Pylori Seropositive Patients Research Articles

Incidence Of Helicobacter Pylori Infection in Association With ABO Blood Groups

Objective: The study aimed to investigate the association between ABO blood groups and helicobacter infection. Method: 150 participants, including 93 females and 57 males between the age group of 18-60 years, were involved in the study. A sample of 3 ml blood was collected and screened against H. pylori antibodies (IgG) by H. pylori rapid diagnostic kit. ABO and Lewis antigen phenotypes were determined with a macroscopic agglutination technique. Results: According to the study's findings, there were 55.42% women (46/83) and 44.5% men (37/83) among the 83 seropositive patients, while 70.14% women (47/67) and 29.85% men (20/67) were found among the 67 seronegative patients. The findings of this study reveal that those with the blood groups O+ and B+ have an estimated 25.3% (21/83) higher risk of H. pylori infection, whereas when seronegative individuals were investigated, it was discovered that blood groups 0+ were also leading, 28.4% (19/67), indicating that there was no significant difference between H. pylori seropositive and seronegative patients (p-value = 0.5146). Other factors, such as gender and family history, did not significantly affect the incidence of H. pylori. Conclusion: It was concluded from the study that no significant difference was observed between trends of H. pylori seropositive patients and seronegative individuals having different blood groups. Keywords: ABO Blood Group, Peptic Ulcer, Seronegative Pyloric patients, Seropositive Pyloric patients.

Helicobacter pylori infection has a detrimental impact on the efficacy of cancer immunotherapies

ObjectiveIn this study, we determined whether Helicobacter pylori (H. pylori) infection dampens the efficacy of cancer immunotherapies.DesignUsing mouse models, we evaluated whether immune checkpoint inhibitors or vaccine-based immunotherapies are effective...

Changes of serum pepsinogen level and ABC classification after bariatric surgery

Very few studies have explored the changes of serum pepsinogen after bariatric surgery and no research has evaluated the feasibility of ABC classification to predict gastric cancer risk after bariatric surgery. We enrolled 94 obese subjects that received bariatric surgery, including 41 sleeve gastrectomy (SG) and 53 Roux-en-Y gastric bypass (RYGB). The serum pepsinogen I (PGI), pepsinogen II (PGII), PGI/II ratio and seropositivity of Helicobacter pylori ( H. pylori ) were measured before and one year after surgery. Patients were classified according to ABC classification and post-operative change was evaluated. Preoperatively, four (4.2%) patients were classified into high risk group (classification C and D) for gastric cancer. Significant reduction of PGI, PGII and decrease of PGI/II ratio were noted after bariatric surgery. H. pylori seropositive patients had a greater postoperative change of PGI (-38.6μg/L vs -22.1μg/L, p=0.003) and PGII (-8.0μg/L vs -2.5μg/L, p <0.001) but a less postoperative change of PGI/II ratio (-0.6 vs -2.1, p =0.04) than H. pylori seronegative patients. One year after surgery, the portion of high risk group of ABC classification for gastric cancer increased markedly from 4.2% to 23.7%. Both of SG and RYGB resulted in significant reduction of serum PGI and PGII after bariatric surgery, and significantly influenced the ABC classification. The application of ABC classification for gastric cancer screening was limited after bariatric surgery.

The Relationship of Gastrinoma in MEN 1 to Helicobacter pylori infection.

Helicobacter pylori and Multiple Endocrine Neoplasia Type 1 (MEN 1) are risk factors for hypergastrinemia. Gastrin-secreting neoplasms of the foregut mucosa are both a source of, and potentially stimulated by, hypergastrinemia. To determine the relationship between H pylori exposure and the prevalence and severity of hypergastrinemia in patients with MEN 1. Cross-sectional analysis of patients with a common MEN1 gene mutation managed at a tertiary referral hospital that underwent fasting serum gastrin and H pylori serum IgG measurement. H pylori IgG and serum gastrin concentration, determined via immunoassay. The prevalence and severity of hypergastrinemia and its relationship to past H pylori exposure. Thirty-four of 95 (36%) patients were H pylori IgG seropositive. H pylori seropositive patients were significantly more likely to exhibit hypergastrinemia compared with seronegative patients (relative risk [RR] 1.72, P = .023). H pylori exposure also predicted severe hypergastrinemia (RR 3.52, P = .026 and RR 9.37, P = .031 for patients with gastrin ≥ ×4 and ≥ ×8 the upper limit of normal [ULN], respectively). Gastrin concentrations ≥ ×10 ULN occurred exclusively in H pylori seropositive patients (0/61 vs 6/34, P = .001). Serum gastrin and alpha subunit were positively associated in H pylori-exposed (β = 0.69, P = .001), but not in H pylori-unexposed patients. Past H pylori exposure was associated with increased prevalence and severity of hypergastrinemia in MEN 1 patients. Past H pylori-related hypergastrinemia may contribute to the pathogenesis of ongoing gastrin hypersecretion by susceptible foregut neuroendocrine tissues.

