Pylori-related Chronic Gastritis Research Articles

Clinical Effect of Clarithromycin Combined with Tinidazole on Helicobacter pylori-Related Gastritis and Its Influence on COX-2 Expression.

Studies have shown that COX-2 expression is upregulated in gastric cancer (GC) as well as in precancerous lesions and in Helicobacter pylori-induced inflammation, suggesting that cyclooxygenase-2 (COX-2) may play an important role in gastric carcinogenesis. We attempted to investigate the role of clarithromycin with tinidazole on Helicobacter pylori-related gastritis from the aspects of clinical effect and COX-2 expression. From January 2016 to January 2019, 130 patients with Helicobacter pylori-related chronic gastritis were collected and grouped into the observation group (OG) and the control group (CG). Altogether, 80 patients in the OG were treated with clarithromycin with tinidazole, while 50 patients in the CG were treated with amoxicillin with metronidazole. Clinical symptom improvement time, content of COX-2 and B cell lymphoma-2 (BCL-2), content of inflammatory factors interleukin-1 (IL-1), IL-4, and C-reactive protein (CRP), expression level of nutritional indicators serum albumin (ALB), realbumin (PA), and transferrin (TF), clearance of Helicobacter pylori, total effective rate, and incidence of adverse reactions were detected. Compared with the CG, the OG had shorter clinical symptom improvement time, lower COX-2 and Bcl-2, lower expression of inflammatory factors IL-1, IL-4, and CRP, higher expression of nutritional indicators ALB, TF, and PA, higher clearance rate of Helicobacter pylori, higher total effective rate, and lower incidence of adverse reactions. Clarithromycin combined with tinidazole can effectively improve the clinical effect of Helicobacter pylori-related gastritis and reduce the expression level of COX-2.

Contribution of Ghrelin to the Pathogenesis of Growth Hormone Deficiency.

In this review we described the interactions between ghrelin and the growth hormone (GH)-insulin-like growth factor 1 (IGF-1) axis in children and adults with growth hormone deficiency (GHD). A possible involvement of these interactions in the pathogenesis of unexplained cases of GHD was suggested. Current research provides more and more details to the knowledge on the circadian rhythm of ghrelin. We gathered reports on the decreasing effect of Helicobacter pylori-related chronic gastritis on the number of ghrelin immunopositive cells and the consequent decrease in ghrelin serum concentration. The gastrointestinal tract microflora modification of the ghrelin action, by the mechanism of molecular mimicry, was also stressed. Moreover, the mutual relationships between ghrelin and the TSH-FT4/FT3 axis in growth and metabolic processes are described. It is to be recalled that FT4 and FT3 exert a permissive impact on IGF-1 action and, in turn, GH, in reaction mediated by IGF-1, enhances the monodeiodination of FT4 to FT3. Finally, we discussed the latest attempts to use the GH secretagogue receptor (GHS-R) analogues for possible diagnostic and therapeutic purposes.

Association of Toll-Like Receptors 2, 4, 9 and 10 Genes Polymorphisms and Helicobacter pylori-Related Gastric Diseases in Saudi Patients

AbstractPurpose:Helicobacter pylori is one of the most prevalent human pathogens worldwide. However, the outcomes of H. pylori infection are markedly variable from asymptomatic mild lesion to malignant transformation. Many factors are suggested to influence these infection outcomes, including host immunity and genetic susceptibility. Toll-like receptors (TLRs) can recognise different microbial components and play an essential role in the mucosal immune response against H. pylori infection. Materials and Methods: The association between the common single nucleotide polymorphisms (SNPs) in the genes of TLR2, 4, 9 and 10 and H. pylori-related gastric diseases were investigated by molecular methods after the confirmation of H. pylori infection. The study included 210 patients in three groups; chronic gastritis (n = 90), peptic ulcer disease (PUD) (n = 75) and gastric carcinoma (n = 45). Results: The results showed a significant association between TLR4 SNPs (rs4986790 and rs4986791) and the presence of H. pylori infection, especially in chronic gastritis patient group. Furthermore, TLR9-rs352140 TT genotype was more prevalent among chronic gastritis patient group. TLR10-rs10004195 TT genotype was found to be less prevalent among H. pylori-related chronic gastritis and PUD and was suspected to have a protective effect. TLR2 SNPs (rs3804099 and rs3804100) showed no significant statistical difference between H. pylori-infected patients and the controls. Conclusion: TLR genes polymorphisms may play a role in H. pylori infection susceptibility and may influence its outcomes; however, the ethnic and other factors may modify this effect.

