Eradication Treatment

Regression of a Large Hyperplastic Polyp after Helicobacter pylori Eradication Treatment

Colonic mucosa-associated lymphoid tissue in a renal transplant recipient: a case report

BackgroundExtra-gastric (particularly colonic) lymphoma of mucosa-associated lymphoid tissue in the immunosuppressed solid organ transplant recipient is rare. We report a case of low-volume mucosa-associated lymphoid tissue lymphoma with colonic and bone marrow involvement in a renal transplant recipient that has been managed conservatively.Case presentationA 62-year-old Caucasian man, 14 years after kidney transplantation, was diagnosed as having extra-nodal marginal zone lymphoma of mucosa-associated lymphoid tissue with bone marrow and colonic involvement, after a colonoscopy identified mucosa-associated lymphoid tissue lymphoma in a sessile sigmoid polyp following surveillance fecal occult blood testing that returned a positive result. A gastric biopsy showed no evidence of Helicobacter pylori, but Helicobacter pylori immunoglobulin G was positive. He received Helicobacter pylori eradication treatment and is being managed expectantly. Immunosuppression was unchanged with prednisolone, mycophenolate mofetil, and cyclosporine A. Renal allograft function has remained stable.ConclusionsThis case highlights the unexpected occurrence of colonic mucosa-associated lymphoid tissue lymphoma in a kidney transplant recipient. The case emphasizes the importance of histopathological diagnosis of colonic lesions in this patient cohort because the unusual diagnosis of low-volume mucosa-associated lymphoid tissue lymphoma can be managed expectantly as it does not appear to be clinically aggressive in the immunosuppressed solid organ transplant.

Helicobacter pylori first-line and rescue treatments in patients allergic to penicillin: Experience from the European Registry on Hpylori management (Hp-EuReg).

Experience in Helicobacter pylori eradication treatment of patients allergic to penicillin is very scarce. A triple combination with a PPI, clarithromycin (C), and metronidazole (M) is often prescribed as the first option, although more recently the use of a quadruple therapy with PPI, bismuth (B), tetracycline (T), and M has been recommended. To evaluate the efficacy and safety of first-line and rescue treatments in patients allergic to penicillin in the "European Registry of Hpylori management" (Hp-EuReg). A systematic prospective registry of the clinical practice of European gastroenterologists (27 countries, 300 investigators) on the management of Hpylori infection. An e-CRF was created on AEG-REDCap. Patients with penicillin allergy were analyzed until June 2019. One-thousand eighty-four patients allergic to penicillin were analyzed. The most frequently prescribed first-line treatments were as follows: PPI+C+M (n=285) and PPI+B+T+M (classic or Pylera® ; n=250). In first line, the efficacy of PPI+C+M was 69%, while PPI+B+T+M reached 91% (P<.001). In second line, after the failure of PPI+C+M, two rescue options showed similar efficacy: PPI+B+T+M (78%) and PPI+C+levofloxacin (L) (71%) (P>.05). In third line, after the failure of PPI+C+M and PPI+C+L, PPI+B+T+M was successful in 75% of cases. In patients allergic to penicillin, a triple combination with PPI+C+M should not be generally recommended as a first-line treatment, while a quadruple regimen with PPI+B+T+M seems to be a better option. As a rescue treatment, this quadruple regimen (if not previously prescribed) or a triple regimen with PPI+C+L could be used but achieved suboptimal (<80%) results.

Does Helicobacter pylori Eradication Reduce the Incidence of Metachronous Gastric Cancer After Curative Endoscopic Resection of Early Gastric Cancer: A Systematic Review and Meta-Analysis.