Association of Interleukin-1B gene Polymorphism with H. pylori infected Dyspeptic Gastric Diseases and Healthy Population.

Objective:The aim of study was to investigate the association of IL 1B gene polymorphism with involvement of H. pylori and other gastric diseases.Methods:Blood samples of dyspeptic patients were collected from endoscopy department of Allied Hospital Faisalabad from January 2017 to January 2019 and were qualitatively assayed for serological detection of CagA H. pylori antibodies. PCR followed by direct sequencing was performed for proinflammatory IL-1B gene polymorphism detection. Sequence analysis was performed in software SnapGene viewer for haplotypes.Results:Demographic characteristics of seropositive patients showed maximum 25% gastritis in age groups of 20-40 years and 41-60 years, predominantly (41.7%) in females. While in seronegative patient’s gastritis (33.3%) was found in age group of 20-40 years mainly in males (41.7%). Among studied groups, higher expression of IL-1B-511 genotype (33.3%) polymorphism was found in healthy individuals as compared to H. pylori seropositive (25%) and seronegative (8.3%). While IL-1B-31 genotype showed maximum 33.3% polymorphism rate in seropositive gastric diseased group. Moreover, haplotypes frequencies IL-1B-511CC and IL-1B-31TT were predominantly (20%) found in seropositive gastric diseased group.Conclusions:In H. pylori seropositive patients, gastric disease was commonly found, however, gastric disease was not only associated with H. pylori as seronegative patients were also carrying gastric complications. Interleukin IL-1B polymorphism was partially associated with H. pylori infection in studied dyspeptic population.

Increased Serum Interleukin-10 Could lead to Allergic Disease Development in Helicobacter pylori Infected Adult

Some research reported a protective effect of increased IL-10 in the development of allergic disease in children with H.pylori infection. Therefore this study aimed to investigate the possible protective effect of increased serum IL-10 levels and allergic disease symptoms in adult infected with H. pylori, furthermore we studied an association between ABO blood group with H. pylori infection. Methodes: Slide heamagglutination test was used to determine the blood group phenotype in 214 patients seropositiveH.pylori which they submitted to Azadi teaching hospital in Kirkuk city-Iraq for diagnosis and treatment, in addition serum levels of anti H. pylori antibody, IL-10, IL-4 and total IgE were assayed using ELISA kits for 70 patients, as well as for 20 healthy control. Results. The result showed significant increasing of the serum levels IL-10 and IL-4(P=0.000,0.003 respectively) and total IgE level (p=0.014) in H. pylori seropositive patients. Also the study showed higher incidence of H.pylori infection within O blood group of patients in compared with general population (p=0.000). Conclusion:H.pylori infection associated with increased IL-10 levels and IL-4 levels, and IL-4 production may responsible for the increase in serum IgE level and higher incidence of infection in O blood phenotype may considered as an etiological risk factor for the development of H. pylori infection.

MOLECULAR DETECTION OF CLARITHROMYCIN AND FLUOROQUINOLONES RESISTANCE IN HELICOBACTER PYLORI INFECTION, DIRECTLY APPLIED TO GASTRIC BIOPSIES, IN AN URBAN BRAZILIAN POPULATION.

