CagA-positive Infection Research Articles

Abstract 3944: Addressing stomach cancer disparities by assessing Helicobacter pylori infections among American Indian adults from the Navajo Nation

Abstract Background. The Navajo Nation, the largest tribe in the United States (US), is experiencing a high burden of stomach cancer, possibly due to a high prevalence of Helicobacter pylori (Hp) infection. Hp is a major risk factor for stomach cancer and Hp strains that carry the cagA-gene are linked to greater gastrointestinal disease severity. Yet little research has investigated the prevalence and correlates of Hp and cagA infection in Navajo people. We assessed the prevalence and correlates of Hp infection and cagA-gene carriage in adult tribal members residing in the Navajo Nation. Methods and Material. We conducted a community-based cross-sectional study in the Navajo Nation in 2021 during the COVID-19 pandemic. Participants were recruited using online and offline platforms, including social media, a study website, newspaper advertisements, flyers, word of mouth, and community outreach. Stool samples collected from participants were analyzed with droplet digital PCR for Hp 16S and cagA virulence genes. Demographic characteristics, health, and dietary factors were collected from self-administered health and food questionnaires sent via mail. Results. Of 99 participants, half (49.5%) were 18-44 years old and 73.7% were female. About sixty percent (57.7%, 95% CI: 47.6-67.3) of participants were infected with Hp, twice the US population prevalence (27%). Among Hp-infected participants, 76.7% (95% CI: 64.0-86.6) were cagA-gene positive, four times the cagA gene prevalence in White people (19%). Controlling for age and sex, monthly use of Navajo herbal medicines was positively associated with Hp infection (OR=3.73, 95% CI: 1.05-17.87). No significant associations with Hp and cagA-gene were observed with other risk factors such as older age, males, lower education, and high sodium intake. Conclusion. A substantial proportion of Navajo adults in our study had Hp and cagA-positive infections. Given studies showing the antibacterial activity of Indigenous herbal medicines, monthly use of Navajo herbal medicines was an unexpected risk factor for Hp infection. This observation may be due to reverse causality, where participants with gastrointestinal conditions used Navajo herbal medicines for gastrointestinal symptom relief, particularly when participants had limited access to healthcare services due to the COVID-19 pandemic. Possible environmental transmission of Hp in the preparation of herbal medicines (i.e., water source, utensils) could be another source of exposure. Given the high burden of Hp and cagA-positive infections, culturally tailored health education strategies and interventions addressing these infections present an opportunity for research and cancer prevention among Navajo adults. Citation Format: Dornell Pete, Nina R. Salama, Johanna W. Lampe, Michael C. Wu, Amanda I. Phipps. Addressing stomach cancer disparities by assessing Helicobacter pylori infections among American Indian adults from the Navajo Nation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 3944.

Structure of cytotoxic associated antigen A protein of Helicobacter pylori from Bali and Lombok isolates of Indonesia.

Background and Aim:Helicobacter pylori is a well-known zoonotic agent with worldwide distribution. In Indonesia, only one report regarding the variation within the cytotoxic associated antigen A (CagA) protein of H. pylori has been described in the literature, which was conducted in Manado, South Sulawesi. There remains no report concerning the structure of this protein, particularly for the Bali and Lombok isolates. The objective of this study was to investigate the diversity of H. pylori CagA amino acid sequences of Bali and Lombok isolates, to predict their molecular structures and conduct toxicity examination of CagA on gastric cells.Materials and Methods:A total of 36 samples were used in equal proportions for each pathologic condition. DNA extraction was performed to subculture H. pylori Bali isolates. The amplification of the CagA 3′ variable region was carried out using the primers P1 (5′-GATAACAGGCAAGCTTTTTGAGG-3′) and P2 (5′-CTGCAAAAGATTGTTTGGCAG-3′). The W2, W9, and W35 fragments were selected as a representation of H. pylori Bali isolates, which were modeled through the threading modeling approach using I-TASSER.Results:According to the 12 CagA sequences obtained and phylogenetic analyses, the H. pylori strain originating from Bali can be grouped within the East Asian genotypes and is identical to the Lombok strain. In addition, the Bali isolates are phylogenetically more closely related to Southeast Asian strains, particularly the Filipino strain. The relationship between degree of inflammation induced and CagA-positive infection was not statistically significant.Conclusion:The structure of the H. pylori Bali isolate is identical to that of Lombok isolate, which belongs to the same group of East Asian genotypes, and bacterial virulence is not related to structure.