Whether Helicobacter pylori eradication could reduce the risk of metachronous gastric cancer remain controversial. In the present study, we performed a systematic review and meta-analysis to evaluate the preventive effect of H. pylori eradication on the occurrence of metachronous gastric cancer after curative endoscopic resection of early gastric cancer. The related studies were identified by searching PubMed and Embase databases. According to the H. pylori infection status and subsequent treatment, all patients were classified into H. pylori negative group, H. pylori eradication group and noneradication group. The relevant data were extracted and pooled effect size was assessed using a fixed effect model or a random effect model. A total of 11 retrospective cohort studies and 3 randomized controlled trials were included in this meta-analysis. The results based on the cohort studies indicated that the risk of metachronous gastric cancer was significantly lower in H. pylori eradication group than in noneradication group (hazard ratios: 0.65, 95% confidence interval: 0.50-0.86, P=0.002; I=0%). The pooled result of 2 randomized controlled trials demonstrated that the patients receiving anti-H. pylori treatment had a lower risk of metachronous gastric cancer than those who did not receive H. pylori eradication treatment (hazard ratios: 0.43, 95% confidence interval: 0.26-0.70, P=0.001; I=0%). In addition, the occurrence of metachronous gastric cancer in H. pylori eradication group was not significantly different from that in H. pylori negative group. Successful H. pylori eradication may be useful for the prevention of metachronous gastric cancer after curative endoscopic resection of early gastric cancer. Thus, anti-H. pylori treatment should be considered for those patients with H. pylori infection after curative endoscopic resection.

10-Day Versus 14-Day Quadruple Concomitant Nonbismuth Therapy for the Treatment of Helicobacter pylori Infection: Results From a Randomized Prospective Study in a High Clarithromycin Resistance Country.

The aim of this study was to investigate the implementation of a 14-day quadruple nonbismuth concomitant regimen, as proposed by recent Guidelines and Consensus Statements. In Greece, a region with >20% clarithromycin resistance where bismuth is unavailable, the 10-day quadruple concomitant scheme has already been adopted as the accepted first-line Helicobacter pylori eradication treatment. Our prospective randomized study included 364 patients with newly diagnosed H. pylori infection, randomized to receive a 10-day or a 14-day nonbismuth quadruple concomitant scheme. Treatment outcome was assessed by C-urea breath test and/or histology at least 4 weeks after therapy. Intention to treat and per protocol analyses of the eradication rates were performed. Secondary endpoints included patient adherence, safety, and the impact of prior antibiotic exposure in treatment efficacy. The overall eradication rates of the 2 treatments were 87.9% versus 87.4% in the intention to treat analysis, P=1.000, and 93% versus 94.1%, P=0.859, in the per protocol analysis for the 10-day and the 14-day treatment group, respectively. Both groups displayed excellent compliance rates (99.5% for the 10-day vs. 96.2% for the 14-day treatment duration, P=0.067). As regards treatment safety, serious adverse events that led to the discontinuation of both regimens were few, with no statistical difference between the 2 groups (0.5% in the 10-day group and 2.2% in the 14-day group, P>0.05). Previous antibiotic exposure was not significant with regard to treatment efficacy. In Greece, the 10-day concomitant nonbismuth quadruple regimen for first-line treatment remains the most efficient strategy for H. pylori eradication.

Family History of Gastric Cancer and Helicobacter pylori Treatment

BackgroundHelicobacter pylori infection and a family history of gastric cancer are the main risk factors for gastric cancer. Whether treatment to eradicate H. pylori can reduce the risk of gastric cancer in persons with a family history of gastric cancer in first-degree relatives is unknown.MethodsIn this single-center, double-blind, placebo-controlled trial, we screened 3100 first-degree relatives of patients with gastric cancer. We randomly assigned 1838 participants with H. pylori infection to receive either eradication therapy (lansoprazole [30 mg], amoxicillin [1000 mg], and clarithromycin [500 mg], each taken twice daily for 7 days) or placebo. The primary outcome was development of gastric cancer. A prespecified secondary outcome was development of gastric cancer according to H. pylori eradication status, assessed during the follow-up period.ResultsA total of 1676 participants were included in the modified intention-to-treat population for the analysis of the primary outcome (832 in the treatment group and 844 in the placebo group). During a median follow-up of 9.2 years, gastric cancer developed in 10 participants (1.2%) in the treatment group and in 23 (2.7%) in the placebo group (hazard ratio, 0.45; 95% confidence interval [CI], 0.21 to 0.94; P=0.03 by log-rank test). Among the 10 participants in the treatment group in whom gastric cancer developed, 5 (50.0%) had persistent H. pylori infection. Gastric cancer developed in 0.8% of participants (5 of 608) in whom H. pylori infection was eradicated and in 2.9% of participants (28 of 979) who had persistent infection (hazard ratio, 0.27; 95% CI, 0.10 to 0.70). Adverse events were mild and were more common in the treatment group than in the placebo group (53.0% vs. 19.1%; P<0.001).ConclusionsAmong persons with H. pylori infection who had a family history of gastric cancer in first-degree relatives, H. pylori eradication treatment reduced the risk of gastric cancer. (Funded by the National Cancer Center, South Korea; ClinicalTrials.gov number, NCT01678027.)