- Antimicrobial resistance is the major factor leading to eradication failure in H. pylori treatment. Molecular tests are useful to detect genetic mutations predictive of clarithromycin and fluoroquinolones resistance. Knowledge of the local prevalence rate of resistance is important to define the best recommended treatment. - To assess the prevalence of primary resistance of H. pylori to clarithromycin and fluoroquinolones, using a molecular test, in a Southeastern urban Brazilian population. - A total of 72 H. pylori seropositive patients [65% female, mean age 39 (19-73) years] never treated before for this infection were studied. All patients underwent gastroscopy in addition to antrum and corpus biopsies and molecular test GenoType HelicoDR (Hain Life Science, Germany) to detect H. pylori and point mutations in genes responsible for clarithromycin and fluoroquinolone resistance. The molecular procedure was divided into three steps: DNA extraction from biopsy samples, a multiplex amplification with biotinylated primers and a reverse hybridization. The most frequent point mutations involved in resistance to the two antibiotics were evaluated. - Resistance to clarithromycin was detected in nine (12.5%) patients and to fluoroquinolones in eight (11.1%) patients. The point mutation A2147G was the most common (77.8%) among resistant strains to clarithromycin. In 50% of the resistant strains to fluoroquinolones, the mutant codon couldn't be identified. - The resistance rates to clarithromycin and fluorquinolones in a large urban population in the Southeast of Brazil were acceptable, suggesting that these drugs remain appropriate options to first and second-line of H. pylori treatment. The molecular test represents an adequate diagnostic tool for monitoring H. pylori resistance.

Increased Exhaled 8-Isoprostane and Interleukin-6 in Patients with Helicobacter pylori Infection.

Helicobacter pylori (H. pylori) infection triggers both local inflammation, usually in gastric mucosa, and chronic systemic inflammation. It is assumed that this local and systemic inflammation is caused by extracellular products excreted by H. pylori. The aim of this study was to investigate the possible association between H. pylori infection and a local inflammatory response in the airway by using exhaled breath condensate technique. This study includes 41 H. pylori seropositive patients who have gastric symptoms and 27 healthy control subjects. Pulmonary function tests (PFT), chest X ray, and physical examination were performed in all patients and interleukin-6 (IL-6), 8-isoprostane and nitrotyrosine levels were measured in exhaled breath condensate. Levels of IL-6 and 8-isoprostane in exhaled breath condensate (EBC) were significantly higher in H. pylori positive patients than control subjects (p < 0.05). Nitrotyrosine levels were also higher in H. pylori positive patients but the difference was not statistically significant. Both groups had similar leukocyte counts, C-reactive protein (CRP) levels and PFT parameters. H. pylori infection causes an asymptomatic airway inflammation which can be detected by exhaled breath condensate. The clinical importance of this inflammation remains unclear.

Association between Helicobacter pylori Seropositivity and the Coronary Artery Calcium Score in a Screening Population

Background/AimsHelicobacter pylori causes numerous extragastric manifestations, including coronary heart disease. The coronary artery calcification (CAC) score, measured using computed tomography (CT) has been used as a screening test for coronary atherosclerosis. This study investigated the association between H. pylori seropositivity and CAC scores in a screening population.MethodsPatients who underwent a health checkup between October 2003 and July 2007 and who did not have a history of ischemic heart disease were enrolled in the study. Subjects were screened with a multidetector CT scan to determine the CAC score and for anti-H. pylori antibody immunoglobulin G; traditional risks for coronary heart disease were evaluated using a structured questionnaire, anthropometric measurements, and laboratory tests.ResultsOf the 2,029 subjects enrolled (1,295 males), 1,214 (59.8%) subjects were H. pylori positive and 815 were H. pylori negative. There were no significant differences in the baseline characteristics of the seropositive and seronegative patients. When the CAC presence or absence scores were considered, multivariate analysis revealed that H. pylori seropositivity was statistically associated with the presence of CAC and that this association was stronger in the mild CAC score category.ConclusionsH. pylori seropositive patients are at a higher risk for coronary atherosclerosis regardless of traditional cardiovascular risk factors. This association is particularly applicable for early coronary atherosclerosis.

Identification and Evaluation of Pre-Malignant Lesions Associated With Helicobacter pylori Infection in Guatemala

routine medical work-up were tested for immunoglobulin G (IgG) against H. pylori and anti-CagA antibodies by specific EIA. Results: The overall seroprevalence of H. pylori infection was 37.9 %. The prevalence of anti-H. pylori IgG in males and females was similar (19.1% and 18.6%, respectively). The prevalence of anti-CagA IgG among H. pylori seropositive patients was 43.3%. When patients were stratified into age groups at decade intervals, a steady age-related increase in seroprevalence of H. pylori infection was not observed (Figure 1). The seroprevalence of H. pylori infection showed a birth-cohort effect with a drop from 40.8% in subjects older than 31 to 18.1% in subjects 30 years old or younger (p<0.05). Conclusions: Serological prevalence of H. pylori-infection shows a significant drop in patients born after 1980 in our population. Changes in housing and increased use of antibiotics are among the possible explanations for this phenomenon.