Sociodemographic and Lifestyle Factors in Relation to Gastric Cancer in a High-Risk Region of China: A Matched Case–Control Study

Objectives: To explore the role of sociodemographic and lifestyle factors in the development of gastric cancer in a high-risk region of China.Methods: In a case–control study, all newly diagnosed patients with gastric cancer were compared with healthy controls matched (1:1) by sex, age (±3 years), and place of residence during 2013–2017.Results: A total of 622 gastric cancer and 622 healthy controls were included. Larger household size (>4 family members) appeared to decrease gastric cancer risk for Helicobacter pylori-negative ones (odd ratio = 0.43, 95% CI = 0.26–0.70). Similarly, longer refrigerator ownership was associated with a 67% decreased risk in H. pylori-negative group (95% CI = 0.15–0.77). Participants with a family history of gastric cancer had nearly fivefold higher risk (odd ratio = 4.88, 95% CI = 2.49–9.55). Smoking attributed to 83% increased risk (odd ratio = 1.83, 95% CI = 1.19–2.80). Tea consumption dramatically decreased risk in whole study population (odd ratio = 0.28, 95% CI = 0.17–0.45).Conclusions: In summary, family history, smoking, H. pylori-related chronic atrophic gastritis, and H. pylori infection were positively associated with gastric cancer. Whereas, tea consumption and refrigerator use negatively associated with gastric cancer and could be promoted to reduce gastric cancer rate in high-risk populations, especially in the developing regions.

Sa1170 – Assessment of Gastroesophageal Reflux Disease by Endoscopically Diagnosed Helicobacter Pylori-Related Chronic Gastritis Stage: A Cohort Study of Health Checkup Koreans

Sa1170 – Assessment of Gastroesophageal Reflux Disease by Endoscopically Diagnosed Helicobacter Pylori-Related Chronic Gastritis Stage: A Cohort Study of Health Checkup Koreans

O3-17-3 - Screening colonoscopy for colorectal tumors in H. pylori-related chronic gastritis with MDM2 SNP309 GG homozygous

O3-17-3 - Screening colonoscopy for colorectal tumors in H. pylori-related chronic gastritis with MDM2 SNP309 GG homozygous

Role of screening colonoscopy for colorectal tumors in Helicobacter pylori-related chronic gastritis with MDM2 SNP309 G/G homozygous: A prospective cross-sectional study in Thailand.

Helicobacter pylori infection is a risk factor for gastric cancer and colorectal cancer (CRC). MDM2 SNP309 G/G homozygosity is known to be the genetic background that influences the severity of inflammation in the gastric mucosa, and it corresponds to CRC development. We examined the role of screening colonoscopy in H. pylori-related chronic gastritis and the association of patients who have MDM2 SNP309 G/G homozygosity and advanced colorectal neoplasia (CRN) susceptibility. A prospective cross-sectional study was used to investigate H. pylori-related gastritis in 331 consecutive asymptomatic patients who had MDM2 SNP309 G/G homozygosity and who were enrolled from November 2014 to July 2017. The MDM2 SNP309 polymorphism was genotyped by real-time PCR hybridization probe assay. Totally, there were 331 patients with H. pylori-related gastritis, of whom 39 (8.76%) had advanced CRN. The H. pylori-positive group comprised 180 patients (54.36%). H. pylori infection was associated with advanced CRN (OR: 2.09, 95% CI: 1.56-2.80; p=0.01) and had an increased risk of advanced CRN (OR: 4.24, 95% CI: 1.76-5.21; p=0.01) after adjusting for confounding factors. Patients with H. pylori infection had a significantly increased risk of high-grade dysplasia or invasive adenocarcinoma (OR: 2.96, 95% CI: 1.48-4.17; p=0.03). Chronic gastritis patients infected with H. pylori and who had MDM2 SNP309 G/G homozygosity had an increased risk of advanced CRN, particularly high-grade dysplasia including invasive adenocarcinoma. Screening colonoscopy in these patients might benefit colorectal polyp diagnosis and prevention and early CRC treatment in the Thai population.