Influence of acotiamide on 13C-urea breath test for Helicobacter pylori diagnosis.

The Helicobacter pylori infection and functional dyspepsia are often coexisted. The effect of acotiamide, a drug for functional dyspepsia, on the result of Helicobacter pylori diagnosis has yet to be studied. We evaluated the influence of acotiamide on the results of Helicobacter pylori diagnosis in the 13C-urea breath test. Twenty patients with Helicobacter pylori-positive functional dyspepsia were treated with 100 mg of acotiamide three times a day for two weeks. Changes in 13C-urea breath test were investigated before and after administration, and two weeks after administration as the follow-up period. The 13C-urea breath test and the medical questionnaire of modified frequency scale for the symptoms of gastroesophageal reflux disease were conducted at every period. Nineteen patients were included for analysis. No patients showed negative in 13C-urea breath test at Weeks 2 and 4. On the symptom scale, dyspepsia and total scores decreased from Week 0 to Week 2 and increased from Week 2 to Week 4, and the improvement rates of the dyspepsia score at Week 2 was 63%. In conclusion, we confirmed that acotiamide is unlikely to influence the result of 13C-urea breath test and it may improve the symptoms of functional dyspepsia during Helicobacter pylori eradication treatment.

Eradication Treatment of Helicobacter pylori Infection Based on Molecular Pathologic Antibiotic Resistance.

BackgroundUnfortunately, the eradication rate of Helicobacter pylori (H. pylori) treatment is markedly decreasing in recent years and the major reason is antibiotic resistance. Our study was designed to determine the effect and safety of H. pylori eradication treatment based on the molecular pathologic antibiotic resistance.Methods261 patients were analyzed retrospectively, including 111 patients who were treated for the first time (one group as First-treated) and 150 patients who failed at least once in bismuth quadruple therapy (another group as Re-treatment). Antibiotic resistance was examined by Real-time PCR detection and conventional PCR and sequencing method. The eradication rate (ER) was compared per intention to treat (ITT) and per protocol (PP) between the two groups.ResultsThe resistance rates to amoxicillin, clarithromycin, fluoroquinolone and tetracycline were 5.5%, 42.1%, 41.7% and 12.9% in the 111 first-treated patients, and 11.7%, 79.7%, 70.7% and 30.0% in the 150 re-treatment patients. The ERs in the ITT and PP analyses were 92.79% (95% CI, 87.98–97.60%, n=111) and 98.10% (95% CI, 95.48–100%, n=105), respectively, in the first-treated patients and 90.67% (95% CI, 86.01–95.32%, n=150) and 95.10% (95% CI, 91.57–98.64%, n=143), respectively, in the re-treatment patients. No significant differences were shown in the ERs between two group patients, and no serious adverse events were found.ConclusionH. pylori eradication treatment based on molecular pathologic antibiotic resistance showed good effect and safety in both first and re-treated patients.

Fundic gland polyp prevalence according to Helicobacter pylori infection status.

The prevalence of fundic gland polyp (FGP) occurrence has not been clarified in individuals with Helicobacter pylori infection post-eradicated status. This study was performed to examine the relationship between FGP prevalence and H. pylori infection status. We enrolled 3400 subjects (2185 male subjects and 1215 female subjects; mean age 54.7 ± 9.5 years) with known H. pylori infection status and who underwent an upper gastrointestinal endoscopy examination as part of an annual check-up. Subjects without and with H. pylori infection numbered 1617 and 239, respectively, while 1544 had a post-eradication status. The presence of FGP and degree of gastric mucosal atrophy were determined in each subject using an endoscopic method. Endoscopy findings showed FGPs in 1029 (30.3%) of all subjects. The prevalence ratio of FGP positivity in H. pylori-negative, H. pylori-positive, and post-eradicated subjects was 51.9%, 1.7%, and 12.0%, respectively. Multiple logistic regression analysis revealed that female gender, older age, milder gastric mucosal atrophy, and anti-secretory therapy were significant risk factors for FGP occurrence. As compared with H. pylori-positive subjects, the odds ratios for H. pylori-negative and post-eradication status were 48.3 and 6.6, respectively (P < 0.001). In the post-eradication status subjects, longer duration following bacterial eradication was a significant risk factor for occurrence of FGPs. The risk of FGP occurrence in individuals who have undergone H. pylori eradication treatment is lower as compared with those who have never been infected. However, that risk increases over time following eradication.

