MATERIALS AND METHODS: This randomized, double-blinded, placebo-controlled trial involved treatment-naïve H. pylori-positive patients. Ninety patients received standard triple therapy for 2 weeks before receiving either a probiotic or placebo for 4 weeks. The posttreatment eradication rate was assessed via a 14 C urea breath test in Week 8. The Gastrointestinal Symptom Rating Scale (GSRS) questionnaire and an interview on treatment adverse effects were conducted during this study.
RESULTS: The eradication rate was higher in the probiotic group than in the placebo group, with a 22.2% difference in the intention-to-treat analysis (91.1% vs. 68.9%; p = 0.007) and 24.3% difference in the per-protocol analysis (93.2% vs. 68.9%; p = 0.007). The probiotic group showed significant pre- to post-treatment reductions in indigestion, constipation, abdominal pain, and total GSRS scores. The probiotic group showed significantly greater reductions in GSRS scores than the placebo group: indigestion (4.34 ± 5.00 vs. 1.78 ± 5.64; p = 0.026), abdominal pain (2.64 ± 2.88 vs. 0.89 ± 3.11; p = 0.007), constipation (2.34 ± 3.91 vs. 0.64 ± 2.92; p = 0.023), and total score (12.41 ± 12.19 vs. 4.24 ± 13.72; p = 0.004). The probiotic group reported significantly fewer adverse headache (0% vs. 15.6%; p = 0.012) and abdominal pain (0% vs. 13.3%; p = 0.026) effects.
CONCLUSIONS: There was a significant increase in H. pylori eradication rate and attenuation of symptoms and adverse treatment effects when L. reuteri was given as an adjunct treatment.
METHODS: We applied H. pylori multiplex serology to measure antibody responses to 13 H. pylori proteins in prediagnostic serum samples from 485 colorectal cancer cases and 485 matched controls nested within the EPIC study. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using multivariable conditional logistic regression to estimate the association of H. pylori overall and protein-specific seropositivity with odds of developing colorectal cancer.
RESULTS: Fifty-one percent of colorectal cancer cases were H. pylori seropositive compared with 44% of controls, resulting in an OR of 1.36 (95% CI, 1.00-1.85). Among the 13 individual H. pylori proteins, the association was driven mostly by seropositivity to Helicobacter cysteine-rich protein C (HcpC; OR: 1.66; 95% CI, 1.19-2.30) and Vacuolating cytotoxin A (VacA) (OR: 1.34; 95% CI, 0.99-1.82), the latter being nonstatistically significant only in the fully adjusted model.
CONCLUSIONS: In this prospective multicenter European study, antibody responses to H. pylori proteins, specifically HcpC and VacA, were associated with an increased risk of developing colorectal cancer.
IMPACT: Biological mechanisms for a potential causal role of H. pylori in colorectal carcinogenesis need to be elucidated, and subsequently whether H. pylori eradication may decrease colorectal cancer incidence.
METHODS: This was a cross-sectional study on gastric biopsies from 234 consecutive patients (mean age 53.5 [14.8] years) who underwent upper gastrointestinal endoscopy between January 2006 and December 2006.
RESULTS: There were 137 (59%) men and 185 (79%) Malay patients. Among 234 biopsies, CAG was found in 99 and non-atrophic gastritis in 135. Intestinal metaplasia and dysplasia were detected in 8 and 6 atrophic gastritis biopsies, respectively, and in 10 and 3 of non-atrophic gastritis biopsies, respectively. H. pylori were detected in 16 (9 Malays, 7 non- Malays) biopsies (p=0.024); intestinal metaplasia was detected in 4 biopsies (p=0.3) and dysplasia in 5 biopsies (p=0.3). Of the 218 biopsies negative for H. pylori, intestinal metaplasia was found in 14 and dysplasia in 4. The risk of intestinal metaplasia as well as dysplasia was associated with presence of H. pylori infection (p=0.029 and p<0.001 respectively).
CONCLUSION: Even in a setting of low prevalence of H. pylori, intestinal metaplasia and dysplasia were significantly associated with H. pylori infection. The frequency of intestinal metaplasia and dysplasia was similar different between biopsies with atrophic gastritis and non-atrophic gastritis.
METHODS: 28 experts from 11 countries reviewed the evidence and modified the statements using the Delphi method, with consensus level predefined as ≥80% of agreement on each statement. The Grading of Recommendation Assessment, Development and Evaluation (GRADE) approach was followed.
RESULTS: Consensus was reached in 26 statements. At an individual level, eradication of H. pylori reduces the risk of GC in asymptomatic subjects and is recommended unless there are competing considerations. In cohorts of vulnerable subjects (eg, first-degree relatives of patients with GC), a screen-and-treat strategy is also beneficial. H. pylori eradication in patients with early GC after curative endoscopic resection reduces the risk of metachronous cancer and calls for a re-examination on the hypothesis of 'the point of no return'. At the general population level, the strategy of screen-and-treat for H. pylori infection is most cost-effective in young adults in regions with a high incidence of GC and is recommended preferably before the development of atrophic gastritis and intestinal metaplasia. However, such a strategy may still be effective in people aged over 50, and may be integrated or included into national healthcare priorities, such as colorectal cancer screening programmes, to optimise the resources. Reliable locally effective regimens based on the principles of antibiotic stewardship are recommended. Subjects at higher risk of GC, such as those with advanced gastric atrophy or intestinal metaplasia, should receive surveillance endoscopy after eradication of H. pylori.