Quadruple therapy versus standard triple therapy for eradication of Helicobacter pylori in Kuwait

Background and study aimsChronic infection caused by Helicobacter pylori (H. pylori) is associated with chronic gastritis, peptic ulcer disease, and gastric cancer. Eradication of H. pylori reduces morbidity of chronic gastritis and incidence of gastric cancer in high-risk population. We aimed at testing the efficacy of clarithromycin-based triple therapy and bismuth-based quadruple therapy for eradicating H. pylori in patients with chronic gastritis in Kuwait. Patients and methodsA total of 218 dyspeptic patients from different countries who were proved to have chronic gastritis by endoscopy and gastric biopsy were enroled. All of them were naïve to H. pylori eradication therapy. They were randomised into two groups: group A, received triple therapy (omeprazole, amoxicillin, and clarithromycin) for 10days; and group B, received quadruple therapy (omeprazole, bismuth subcitrate potassium, tetracycline, and metronidazole) for 10days. All patients were tested for eradication of H. pylori by carbon-13 urea breath test 4weeks after treatment. ResultsTotal response rate of eradication therapy in both groups was 77.5% (n=169). However, group B (n=100) had a higher eradication rate (88%) than group A (n=118) (68.6%). H. pylori eradication rate was significantly higher in males (84.2%) than females (70.2%) in both groups (p<0.01). There were no differences in eradication rates with regard to median age or nationality. ConclusionBismuth-based quadruple therapy is more effective as a first-line therapy than clarithromycin-based triple therapy for eradicating H. pylori in patients with H. pylori-related chronic gastritis in Kuwait.

Gastroduodenal Changes Two Years After Eradication of Helicobacter pylori in a Population-Based Cohort

BackgroundThe main cause of chronic gastritis is Helicobacter pylori (H. pylori) infection. Some individuals with H. pylori-related chronic gastritis develop atrophy of the gastric mucosa, a risk factor for gastric neoplasia. When H. pylori-associated gastritis is encountered, it is important to be aware of its natural history and reversibility of associated histopathological and hormonal changes.MethodsA sample of 501 volunteers from the general population in the municipality of Linkoping, Sweden, was examined with esophago-gastro-duodenoscopy (EGD) with biopsy. Blood samples were collected in the fasting state and the subjects answered a questionnaire concerning lifestyle factors, medications and disease history. At a primary follow-up examination, after 8 years, 314 participants were re-examined and those infected with H. pylori received eradication. Two years after successful eradication therapy, 82 participants attended re-examination with EGD and blood sampling, as in the previous examinations.ResultsIn this prospective cohort study of a sample of volunteers from the general population, all of the 82 participants had chronic gastritis with at least one positive H. pylori test before eradication therapy. During follow-up, non-steroid-inflammatory-drug (NSAID) use had decreased significantly (P = 0.007, McNemar). The H. pylori serology was still positive in 79/82 subjects (P = 0.007, McNemar). The basal gastrin and cholecystokinin (CCK) concentrations both had decreased (P < 0.001 for both, Wilcoxon), whereas the P-somatostatin had increased (P < 0.001, Wilcoxon). Symptoms included in the self-administered symptom questionnaire concerned the last 3 months showed no big difference at all. The inflammation had decreased in both antrum (before 2/38/42/0 and after 60/22/0/0, P < 0.0001) and corpus (before 3/54/22/3 and after 58/23/1/0, P < 0.0001). Changes in the inflammatory activity had decreased significantly in both the antrum (P < 0.001) and the corpus (P < 0.001). Intestinal metaplasia was without changes. Regarding the duodenal bulb, the inflammation decreased.ConclusionsBeing aware of the natural history of chronic gastritis, even beyond eradication of H. pylori, is important because of the associations to gastric neoplasia and ulcer disease. The blood mirror of gastroduodenal parameters showed decreased values, except for somatostatin that increased and a symptomatology with no significant changes although, morphologically determined, both inflammation and atrophy had decreased.