Helicobacter pylori infection may increase the severity of nonalcoholic fatty liver disease via promoting liver function damage, glycometabolism, lipid metabolism, inflammatory reaction and metabolic syndrome.

Background and aimRecent clinical trials have confirmed that Helicobacter pylori infection is positively associated with nonalcoholic fatty liver disease (NAFLD), although some research has shown a negative association. Therefore, to confirm whether H. pylori eradication treatment is feasible for NAFLD patients in our hospital, we aimed to establish the association between H. pylori infection and NAFLD.MethodsWe enrolled 91 patients with NAFLD diagnosed by abdominal B-mode ultrasonography between January and December 2018. H. pylori infection was confirmed by C13 urea breath test, and liver function, glycometabolism, insulin sensitivity, lipid metabolism, as well as inflammatory reaction were assessed through blood biochemical analyses.ResultsA minority of NAFLD patients had liver dysfunction, increased fasting glucose and insulin levels, a score of insulin-resistance (HOMA-Ir), lipid metabolism, slight inflammatory response, fasting hyperglycemia and hypertension. Most patients were complicated with overweight/visceral obesity and dyslipidemia. Moreover, these abnormal indicators were closely associated with the severity of NAFLD and H. pylori infection. Notably, the prevalence of H. pylori infection showed a significant difference between mild, moderate and severe NAFLD, and hepatic steatosis with coexistent NAFLD also revealed a striking difference between H. pylori-positive and H. pylori-negative patients (P < 0.01).ConclusionOur results suggest that H. pylori infection may be an independent risk factor in NAFLD progress.

Metformin use and risk of gastric adenocarcinoma in a Swedish population-based cohort study

BackgroundWhether or not the use of metformin decreases the risk of gastric adenocarcinoma is unclear.MethodsThis was a population-based cohort study in 2005–2015. Associations between metformin use and gastric non-cardia and cardia adenocarcinomas were examined within two cohorts; a diabetes cohort of participants using anti-diabetes medications, and a matched cohort of common-medication users, where metformin non-users were frequency matched (10:1) with metformin users for sex and age. Multivariable Cox proportional hazard regression analyses provided hazard ratios (HR) and 95% confidence intervals (CI), adjusting for sex, age, calendar year, comorbidity, Helicobacter pylori eradication treatment, use of non-steroidal anti-inflammatory drugs or aspirin and use of statins.ResultsDuring the follow-up for a median of 5.8 years, 892 (0.1%) participants in the diabetes cohort and 6395 (0.1%) participants in the matched cohort of common-medication users developed gastric adenocarcinoma. Metformin users had no significantly decreased risk of gastric non-cardia adenocarcinoma (diabetes cohort: HR 0.93, 95% CI 0.78–1.12; matched cohort: HR 1.30, 95% CI 1.18–1.42) or cardia adenocarcinoma (diabetes cohort: HR 1.49, 95% CI 1.09–2.02; matched cohort: HR 1.58, 95% CI 1.38–1.81) compared with non-users in both cohorts.ConclusionsThis cohort study with <10 years of follow-up suggests metformin use may not prevent gastric adenocarcinoma.

Helicobacter Pylori Cytotoxin-Associated Gene A (CagA) and Gastric Carcinoma

Gastric cancer is a highly lethal disease. Establishment of H. pylori infection as a risk factor for this malignancy help identifying persons at increased risk. Studying the association between the genotypes of H pylori virulence factors and gastric carcinoma would have clinical implications in selecting patients who would benefit from H. pylori eradication treatment, with a subsequent reduced risk of gastric cancer. Many virulence factors are involved in the pathogenicity of H. pylori, including urease, vacuolating cytotoxin (a product of the vacA gene), and the immunogenic protein cagA, encoded by the cytotoxin-associated gene A (cagA). These virulence factors interact and modulate different cellular signaling pathways to induce a pro-inflammatory response or alter tight junctions and cell polarity, which finally favor metastasis. The cagA gene is a virulence gene located in the cag pathogenicity island of the bacterial genome and is frequently associated with more severe clinical outcomes. The cagA proteins can increase the virulence potencies of strains, by increasing host-cell cytokine production and altering protein tyrosine phosphorylation. Many studies revealed a possible association between H. pylori virulence factor cagA and its genotypes and the development of gastric carcinoma among patients, which would help in minimizing the risk of gastric carcinoma development by selecting patients who would benefit from H. pylori eradication. This review highlights how the upregulation of cagA gene could be a risk factor for developing gastric carcinoma and its potential relationship on the selection of patients who would benefit from H. Pylori treatment. Keywords:Cancer, cytokine, virulence