Epidemiology of Helicobacter pylori and CagA-Positive Infections and Global Variations in Gastric Cancer.

Gastric cancer is a major health burden and is the fifth most common malignancy and the third most common cause of death from cancer worldwide. Development of gastric cancer involves several aspects, including host genetics, environmental factors, and Helicobacter pylori infection. There is increasing evidence from epidemiological studies of the association of H. pylori infection and specific virulence factors with gastric cancer. Studies in animal models indicate H. pylori is a primary factor in the development of gastric cancer. One major virulence factor in H. pylori is the cytotoxin-associated gene A (cagA), which encodes the CagA protein in the cag pathogenicity island (cag PAI). Meta-analysis of studies investigating CagA seropositivity irrespective of H. pylori status identified that CagA seropositivity increases the risk of gastric cancer (OR = 2.87, 95% CI: 1.95–4.22) relative to the risk of H. pylori infection alone (OR = 2.31, 95% CI: 1.58–3.39). Eradicating H. pylori is a strategy for reducing gastric cancer incidence. A meta-analysis of six randomised controlled trials (RCTs) suggests that searching for and eradicating H. pylori infection reduces the subsequent incidence of gastric cancer with a pooled relative risk of 0.66 (95% CI: 0.46–0.95). The introduction in regions of high gastric cancer incidence of population-based H. pylori screening and treatment programmes, with a scientifically valid assessment of programme processes, feasibility, effectiveness and possible adverse consequences, would impact the incidence of H. pylori-induced gastric cancer. Given the recent molecular understanding of the oncogenic role of CagA, targeting H. pylori screening and treatment programmes in populations with a high prevalence of H. pylori CagA-positive strains, particularly the more oncogenic East Asian H. pylori CagA strains, may be worth further investigation to optimise the benefits of such strategies.

Interleukin-17C in Human Helicobacter pylori Gastritis.

The interleukin-17 (IL-17) family of cytokines (IL-17A to IL-17F) is involved in many inflammatory diseases. Although IL-17A is recognized as being involved in the pathophysiology of Helicobacter pylori-associated diseases, the role of other IL-17 cytokine family members remains unclear. Microarray analysis of IL-17 family cytokines was performed in H. pylori-infected and uninfected gastric biopsy specimens. IL-17C mRNA was upregulated approximately 4.5-fold in H. pylori-infected gastric biopsy specimens. This was confirmed by quantitative reverse transcriptase PCR in infected and uninfected gastric mucosa obtained from Bhutan and from the Dominican Republic. Immunohistochemical analysis showed that IL-17C expression in H. pylori-infected gastric biopsy specimens was predominantly localized to epithelial and chromogranin A-positive endocrine cells. IL-17C mRNA levels were also significantly greater among cagA-positive than cagA-negative H. pylori infections (P = 0.012). In vitro studies confirmed an increase in IL-17C mRNA and protein levels in cells infected with cagA-positive infections compared to cells infected with either cagA-negative or cag pathogenicity island (PAI) mutant. Chemical inhibition of IκB kinase (IKK), mitogen-activated protein extracellular signal-regulated kinase (MEK), and Jun N-terminal kinase (JNK) inhibited induction of IL-17C proteins in infected cells, whereas p38 inhibition had no effect on IL-17C protein secretion. In conclusion, H. pylori infection was associated with a significant increase in IL-17C expression in human gastric mucosa. The role of IL-17C in the pathogenesis of H. pylori-induced diseases remains to be determined.

Methylation ofDAPKandTHBS1genes in esophageal gastric-type columnar metaplasia

To explore methylation of DAPK, THBS1, CDH-1, and p14 genes, and Helicobacter pylori (H. pylori) status in individuals harboring esophageal columnar metaplasia. Distal esophageal mucosal samples obtained by endoscopy and histologically diagnosed as gastric-type (non-specialized) columnar metaplasia, were studied thoroughly. DNA was extracted from paraffin blocks, and methylation status of death-associated protein kinase (DAPK), thrombospondin-1 (THBS1), cadherin-1 (CDH1), and p14 genes, was examined using a methyl-sensitive polymerase chain reaction (MS-PCR) and sodium bisulfite modification protocol. H. pylori cagA status was determined by PCR. In total, 68 subjects (33 females and 35 males), with a mean age of 52 years, were included. H. pylori cagA positive was present in the esophageal gastric-type metaplastic mucosa of 18 individuals. DAPK, THSB1, CDH1, and p14 gene promoters were methylated by MS-PCR in 40 (58.8%), 33 (48.5%), 46 (67.6%), and 23 (33.8%) cases of the 68 esophageal samples. H. pylori status was associated with methylation of DAPK (P = 0.003) and THBS1 (P = 0.019). DNA methylation occurs in cases of gastric-type (non-specialized) columnar metaplasia of the esophagus, and this modification is associated with H. pylori cagA positive infection.