Strategy for the Treatment of Helicobacter pylori Infection

The eradication of Helicobacter pylori not only heals peptic ulcers but also prevents their recurrence and reduces the risk of development of gastric cancer and other H. pylori-associated disorders. H. pylori eradication heals gastritis and may prevent the spread of infection, reducing the future costs required for the treatment of subsequent H. pylori-associated diseases. There are various guidelines for the management of H. pylori infection worldwide, such as the guidelines of the American College of Gastroenterology, Maastricht IV, the Second Asia-Pacific Consensus Conference, and Japan. The Japanese health insurance system approved H. pylori eradication therapy for H. pylori-related chronic gastritis in 2013. Triple therapy regimens comprising 1 proton pump inhibitor and 2 antimicrobial agents such as amoxicillin, clarithromycin, metronidazole, levofloxacin, or tetracycline have been widely used to eradicate this bacterium. The rate of successful eradication has declined owing to the increased rate of drug resistance stemming from the wide usage of antibiotics. This issue is of particular relevance with regard to clarithromycin. In worldwide, clarithromycin-based triple therapy should be abandoned, as it is no longer effective. Quadruple therapy and sequential therapy are reasonable alternatives for initial therapy. First-line treatment should be recommended on the basis of an understanding of the local prevalence of H. pylori antimicrobial resistance.

Su1182 Usefulness of the Non-Invasive Rapid Urease Test Using Gastric Mucus for the Diagnosis of Helicobacter pylori Infection

Background: Eradication therapy for Helicobacter pylori-related chronic gastritis was approved for coverage by the Japanese national insurance in February 2013. Therefore, the use of eradication therapy has rapidly increased in Japan. The primary eradication rate of H. pylori using the 7-day triple therapy has gradually decreased in recent years. Drug resistance to clarithromycin (CAM), poor treatment compliance, and smoking are factors associated with eradication failure. A recent study showed that combination of eradication agents is useful for increasing eradication success, because combination treatments are prepared using daily dosages on one sheet. In our study, we prospectively compared the eradication rate in patients receiving conventional therapy with three drugs to that in patients receiving combination therapy. Patients and methods: Between July 2012 and September 2013, we included 276 patients (147 men and 129 women; mean age, 62.2 years) with H. pylori-positive peptic ulcers and gastritis. Combination therapy (Lansap®; lansoprazole 30 mg plus amoxicillin 750 mg plus CAM 200 mg) was administered to 54 patients twice a day for 7 days, and conventional therapy (omeprazole 20 mg or esomeprazole 20 mg or rabeprazole 20 mg plus amoxicillin 750 mg plus CAM 200 mg) was administered to 221 patients as individual drugs twice a day for 7 days. The 13C-urea breath test was used to confirm the eradication of H. pylori at least 6 weeks after the completion of eradication therapy. Patients who had undergone H. pylori eradication therapy in the past and patients who used proton pump inhibitors and antibiotics within 4 weeks were excluded. Results: No significant difference was observed in the background criteria of patients between the combination group and conventional group. The eradication rate (per protocol analysis) in the combination group was 90.3% (47/52), which was significantly different from that in the conventional group (74.9%; 161/215; p< 0.01). In addition, the eradication rate in intention-to-treat (ITT) analysis was significantly higher in the combination group (85.4%, 47/55) than in the conventional group (72.8%, 161/221; p< 0.01). No significant difference was observed in the incidence of adverse drug reactions (such as diarrhea, dysgeusia, and eruption) between the two groups (combination group 4.1%; conventional group 4.7%). Conclusions: Our study suggested that combination therapy with eradication agents is more useful for successful eradication of H. pylori than conventional therapy, although the primary eradication rate has decreased in Japan in the recent years. The underlying reason for the decrease in the primary eradication rate might be greater compliance to combination therapy.