1911 Acquired Double Pylorus: The Road Less Traveled

INTRODUCTION: A double pylorus channel can be congenital or acquired. Acquired double pylorus is thought to be the result of a gastric or duodenal ulcer forming a fistula between the prepyloric antrum and the duodenal bulb. Although it is a rare endoscopic finding, seen in only 0.001%–0.4% of upper gastrointestinal endoscopies1, when acquired, it signifies peptic ulcer disease (PUD) which needs risk factor modification and treatment. CASE DESCRIPTION/METHODS: A 50-year-old man with alcohol use disorder, newly diagnosed alcoholic cirrhosis and recent NSAID use presented with confusion, melena and dark emesis. His physical exam was notable for hypotension (BP 86/55 mmHg), somnolence, confusion and positive asterixis. Laboratory values were remarkable for hemoglobin of 5 g/dL, BUN of 48 mmol/L, platelets of 271 × 109/L and INR of 2. Management included fluid resuscitation, blood transfusion, proton pump inhibitor and octreotide drip. Once hemodynamically stabilized, an upper endoscopy was performed revealing blood in the gastric body, two antral ulcers with visible vessels, but no endoscopic stigmata of liver disease. Adjacent to the pylorus, a slit-like channel connecting the prepyloric antrum to the duodenal bulb was noted and traversed with the endoscope. Helicobacter pylori work up revealed a positive serum antibody. Patient did well post-procedure and received Helicobacter pylori eradication treatment and counseling on alcohol cessation and NSAID avoidance. DISCUSSION: In contrast to congenital double pylorus which is an incidental finding, patients with acquired double pylorus often present with symptoms of PUD. In this case, likely culprits included NSAIDs and Helicobacter pylori. It should be distinguished from other similar appearing endoscopic findings such as gastric diverticulum, as risk factors for PUD need to be investigated in patients with an acquired double pylorus. While treatment with acid suppression and Helicobacter pylori eradication should be pursued, the fistula tract often persists despite treatment2. Endoscopic recognition and familiarity are key to ensure appropriate risk modification, treatment and prevention of endoscopic complications with side-viewing scopes.

Helicobacter pylori eradication treatment for gastric carcinoma prevention in asymptomatic or dyspeptic adults: systematic review and Bayesian meta-analysis of randomised controlled trials

ObjectivesRecent meta-analyses of eradication therapy in Helicobacter pylori-infected adults reported significant reductions in gastric carcinoma risk. However, concerns about supporting unfocused screening and eradication programme in healthy, asymptomatic populations have...

Final results of early non-invasive gastric cancer detection study using the serum pepsinogen test method in Croatian patients.