RUNX3 Methylation, Loss of RUNX3 Expression and Clinicopathologic Findings according to Helicobacter pylori CagA in Gastric Carcinoma.

Helicobacter pylori cytotoxin-associated gene A (CagA) has been suggested to be involved in the inactivation of Runt-related transcription factor 3 (RUNX3), a known gastric carcinoma tumor suppressor gene. It remains unclear how H. pylori CagA initiates or maintains RUNX3 promoter methylation and inactivates its protein expression in gastric carcinoma. RUNX3 promoter methylation status, RUNX3 expression, and H. pylori CagA were investigated in 76 sample pairs of gastric carcinoma tissue. The patients' medical records were reviewed. The association between RUNX3 methylation or loss of RUNX3 expression and clinicopathologic variables according to H. pylori CagA status were investigated. In gastric carcinoma patients with H. pylori CagA-positive infection, RUNX3 methylation did not show association with lymphatic invasion, venous invasion, and TNM stages. However RUNX3 methylation was observed more frequently in poorly differentiated adenocarcinoma and signet ring cell carcinoma (77.8% vs. 20.0%, p=0.023) in early stage. In gastric carcinoma patients with H. pylori CagA-positive infection, loss of RUNX3 expression did not show association with lymphatic invasion, venous invasion, and TNM stages. However loss of RUNX3 expression was observed more frequently in early gastric carcinoma than in advanced gastric carcinoma (84.2% vs. 75.0%, p=0.51), but this difference was not significant. In gastric carcinoma patients with H. pylori CagA-positive infection, RUNX3 methylation or loss of RUNX3 expression did not show correlation with lymphovascular invasion and TNM stages. In early gastric carcinoma patients with H. pylori CagA-positive infection, RUNX3 methylation was observed more in poorly differentiated adenocarcinoma and signet ring cell carcinoma.

STUDY OF THE DYNAMIC OF HELICOBACTER PYLORI INFECTION PREVALENCE IN DIFFERENT AGE GROUPS OF ST. PETERSBURG POPULATION IN 2007-2011

Abstract. Presence of specific antibodies to H. pylori and to its Cag A toxin was studied in 1917 persons, including 860 children and 1057 adults, in Pasteur Research Institute of Epidemiology and Microbiology, St. Petersburg, Russia. The studied group was presented by the subjectively healthy individuals and blood donors living in St. Petersburg. The growth and stabilization of serological positive rates to H. pilory at high level, as well as increasing the proportion of CagA-positive infection among children and adults in St. Petersburg in 2007–2011 have been established. There are 3 age risk groups of H. pylori infection among children population: 4–5 years, 7–8 years and 14–15 years. The shift of the maximum H. pylori seropositivity rates from age group of 30–39 years in 2007 to age group 40–49 years in 2011 was detected.

Relationship Between Drug Resistance and cagA Gene in Helicobacter pylori

Background: Currently, there are evidences for the existence of diverse strains of Helicobacter pylori with different levels of virulence. In other way, the most important reason of therapeutic failure is resistance to the antibiotics. Objectives: The aim of this study was to evaluate the relationship between H. pylori drug resistance and the presence of cagA gene. Patients and Methods: Gastric biopsy specimens were cultured for H. pylori isolation. Resistance to antimicrobial agents, including clarithromycin, metronidazole, and amoxicillin were detected by modified disk agar diffusion tests. The cagA gene was detected using PCR, and the results were analyzed by χ2 and Fishers exact tests using SPSS software version 16. Results: A total of 123 H. pylori-positive patients (68 males, 55 females, mean age 35 ± 18 years old) were studied. The rate of resistance to clarithromycin, metronidazole and amoxicillin were 17.07, 78.86 and 27.64%, respectively. In this study, the cagA was detected in 84 of 123 strains (68.3%). The frequency of resistance to clarithromycin, metronidazole and amoxicillin in cagA positive confirmed microorganisms were, 16 (13.01%), 67 (54.47%) and 24 (19.51%), respectively. While the results for cagA negative ones were 5 (4.06%), 30 (24.39%) and 10 (8.13%), respectively. Conclusions: Our results indicated that the overall antibiotic resistance of H. pylori was high, and the relationship between drug resistance and cagA status was not statistically significant. Therefore, different treatment regimens are not recommended for patients with H. pylori- cagA positive infections.