The Cost of Inflammatory Bowel Disease Inpatient Care

routine medical work-up were tested for immunoglobulin G (IgG) against H. pylori and anti-CagA antibodies by specific EIA. Results: The overall seroprevalence of H. pylori infection was 37.9 %. The prevalence of anti-H. pylori IgG in males and females was similar (19.1% and 18.6%, respectively). The prevalence of anti-CagA IgG among H. pylori seropositive patients was 43.3%. When patients were stratified into age groups at decade intervals, a steady age-related increase in seroprevalence of H. pylori infection was not observed (Figure 1). The seroprevalence of H. pylori infection showed a birth-cohort effect with a drop from 40.8% in subjects older than 31 to 18.1% in subjects 30 years old or younger (p<0.05). Conclusions: Serological prevalence of H. pylori-infection shows a significant drop in patients born after 1980 in our population. Changes in housing and increased use of antibiotics are among the possible explanations for this phenomenon.

Impact of Helicobacter pylori Infection on the Humoral Immune Response to MUC1 Peptide in Patients with Chronic Gastric Diseases and Gastric Cancer

Many investigators have demonstrated alteration of gastric mucins in H. pylori infected individuals. The inflammatory environment induced by H. pylori leading to aberrant glycosylation of MUC1 and demasking of core peptide MUC1 epitope could enhance immune responses to MUC1. IgG and IgM immune response to MUC1 in patients with gastric cancer (n = 214) chronic gastroduodenal diseases (n = 160) and healthy blood donors (n = 91) was studied with ELISA using bovine serum albumin-MUC1 60-mer peptide as antigen. H. pylori serologic status was evaluated with ELISA and CagA status by immunoblotting. Gastric mucosa histology was scored according to the Sydney system. Compared to H. pylori seronegative individuals, higher levels of IgG antibody to MUC1 were found in H. pylori seropositive patients with benign gastric diseases (p < 0.01) and blood donors (p < 0.03). Higher MUC1 IgG antibody levels were associated with a higher degree of gastric corpus mucosa inflammation in patients with chronic gastroduodenal diseases (p < 0.0025). There was a positive correlation between the levels of anti-H. pylori IgG and MUC1 IgG antibody levels in blood donors (p = 0.03), and in patients with benign diseases (p < 0.0001). In patients with gastric cancer (n = 214) a significantly higher level of anti-MUC1 IgG than in blood donors was observed (p < 0.001) irrespective of H. pylori status or stage of cancer. MUC1 IgM antibody levels were not related to the H. pylori serology. IgG immune response to tumor-associated MUC1 is up regulated in H. pylori infected individuals. This increase is associated with a higher IgG immune response to H. pylori and with a higher degree of gastric mucosa inflammation. High levels of MUC1 IgG antibody irrespective of H. pylori serologic status characterized patients with gastric cancer. The findings suggest that, in some individuals, the H. pylori infection may stimulate immune response to tumor-associated MUC1 peptide antigen thus modulating tumor immunity.

Comparative Immunoproteomics of Identification and Characterization of Virulence Factors from Helicobacter pylori Related to Gastric Cancer

Helicobacter pylori is an important risk factor of gastric cancer (GC). Although many H. pylori virulence factors have been reported, the pathogenic mechanism by which H. pylori infection causes GC remains unclear. The aims of this study were to identify GC-related antigens from H. pylori and characterize their roles in the development of GC. As GC and duodenal ulcer (DU) are considered clinically divergent, we compared two-dimensional immunoblots of an acid-glycine extract of H. pylori probed with serum samples from 15 patients with GC and 15 with DU to find GC-related antigens, which were subsequently identified by mass spectrometry. Many protein spots were recognized by more than one serum, and 24 of these were better recognized by GC sera. The proteins showing higher frequency of recognition in GC group are threonine synthase, rod shape-determining protein, S-adenosylmethionine synthetase, peptide chain release factor 1, DNA-directed RNA polymerase alpha subunit, co-chaperonin GroES (monomeric and dimeric forms), response regulator OmpR, and membrane fusion protein. Of these proteins, GroES was identified as a dominant GC-related antigen with a much higher seropositivity of GC samples (64.2%, n = 95) compared with 30.9% for gastritis (n = 94) and 35.5% for DU (n = 124). GroES seropositivity was more commonly associated with antral GC than with non-antral GC (odds ratio = 2.7; 95% confidence interval, 1.1-6.7). In peripheral blood mononuclear cells, GroES stimulated production of interleukin (IL)-8, IL-6, granulocyte macrophage colony-stimulating factor, IL-1beta, tumor necrosis factor-alpha, cyclooxygenase-2, and prostaglandin E(2). Moreover when incubated with gastric epithelial cells, GroES induced expression of IL-8, cell proliferation, and up-regulation of c-jun, c-fos, and cyclin D1 but caused down-regulation of p27(Kip1). We conclude that GroES of H. pylori is a novel GC-associated virulence factor and may contribute to gastric carcinogenesis via induction of inflammation and promotion of cell proliferation.