Su1183 Rebamipide, Mucosal-Protective and Ulcer-Healing Drug, Improves Chronic Inflammation of the Corpus After H. pylori Eradication: A Multicenter Study in Japan

Background: Eradication therapy for Helicobacter pylori-related chronic gastritis was approved for coverage by the Japanese national insurance in February 2013. Therefore, the use of eradication therapy has rapidly increased in Japan. The primary eradication rate of H. pylori using the 7-day triple therapy has gradually decreased in recent years. Drug resistance to clarithromycin (CAM), poor treatment compliance, and smoking are factors associated with eradication failure. A recent study showed that combination of eradication agents is useful for increasing eradication success, because combination treatments are prepared using daily dosages on one sheet. In our study, we prospectively compared the eradication rate in patients receiving conventional therapy with three drugs to that in patients receiving combination therapy. Patients and methods: Between July 2012 and September 2013, we included 276 patients (147 men and 129 women; mean age, 62.2 years) with H. pylori-positive peptic ulcers and gastritis. Combination therapy (Lansap®; lansoprazole 30 mg plus amoxicillin 750 mg plus CAM 200 mg) was administered to 54 patients twice a day for 7 days, and conventional therapy (omeprazole 20 mg or esomeprazole 20 mg or rabeprazole 20 mg plus amoxicillin 750 mg plus CAM 200 mg) was administered to 221 patients as individual drugs twice a day for 7 days. The 13C-urea breath test was used to confirm the eradication of H. pylori at least 6 weeks after the completion of eradication therapy. Patients who had undergone H. pylori eradication therapy in the past and patients who used proton pump inhibitors and antibiotics within 4 weeks were excluded. Results: No significant difference was observed in the background criteria of patients between the combination group and conventional group. The eradication rate (per protocol analysis) in the combination group was 90.3% (47/52), which was significantly different from that in the conventional group (74.9%; 161/215; p< 0.01). In addition, the eradication rate in intention-to-treat (ITT) analysis was significantly higher in the combination group (85.4%, 47/55) than in the conventional group (72.8%, 161/221; p< 0.01). No significant difference was observed in the incidence of adverse drug reactions (such as diarrhea, dysgeusia, and eruption) between the two groups (combination group 4.1%; conventional group 4.7%). Conclusions: Our study suggested that combination therapy with eradication agents is more useful for successful eradication of H. pylori than conventional therapy, although the primary eradication rate has decreased in Japan in the recent years. The underlying reason for the decrease in the primary eradication rate might be greater compliance to combination therapy.

Su1181 Combination Therapy With Eradication Agents Is Useful for Successful Eradication of Helicobacter pylori in Japan