IL-4 -588C>T polymorphism and IL-4 receptor alpha [Ex5+14A>G; Ex11+828A>G] haplotype concur in selecting H. pylori cagA subtype infections

BackgroundThe Th2 cytokine IL-4 might limit H. pylori associated gastric inflammation and favour H. pylori clearance. The aim of the study was to verify whether IL-4 -588C>T SNP, or two SNPs of the gene coding the alpha chain of IL-4 receptor (IL-4RA Ex5+14A>G, IL-4RA Ex11+828A>G) considered singly or as haplotypes, are correlated with H. pylori virulence genes or H. pylori associated diseases. MethodsWe studied 144 patients with non-cardia gastric cancer (NCGC)(41/50 with present or past H. pylori infection), 75 with duodenal ulcer (DU)(66 H. pylori infected) and 171 with gastritis (CG)(107 H. pylori infected). cagA gene was present in 24/28 NCGC, 45/59 DU and 56/107 CG. ResultsAll SNPs were in Hardy–Weinberg equilibrium. IL-4RA haplotypes frequencies were estimated using Arlequin software. Neither the SNPs nor the IL-4RA haplotype correlated with disease diagnosis, H. pylori infection, degree of mucosal inflammation or intestinal metaplasia. IL-4 -588T allele (OR=3.69, 95% CI:1.34–10.16) and IL-4RA GA haplotype (p<0.05) enhanced the risk for cagA positive infections. IL-4RA GA haplotype correlated with IL-4 protein levels in H. pylori infected gastric mucosa. ConclusionsIL-4 and IL-4RA gene polymorphisms concur in selecting the H. pylori infecting strain, probably influencing the IL-4 signalling pathway.

Gastric cancer risk in a Mexican population: Role of Helicobacter pylori CagA positive infection and polymorphisms in interleukin‐1 and ‐10 genes

Several polymorphisms of the IL1B and IL10 gene promoters have been reported to be associated with gastric cancer risk in Caucasians. However, studies in other populations have shown differing results. We aimed to test for associations between polymorphisms in IL1B (-31 and +3954), IL10-592 and IL1RN variable number of tandem repeats (VNTR) and risk of gastric cancer in a Mexican population. DNA was extracted from sera of 183 gastric adenocarcinoma patients and 377 controls. The IL1B-31, IL1B+3954 and IL10-592 biallelic polymorphisms were discriminated using 5' Nuclease (TaqMan) assays and Pyrosequencing. The IL1RN penta-allelic VNTR polymorphism was genotyped using PCR followed by GeneScan analysis. A significant interaction was found between IL1B-31 and CagA status for the risk of intestinal-type gastric cancer (p = 0.023). Among CagA positive subjects, those with IL1B-31CC genotype had an increased risk of intestinal-type gastric cancer (OR 3.19, 95%CI = 1.05-9.68), compared to carriers of IL1B-31TT genotype. In contrast, among CagA negative subjects, no significant association of IL1B-31CC genotype with gastric cancer was observed. The IL10-592CC genotype was associated with more than doubling of the risk of the intestinal-type gastric cancer (OR, 2.20, 95%CI = 1.04-4.65). A nonsignificantly increased risk for intestinal-type gastric cancer was found in IL1RN*2 carriers (OR 1.49, 95%CI = 0.89-2.50). None of these polymorphisms was significantly related to the risk of diffuse-type gastric cancer. No significant association was found between risk of gastric cancer and the IL1B+3954 polymorphism. Individuals carrying 2 or more of the risk-associated alleles (IL1B-31C, IL1RN *2 and IL10-592C) were at increased risk for intestinal-type gastric cancer, compared to those with 0 or 1 risk-associated allele. The risk from multiple risk-associated alleles was especially high in subjects infected with CagA positive H. pylori. Our results support the identification of the IL1B-31 promoter polymorphism as a useful marker for risk of intestinal type gastric cancer in persons with CagA positive H. pylori infections.

CagA in Barrett’s oesophagus in Colombia, a country with a high prevalence of gastric cancer

Background: In the USA, atrophic gastritis and gastric cancer are rare, whereas gastro-oesophageal reflux disease (GERD) is common. Infection with Helicobacter pylori, especially a CagA positive strain, is unusual in...