e15551 Background: Gastric cancer (GC) is the 8th most common cancer cause of cancer deaths in Croatia and 2nd most common cause of cancer deaths worldwide. GC of the intestinal type is usually preceded by a chronic atrophic gastritis which is a precancerous change in the stomach. Methods: A reliable diagnostic tool for the early detection of the GC is essential. Screening programs have led to an improvement of overall 5-y survival rate for GC in Japan and Pepsinogen test method was suggested to reduce mortality from gastric cancer. The gold standard for the diagnosis of GC is the pathohistological study of biopsies obtained during an upper GI endoscopy, an invasive method that is too complicated for use in population screening and patients with comorbidity. We have conducted a prospective single center clinical study over a period of &gt; 2 years to evaluate sensitivity and specificity of reagents, and to determine if these reagents can be part of routine. Inclusion criteria for the study were: signed informed consent, life expectancy &gt; 12, and exclusion criteria were: previous treatments for any malignancy, current usage of IPP or NSAIDs medication, poor ECOG performance status ≥3, known history of H. pylori eradication treatment or gastric surgery. We previously reported preliminary results of PG test method in Croatian population. Here, we present mature data after median follow-up of 26 months. Statistical analyses were performed by using a Mann-Whitney U test, multiple logistic regression and the receiver operating characteristics (ROC) to evaluate the predictive power of biomarkers. Results: Blood samples have been collected from patients with suspicious to GC attending for endoscopy or surgery. We used cut off points to evaluate gastric cancer risk: PGI ≤ 70 and PGI/II ratio ≤ 3.0. Of the 116 patients, 25 patients had GC and 91 had non-malignant pathology on tissue biopsy (like atrophic gastritis). Based on an optimal cut-off value calculated by ROC curve analysis had accuracy, sensitivity, specificity, positive predictive value, and negative predictive value of 86.2%, 60.0%, 93.4%, 65.2%and 89.47%, respectively, for the diagnosis of GC. AUC was 0.767 (95% CI 64.0-89.0). Conclusions: The single use of pepsinogen tests is not sufficient for stomach cancer detection; however, it provides a valuable test for selecting a population that needs further diagnosing. Meanwhile, its high specificity could also help to avoid unnecessary endoscopy, especially in older population or patients with heavy burden of comorbidity. Clinical trial information: 2016-0019-34.

Role of Probiotics in Prophylaxis of Helicobacter pylori Infection.

Helicobacter pylori, a pathogenic bacterium, has been known to be the root cause of numerous gastrointestinal disorders. In patients showing symptoms of its infection, antibiotic therapy is a likely treatment. However, the high cost of antibiotic therapy, associated antibiotic resistance along with other adverse effects has led to the use of probiotics for Helicobacter pylori treatment. In recent times, probiotics have played an essential role as complementary prophylaxis for gastrointestinal diseases, thus minimizing antibiotics' usage and their side effects. Probiotics are live microbial agents that exude beneficial effects on their hosts when administered in the proper dosage. The growth of the organism has been reported to be inhibited to a great extent by probiotics and research employing animal models has shown a significant reduction in H. pylori-associated gastric inflammation. In human clinical trials, it has been observed that treatment with probiotics alleviated gastritis symptoms caused by H. pylori and reduced colonization of the organism. As expected, complete eradication of H. pylori infection has not yet been reported by the administration of probiotics alone. Complement treatments using probiotics have shown to benefit infected individuals by decreasing the harmful effects of H. pylori eradication treatment using antibiotics. Long-term administration of probiotics might have favourable outcomes in H. pylori infection especially by decreasing the risk of development of diseases caused by increased levels of gastric inflammation. One such chronic condition is gastric ulcer which occurs due to considerable damage to the mucosal barrier by H. pylori colonization. This review provides a brief description of the promising role of probiotics as a complementary treatment to control H. pylori infection and consequently the management of various gastrointestinal disorders among populations with a special focus on gastric ulcer.

High dose dual therapy versus bismuth quadruple therapy for Helicobacter pylori eradication treatment: A systematic review and meta-analysis.

The aim of this study was to perform a systematic review and meta-analysis on high-dose dual therapy (HDDT) versus bismuth quadruple therapy (BQT) for Helicobacter pylori infection. Comparing HDDT to BQT were identified from PubMed, EMBASE, Cochrane library, CNKI, and Wanfang databases in Chinese up to March 2018. Statistical analyses were conducted using Review Manager 5.3 to compare the efficacy and side effects of these 2 therapies for H pylori infection. Dichotomous data were pooled to score the relative risk (RR) with 95% confidence intervals (CIs). Four randomized clinical trials (RCTs) including 829 patients with a diagnosis of H pylori infection were assessed. Overall the meta-analysis showed that both HDDT and BQT achieved similar efficacy of intention-to-treat (ITT) eradication rate, 85.5% versus 87.2%, RR 1.01 (95% CI: 0.96-1.06), P = .63, and of per-protocol (PP) eradication rate, 88.4% versus 91.5%, RR 1.00 (95% CI: 0.96-1.04), P = .99, and adherence 97.8% versus 95.0%, RR 1.01 (95% CI: 0.99-1.04), P = .32, but side effects were more likely in BQT (14.4% vs 40.4%, RR 0.42 (95% CI: 0.32-0.54), P <.00001). Both HDDT and BQT can achieve similar eradication rate for H pylori infection and adherence, and generally HDDT causes fewer side effects.