Background: Eradication therapy for Helicobacter pylori-related chronic gastritis was approved for coverage by the Japanese national insurance in February 2013. Therefore, the use of eradication therapy has rapidly increased in Japan. The primary eradication rate of H. pylori using the 7-day triple therapy has gradually decreased in recent years. Drug resistance to clarithromycin (CAM), poor treatment compliance, and smoking are factors associated with eradication failure. A recent study showed that combination of eradication agents is useful for increasing eradication success, because combination treatments are prepared using daily dosages on one sheet. In our study, we prospectively compared the eradication rate in patients receiving conventional therapy with three drugs to that in patients receiving combination therapy. Patients and methods: Between July 2012 and September 2013, we included 276 patients (147 men and 129 women; mean age, 62.2 years) with H. pylori-positive peptic ulcers and gastritis. Combination therapy (Lansap®; lansoprazole 30 mg plus amoxicillin 750 mg plus CAM 200 mg) was administered to 54 patients twice a day for 7 days, and conventional therapy (omeprazole 20 mg or esomeprazole 20 mg or rabeprazole 20 mg plus amoxicillin 750 mg plus CAM 200 mg) was administered to 221 patients as individual drugs twice a day for 7 days. The 13C-urea breath test was used to confirm the eradication of H. pylori at least 6 weeks after the completion of eradication therapy. Patients who had undergone H. pylori eradication therapy in the past and patients who used proton pump inhibitors and antibiotics within 4 weeks were excluded. Results: No significant difference was observed in the background criteria of patients between the combination group and conventional group. The eradication rate (per protocol analysis) in the combination group was 90.3% (47/52), which was significantly different from that in the conventional group (74.9%; 161/215; p< 0.01). In addition, the eradication rate in intention-to-treat (ITT) analysis was significantly higher in the combination group (85.4%, 47/55) than in the conventional group (72.8%, 161/221; p< 0.01). No significant difference was observed in the incidence of adverse drug reactions (such as diarrhea, dysgeusia, and eruption) between the two groups (combination group 4.1%; conventional group 4.7%). Conclusions: Our study suggested that combination therapy with eradication agents is more useful for successful eradication of H. pylori than conventional therapy, although the primary eradication rate has decreased in Japan in the recent years. The underlying reason for the decrease in the primary eradication rate might be greater compliance to combination therapy.

Helicobacter pylori-related chronic gastritis as a risk factor for colonic neoplasms

To summarize the current views and insights on associations between Helicobacter pylori (H. pylori)-related chronic gastritis and colorectal neoplasm, we reviewed recent studies to clarify whether H. pylori infection/H. pylori-related chronic gastritis is associated with an elevated risk of colorectal neoplasm. Recent studies based on large databases with careful control for confounding variables have clearly demonstrated an increased risk of colorectal neoplasm associated with H. pylori infection. The correlation between H. pylori-related chronic atrophic gastritis (CAG) and colorectal neoplasm has only been examined in a limited number of studies. A recent large study using a national histopathological database, and our study based on the stage of H. pylori-related chronic gastritis as determined by serum levels of H. pylori antibody titer and pepsinogen, indicated that H. pylori-related CAG confers an increased risk of colorectal neoplasm, and more extensive atrophic gastritis will probably be associated with even higher risk of neoplasm. In addition, our study suggested that the activity of H. pylori-related chronic gastritis is correlated with colorectal neoplasm risk. H. pylori-related chronic gastritis could be involved in an increased risk of colorectal neoplasm that appears to be enhanced by the progression of gastric atrophy and the presence of active inflammation.

Potential usefulness of DNA methylation as a risk marker for digestive cancer associated with inflammation

DNA methylation has been deeply involved in the development and progression of digestive cancer, while aberrant DNA methylation has also often been observed in aged and inflammatory digestive tissues. Helicobacter pylori-related chronic gastritis, ulcerative colitis, and hepatitis B virus- and hepatitis C virus-related chronic hepatitis, are significant risk factors for developing cancer. A number of studies have revealed the specific methylation patterns for specific tissue types. DNA methylation status is stably transmitted to daughter cells. Also, unlike genetic mutations, it is possible to detect very tiny amounts of methylated DNA among tissues. Therefore, the use of aberrant methylation as a marker could be applicable to risk estimation of cancer development. We discuss the potential usefulness of DNA methylation as a risk marker for inflammation-associated digestive cancer, especially with attempts on gastric cancer, ulcerative colitis-associated cancer, and hepatitis B virus- and hepatitis C virus-related hepatocellular carcinoma.