Histology and culture results among subjects with antibodies to CagA but no evidence of Helicobacter pylori infection with IgG ELISA

Objective. Serological evidence of antibodies to cytotoxin-associated gene A (CagA) antigens may exist without concomitant Helicobacter pylori IgG enzyme linked immunosorbent assay (ELISA) seropositivity. In a recent case-control study, this serological pattern was strongly linked to stomach cancer, and it was hypothesized to represent “burned-out” CagA-positive infections. The aim of this analysis was to test this hypothesis.Material and methods. We used data from a Swedish endoscopy clinic-based case-control study with 64 gastric cancer cases and 281 age-matched and gender-matched non-cancer patients who had other gastric diseases or normal endoscopy. HM-CAP® ELISA and Helicoblot® 2.0 immunoblot results were compared with culture and histology.Results. Overall, 86 out of 345 (25%) subjects were CagA seropositive but ELISA seronegative. This proportion was similar among cancer and non-cancer patients. Current H. pylori infection could be verified by culture or histology in only 15% of these patients. Forty-three percent of subjects with this isolated CagA seropositivity had histological evidence of corpus and/or antral atrophy. This was higher than in those who were negative in both tests (15%), but lower than among those seropositive for both tests (53%). The percentage of isolated CagA-seropositive patients who had atrophy was similar among those with or without evidence of current infection.Conclusions. Although false-positive tests for CagA, or false-negative ELISA tests, may explain the serologic pattern in some of the subjects with isolated CagA seropositivity, healed infections are estimated to account for the majority. Unless the histology is often restituted after spontaneous disappearance of the infection, atrophy does not appear to be a mandatory intermediate step leading to this serology.

Pro- and anti-inflammatory cytokines gene polymorphisms and Helicobacter pylori infection: interactions influence outcome

The aim of this study was to evaluate whether there was any correlation between Helicobacter pylori-associated diseases and (1) H. pylori virulence genes or (2) IL-1B, IL-1RN, IFN-G, TNF-A, IL-10 genetic polymorphisms. Patients with non-cardia gastric cancer (NCGC, n = 129) or benign gastroduodenal diseases ( n = 792) were studied. IL-1RN intron 2 VNTR polymorphism (PCR), IL-1B −31 C/T (RFLP), the SNPs of IFN-G (+874 A/T), TNF-A (−1031 C/T, −857 C/T, −376 A/G, −308 A/G, −238 A/G), IL-10 (−1082 A/G, −819 C/T, −592 A/C) (Taqman chemistry) were studied. cagA, s1 and m1 vacA, were PCR amplified. Duodenal ulcer was more frequent in TNF-A −857 TT and in IL-1RN 1,2 subjects. TNF-A −857 TT genotype was also correlated with gastric ulcer. IL-10 −819 TT genotype was associated with intestinal metaplasia and NCGC. Antral inflammation was associated with TNF-A −1031 TT, while corpus activity with IL-10 −819 CC. H. pylori infection was associated with TNF-A −308 AG genotype, while IFN-G +874 AA genotype was associated with cagA. In conclusion, among host genetic factors contributing to H. pylori disease outcome, IFN-G +874 AA genotype favors cagA positive infections, TNF-A −857 TT duodenal ulcer while IL-10 −819 TT intestinal metaplasia and NCGC.

Helicobacter pylori CagA status, mucosal oxidative damage and gastritis phenotype: a potential pathway to cancer?

Oxidative DNA damage is associated with Helicobacter pylori infection, atrophy and intestinal metaplasia. H. pylori-cagA-positive strains are associated with the highest risk of gastric cancer. To ascertain whether cagA-positive H. pylori infection correlates with higher concentrations of 8OHdG and the presence of precancerous changes. 118 patients were studied (65M/53F, age 61 +/- 14 years). Twelve were H. pylori-negative. Among the H. pylori-positive patients, 34 were cagA-positive and 40 were cagA negative. In 32 patients H. pylori had been eradicated at least 6 months before endoscopic sampling. The phenotype of the gastritis (atrophic compared with nonatrophic, with and without intestinal metaplasia) was scored in biopsy samples obtained from the antrum, corpus, and angularis incisura. In antral biopsy samples, 8-hydroxydeoxyguanosine was assessed by HPLC (electrochemical detector). CagA status was determined by PCR. The highest scores for both mononuclear inflammation and activity of gastritis were significantly associated with cagA status (p = 0.036 antrum and p = 0.02 corpus). cagA-positive infection significantly correlated with a higher prevalence of atrophic-metaplastic lesions (p = 0.04). cagA-positive patients had higher 8-hydroxydeoxyguanosine levels than both cagA-negative and H. pylori-negative cases (p = 0.01). The 8-hydroxydeoxyguanosine levels were significantly higher in multifocal atrophic gastritis (p = 0.04). The odds ratio for cagA-positive patients having 8OHdG levels above a cut-off calculated on the basis of the ROC curves were 7.12, overall, reaching 11.25 when only patients younger than 50 were considered. cagA-positive patients were characterized: first, for higher scores for gastritis, activity and atrophic and metaplastic lesions; and second for greater oxidative DNA damage overall, at younger age and in the presence of multifocal atrophy. This setting may represent a cancer-prone biological context.