Effect of Helicobacter pylori eradication in the treatment of Japanese patients with chronic idiopathic urticaria

Infection with Helicobacter pylori has been associated with chronic idiopathic urticaria (CIU). The aim of this study was to investigate the efficacy of H. pylori eradication in the treatment of patients with CIU. Fifty patients with CIU (16 men and 34 women; age 25-75 years) and 100 sex- and age-matched control subjects were enrolled in the study. Presence of IgG antibody to H. pylori was examined by serology. H. pylori-seropositive patients with CIU received endoscopy to confirm H. pylori infection. Patients infected with H. pylori received eradication therapy comprising lansoprazole, amoxicillin, and either clarithromycin or metronidazole. At least 2 months after finishing the eradication therapy, a (13)C-urea breath test was performed, and the effect of eradication therapy on the CIU was scored, using a three-point scale, as complete remission, partial remission, or no improvement. In the 50 patients with CIU, 26 (52%) were H. pylori-seropositive, while 48% (48/100) of the control subjects were seropositive (statistically not significant). Nineteen out of the 26 patients with CIU infected with H. pylori received eradication therapy, and eradication was successful in 17 patients. In the 17 H. pylori-eradicated patients, 6 (35%) had complete remission and 11 (65%) had complete remission or partial remission. On the other hand, in the 9 patients without H. pylori eradication, only 2 (22%) showed partial remission and 7 (78%) had no improvement. Eradication of H. pylori would be a valid choice for patients with CIU, although the prevalence of H. pylori infection is not higher in patients with CIU than it is in controls.

Relation between seroreactivity to low-molecular-weight Helicobacter pylori-specific antigens and disease presentation.

The identification of Helicobacter pylori-strain specific factors that correlate with clinical outcome has remained elusive. We investigated possible relationships between a group of H. pylori antigens and clinical outcome and compared an immunoblot assay kit (HelicoBlot, version 2.1 [HB 2.1]; Genelabs Diagnostics) with an established serological test, the high-molecular-weight cell-associated protein test (HM-CAP). We used sera from 156 Thai patients with different disease presentations, including 43 patients with gastric cancer, 64 patients with gastric ulcer, and 49 patients with nonulcer dyspepsia (NUD). HB 2.1 was compared to HM-CAP as a diagnostic test for H. pylori infection. The seroprevalence of H. pylori was significantly higher among gastric cancer patients than among patients with NUD (93 and 67%, respectively; P < 0.01). Among the H. pylori-seropositive patients, the presence of the antibody to the 37,000-molecular-weight antigen (37K antigen) was inversely related to the presence of gastric cancer (e.g., for gastric cancer patients compared with NUD patients, odds ratio [OR] = 0.28 and 95% confidence interval [CI] = 0.1 to 0.8). The presence of antibody to the 35K antigen was higher in gastric ulcer patients than in NUD patients (OR = 11.5; 95% CI = 2.4 to 54.3). The disease associations of antibodies to the 35K and 37K antigens are consistent with the possibility that these antigens are either indirect markers for H. pylori-related diseases or have specific active or protective roles in H. pylori-related diseases.

Yield of endoscopy in dyspepsia and concurrent treatment with proton pump inhibitors: The blind leading the blind?

Yield of endoscopy in dyspepsia and concurrent treatment with proton pump inhibitors: The blind leading the blind?