Clinical practice guideline of Chinese medicine for chronic gastritis

Chronic gastritis (CG) is an inflammatory condition of the gastric mucosa, induced by various causes. A commonly-seen disease in clinical practice, it is found in about 80%-90% of patients undergoing gastroscopic examination. The prevalence rate in the general population remains unclear. It is generally considered that its incidence rate accords with Helicobacter. pylori infection rate and the prevalence of CG is 30%-80% in China. Possible etiological factors include H. pylori infection, smoking, drinking alcohol, food allergies, duodenal juice reflux, drug-induced injuries, heredity, immunity, and radiation. (1-8) Some patients with CG have no obvious clinical manifestations, and symptomatic patients mainly show symptoms of non-specific dyspepsia. In H. pylori related CG, the disease will persist unless the H. pylori infection is eradicated. There is a higher risk of gastric cancer if chronic atrophic gastritis (CAG) is accompanied by intestinal metaplasia or dysplasia; it is commonly believed that the canceration rate of atrophic gastritis is 0.5%-1% annually. (9)

Elevated risk of colorectal adenoma with Helicobacter pylori‐related chronic gastritis: A population‐based case‐control study

This study investigated correlations between Helicobacter pylori infection or chronic atrophic gastritis (CAG) and risk of colorectal adenoma in a population-based case-control study. Subjects comprised asymptomatic, middle-aged, male Japanese factory workers who participated in an annual health check-up program, including cancer screening with colonoscopy. We selected 239 colorectal adenoma cases based on histological evaluation and 239 age-matched adenoma-free controls, and evaluated colorectal adenoma risk according to stage of H. pylori-related chronic gastritis as determined by serum tests for H. pylori antibody titer and pepsinogen. Subjects with colorectal adenoma were more likely to be smokers and have hypercholesterolemia. H. pylori infection was a risk factor for adenoma as a whole (crude odds ratio [OR]: 2.26, 95% confidence interval [CI]: 1.44-3.55). Analysis of distal adenoma cases showed that adenoma risk was significantly increased in the presence of H. pylori infection, but there was no further increase in risk with CAG. In contrast, proximal adenoma risk increased stepwise with the presence and progression of H. pylori-related chronic gastritis and showed a maximal and significant increase with CAG (crude OR: 4.51, 95% CI: 1.43-14.2). Subjects with more extensive and severe gastritis showed still higher risk not only for proximal but also for distal adenoma. H. pylori-related chronic gastritis is likely to be involved in the development of colorectal neoplasms, and its progression appears to increase the risk, particularly for proximal adenomas. Knowing the H. pylori-related chronic gastritis stage will probably be useful for evaluation of risk for colorectal neoplasia.

Assessment of gastroesophageal reflux disease by serodiagnosis of Helicobacter pylori-related chronic gastritis stage

To evaluate the association of Helicobacter pylori (H.pylori)-related chronic gastritis stage with upper gastrointestinal symptoms and gastroesophageal reflux disease (GERD). Subjects underwent upper gastrointestinal endoscopy, a questionnaire using a frequency scale for symptoms of GERD (FSSG), and measurements of serum H.pylori-antibody and pepsinogen (PG) levels. They were classified into the following 4 groups in terms of H.pylori-related chronic gastritis stage: Group A (n = 219), H.pylori(-)PG(-); Group B (n = 310), H.pylori(+)PG(-); Group C (n = 279), H.pylori(+)PG(+); and Group D (n = 17), H.pylori(-)PG(+). Reflux esophagitis occurred in 30.6% of Group A, 14.5% of Group B, 6.8% of Group C, and 0% of Group D (P < 0.001). Scores for acid reflux symptoms decreased significantly with chronic gastritis stage (from Group A to D) (P < 0.05), while scores for dysmotility symptoms did not differ significantly. The prevalence of non-erosive reflux disease (NERD) did not differ among groups. However, in subjects with GERD, the prevalence of NERD tended to increase with chronic gastritis stage (P = 0.081). Acid reflux symptoms and the prevalence of reflux esophagitis can be assessed by measuring both serum H.pylori-antibody and PG levels.