CONCLUSION: Evidence supports the proposal that eradication therapy should be offered to all individuals infected with H. pylori. Vulnerable subjects should be tested, and treated if the test is positive. Mass screening and eradication of H. pylori should be considered in populations at higher risk of GC.
DESIGN: A cross-sectional study on consecutive patients with dyspepsia undergoing upper gastrointestinal endoscopy.
SETTING: A large general hospital in Kuala Lumpur, Malaysia.
PARTICIPANTS: Consecutive patients undergoing endoscopy for upper abdominal discomfort were examined for the presence of reflux oesophagitis, hiatus hernia and Barrett's oesophagus. The diagnosis and classification of reflux oesophagitis was based on the Los Angeles classification. Patients with predominant symptoms of heartburn or acid regurgitation of at least one per month for the past 6 months in the absence of reflux oesophagitis were diagnosed as having NERD. The prevalence of GORD, reflux oesophagitis and NERD were analysed in relation to age, gender, race, body mass index (BMI), presence of hiatus hernia, Helicobacter pylori status, alcohol intake, smoking and level of education.
RESULTS: One thousand patients were studied prospectively. Three hundred and eighty-eight patients (38.8%) were diagnosed as having GORD based on either predominant symptoms of heartburn and acid regurgitation and/or findings of reflux oesophagitis. One hundred and thirty-four patients (13.4%) had endoscopic evidence of reflux oesophagitis. Two hundred and fifty-four (65.5%) were diagnosed as having NERD. Hiatus hernia was found in 6.7% and Barrett's oesophagus in 2% of patients. Of our patients with reflux oesophagitis 20.1% had grade C and D oesophagitis. No patients had strictures. Following logistic regression analysis, the independent risk factors for GORD were Indian race (odds ratio (OR), 3.25; 95% confidence interval (CI), 2.38-4.45), Malay race (OR, 1.67; 95% CI, 1.16-2.38), BMI > 25 (OR, 1.41; 95% CI, 1.04-1.92), presence of hiatus hernia (OR, 4.21; 95% CI, 2.41-7.36), alcohol consumption (OR, 2.42; 95% CI, 1.11-5.23) and high education level (OR, 1.52; 95% CI, 1.02-2.26). For reflux oesophagitis independent the risk factors male gender (OR, 1.64; 95% CI, 1.08-2.49), Indian race (OR, 3.25; 95% CI, 2.05-5.17), presence of hiatus hernia (OR, 11.67; 95% CI, 6.40-21.26) and alcohol consumption (OR, 3.22; 95% CI, 1.26-8.22). For NERD the independent risk factors were Indian race (OR, 3.45; 95% CI, 2.42-4.92), Malay race (OR, 1.80; 95% CI, 1.20-2.69), BMI > 25 (OR, 1.47; 95% CI, 1.04, 2.06) and high education level (OR, 1.66; 95% CI, 1.06-2.59).
CONCLUSIONS: Reflux oesophagitis and Barrett's oesophagus were not as uncommon as previously thought in a multiracial Asian population and a significant proportion of our patients had severe grades of reflux oesophagitis. NERD, however, still constituted the larger proportion of patients with GORD. Indian race was consistently a significant independent risk factor for reflux oesophagitis, NERD and for GORD overall.
METHODS: We used multiple search strategies in MEDLINE through PubMed to seek for suitable articles that had case-control design with gastric cancer as outcome.
RESULTS: The outcomes of our study shows protection (odds ratio [OR] 0.55, P = 0.003) and susceptibility (OR 1.94, P = 0.0004), both significant with low and medium-high intake of capsaicin, respectively, although under relatively heterogeneous conditions (P(heterogeneity) = <0.0001). Outlier analysis resulted in loss of overall heterogeneity (P = 0.14) without affecting the pooled ORs. Among the subgroups, low intake elicited protection in both Korean (OR 0.37) and Mexican (OR 0.63) populations while high intake rendered these subgroups susceptible (OR 2.96 and OR 1.57, respectively). These subgroup values were highly significant (P = 0.0001-0.01) obtained in heterogeneous conditions (P(heterogeneity)
Materials and Methods: The study comprised 20 patients in Group I presenting with various symptoms of gastritis and 10 asymptomatic subjects in Group II. The intestinal endoscopy antral biopsies were collected from 20 symptomatic patients with gastroduodenal disorders. The saliva specimens were taken from all patients before endoscopy. PCR was performed using genomic DNA, isolated from the saliva and the biopsies of the patients as the template to detect the presence of the 16S ribosomal RNA gene in H. pylori.
Results: In Group I, 10 (50%) cases of clinical gastritis were positive for H. pylori by endoscopy biopsy and 10 (50%) were negative. Of the 10 endoscopy biopsy positive cases for H. pylori, eight were PCR positive in saliva and two were negative. Of the 10 endoscopy biopsy negative cases, three were PCR positive for H. pylori in saliva and seven were negative. In Groups II, four were symptomatic for gastritis and six were negative. Of the six gastritis negative cases, three were PCR positive, four were gastritis positive, and three were PCR positive. Sensitivity and specificity of PCR were found to be 80% and 70%, respectively. The positive predictive and negative predictive values of PCR in saliva were 72.7% and 77.7%, respectively.
Conclusion: PCR analysis of saliva may be handy in identification of H. pylori and serves as a noninvasive technique to diagnose and monitor the prognosis.