The phenotype of gastric mucosa coexisting with Barrett's oesophagus

Background/Aims—Barrett's oesophagus complicates the gastro-oesophageal acid reflux. Helicobacter pylori infection, particularly with cagA positive strains, induces inflammatory/atrophic lesions of the gastric mucosa, which may impair acid output. No systematic study...

Interleukin 10 in Helicobacter pylori associated gastritis: immunohistochemical localisation and in vitro effects on cytokine secretion

Background/Aims—Interleukin 10 (IL-10) is a counterinflammatory peptide implicated in the downregulation of human intestinal immune responses. Enhanced secretion of IL-10 has been documented in gastric biopsy organ culture in Helicobacter...

Increased expression of IL-10 and IL-12 (p40) mRNA in Helicobacter pylori infected gastric mucosa: relation to bacterial cag status and peptic ulceration.

AIMS: To investigate interleukin (IL)-12 (p40) and IL-10 mRNA expression levels in the gastric mucosa in relation to H pylori cag status, peptic ulceration, and histopathology. METHODS: In 81 dyspeptic...

Gastric cancer, cytotoxin-associated gene A–positive Helicobacter pylori, and serum pepsinogens: An international study

Background & Aims: CagA-positive Helicobacter pylori infection has been more closely associated with gastric disease than CagA-negative infection. This study evaluated whether geographic variation in the prevalence of CagA could explain variation in gastric cancer rates. Methods: The Eurogast study was conducted in 17 centers in 13 countries. Gastric cancer rates were calculated for each center, and serum samples from approximately 2850 subjects were assayed for immunoglobulin G antibodies to H. pylori and CagA and for pepsinogens A and C. Results: The proportion of CagA-positive H. pylori infections varied across the centers, but this variation did not explain any more of the variation in gastric cancer rates than H. pylori alone. Subjects with CagA-positive infection had, however, significantly higher pepsinogen levels and a lower pepsinogen A/C ratio than subjects with CagA-negative infection; this pattern was observed consistently across the study centers. Conclusions: Variation in the seroprevalence of CagA did not explain geographic variation in gastric cancer rates any better than H. pylori alone. However, the consistent variation in pepsinogen levels with CagA status across the study centers supports the importance of the role of CagA in the development of gastric disease. GASTROENTEROLOGY 1999;116:269-276

Chemokine mRNA expression in gastric mucosa is associated with Helicobacter pylori cagA positivity and severity of gastritis.

AIM: To investigate the association between the quantity of gastric chemokine mRNA expression, severity of gastritis, and cagA positivity in Helicobacter pylori associated gastritis. METHODS: In 83 dyspeptic patients, antral...

Are dyspeptic symptoms associated with Helicobacter pylori CagA-positive infection in the general population?

• G1074 ARE DYSPEPTIC SYMPTOMS ASSOCIATED WITH HELICOBACTER PYLORI CAGA-POSITIVE INFECTION IN THE GENERAL POPULATION? S. Pretolani, F. Miglio, tL. Baldini, IF, Bonvieini, IV. Arienti, 2N. Figura, 3ML. Stefanelli, .~G. Giulianelli, 3C. Cecchetti, 3GC. Ghironzi, M. Polini, 4A. Gasbarrini and 4G: Gasbarrini. Dpt. of Emergency Medicine, Policlinico S. Orsola-Malpighi, Bologna, Italy; lDpt. of Internal Medicine, Cardioangiology, Hepathology, University of Bologna, Italy; 2Inst. of Medical Pathology, University of Siena, Italy; 3Ospedale di Stato, Republic of San Marino; 4Dpt. of Internal Medicine and Geriatrie, Catholic University, Rome, Italy