Ancillary Stains Modestly Improve Helicobacter pylori Detection in Patients with Rapid Urease Test Positive, Histology Negative Infection

Purpose: To determine whether ancillary staining increases detection rates of Helicobacter pylori (H. pylori) in patients with positive rapid urease test (RUT) but H&E negative biopsies. H. pylori is a gram-negative bacterium that causes gastric inflammation, ulcers and cancer. Endoscopy and mucosal biopsy play a major role in H. pylori detection. H. pylori organisms may be missed on careful H&E stain and found only by RUT, perhaps due to suppression by proton pump inhibitors. We studied a unique group of patients in whom H. pylori was found at endoscopy only by RUT with negative histopathologic specimens, to identify whether ancillary staining techniques would create concordance between the studies. Methods: We identified 32 study patients, all with positive RUT at endoscopy, but negative H&E stains of biopsies of the antrum and fundus. Each case was subjected to 3 histochemical stains (Giemsa, Warthin-Starry, and Acridine Orange) and H. pylori immunohistochemistry (IHC). Ten RUT-positive patients with H. pylori-related chronic active gastritis on biopsy and 10 RUT-negative patients with normal gastric histology served as positive and negative controls, respectively. Results: The study group H&E stained sections showed normal histology (n=12, 38%), chemical gastropathy (n=9, 28%) chronic active gastritis (n=3, 9%), and mild chronic inactive gastritis (n=8, 25%). Two (6%) study patients had detectable H. pylori by ancillary techniques, which were equally useful in detection of bacteria. In retrospect, both of these cases showed mild chronic inactive gastritis and rare H. pylori in H&E stained sections. Essentially all RUT-positive, H&E negative patients had a follow up RUT-negative study after antibiotic treatment. Conclusion: Routine evaluation of H&E stained sections reliably detects H. pylori in most infected patients. However, bacteria may be overlooked, particularly when inflammation is mild, suggesting one have a low threshold for ordering ancillary stains and obtaining a simultaneous RUT. Giemsa, Warthin-Starry and Acridine Orange stains detect H. pylori at rates comparable to IHC and, thus, represent cheaper, faster alternatives to IHC assays.

Inhibitory effects of Japanese apricot (Prunus mume Siebold et Zucc.; Ume) on Helicobacter pylori-related chronic gastritis

We investigated the correlation between Japanese apricot (JA) intake and Helicobacter pylori-related chronic atrophic gastritis (CAG). A questionnaire was administered and serum anti-H. pylori IgG antibodies measured in 1358 asymptomatic adults. The subjects were divided into high-intake and low-intake groups. Histological and serological evaluation of H. pylori-related CAG was performed in 68 non-elderly volunteers. The H. pylori-negative rate did not differ significantly between the high-intake and low-intake groups. Mean antibody titers were lower in the high-intake group, but the difference was not significant. There was no significant difference in the rate of H. pylori infection on the basis of JA intake when subjects were stratified by age. Among H. pylori-positive non-elderly subjects, antibody titers were significantly lower in the high-intake group (P=0.041). Endoscopic tissue biopsy from the 68 volunteers showed less H. pylori bacterial load and mononuclear infiltration irrespective of gastric site in the high-intake group. In the high-intake group, antral neutrophil infiltration was significantly less pronounced and corporal atrophy was less extensive. Serological evaluation using serum PG levels also confirmed these histopathological data. Our findings strongly indicate a preventive effect of JA intake on CAG by inhibiting H. pylori infection and reducing active mucosal inflammation.