Better Survival of Helicobacter pylori Infected Patients with Early Gastric Cancer Is Related to a Higher Level of Thomsen‐Friedenreich Antigen‐Specific Antibodies

The survival of patients with histologically verified gastric carcinoma at stage I (n = 44) and stage II (n = 43) was analysed by the Kaplan‐Meier method depending on H. pylori serological status and a level of IgG and IgM antibody to tumor‐associated Thomson‐Friedenreich antigen (T Ag). In cancer patients at stage I, significantly better survival for H. pylori seropositive patients was observed compared to H. pylori‐seronegative patients (median±SE survival time: 60.0±3.8 mths and 37.0±7.8 mths, respectively; P < 0.0004, log‐rank test). Patients with higher level of T Ag‐specific IgG antibody (strong responders) showed significantly and dramatically better (P < 0.00001) survival rate than weak responders. However, an association of better survival with a higher level of anti‐T antibody level was limited to the H. pylori seropositive patients exclusively (P < 0.00001) with no difference for H. pylori seronegative group of patients. The level of IgM anti‐T Ag antibody was not significantly related to the survival of patients at both stages of the disease, though better survival was noted in H. pylori seropositive IgM strong responders at ~40–60 months of observation. Statistically insignificant associations between survival and H. pylori status or anti‐T antibody levels were also observed in a group of gastric cancer patients at stage II. In summary, the survival of patients with early gastric cancer (stage I) is significantly better in H. pylori seropositive patients, and this phenomenon may be in part explained by up‐regulation of T Ag‐specific IgG immune response in H. pylori infected individuals.

Lack of association of Helicobacter pylori infection with coronary artery disease and frequency of acute myocardial infarction or death

We investigated the association between Helicobacter pylori (H. pylori) infection and coronary artery disease (CAD) in 2 study populations: (1) a cross-sectional study to determine risk of having CAD, and (2) a longitudinal study to determine risk of acute myocardial infarction (AMI) or death over a mean follow-up period of 3 years in patients with angiographically documented CAD. Blood samples were tested for serum immunoglobulin G antibodies to H. pylori and C-reactive protein (CRP) levels. Study 1: Of 391 patients (62% men, mean age 57 years), 41% had antibodies to H. pylori. CAD prevalence was 70% in H. pylori seropositive patients and 59% in seronegative patients (p = 0.03). Elevated CRP levels (>0.5 mg/dl) were significantly higher in patients with than without CAD (p = 0.02). By univariate analysis, CAD prevalence significantly increased stepwise depending on H. pylori seropositivity and elevated CRP levels (p = 0.008). Significance was lost after adjustment for traditional risk factors. Further analyses revealed that age was the critical confounder. Study 2: Of 929 patients (77% men, mean age 65 years), 56% had antibodies to H. pylori. By univariate analysis, the incidence of AMI or death was 22% in H. pylori seropositive patients and 18% in seronegative patients (p = 0.1). The adjusted hazard ratio of AMI or death for H. pylori seropositivity was 1.12 (95% confidence interval 0.81 to 1.54). Our data suggest that prior infection with H. pylori is not a major factor determining either risk of CAD, AMI, or death in patients with CAD.

Seroprevalence of Helicobacter pylori Infection in Inflammatory Bowel Disease: Is Helicobacter pylori Infection a Protective Factor?

Background: The mechanisms for the observed low prevalence of Helicobacter pylori infection in inflammatory bowel disease (IBD) are unknown, but might be important for the pathogenesis of IBD. We have studied the seroprevalence of H. pylori in different categories of IBD and evaluated the role of medical therapy, smoking and social status. We also analysed the effect of seropositivity on the age of onset of IBD in order to find possible evidence for the protective effect of the infection. Methods: We studied 296 (mean age 43 years, range 18-79; women 144) unselected patients with IBD, including 185 with ulcerative colitis (UC), 94 with Crohn disease (CD), and 17 with indeterminate colitis (IC). Seventy healthy age- and sex-matched subjects served as controls. Serum samples were studied for H. pylori antibodies. Detailed clinical history was obtained from patient records and by face-to-face interview. Results: The prevalence of H. pylori infection was lower in IBD patients (24%) than in controls (37%; P = 0.029), and in CD lower (13%) than in UC (30%; P = 0.002). Seropositivity was not related to sulphasalazine treatment or smoking. Age of onset of IBD was higher in seropositive (mean 40 years) than in seronegative patients (30 years; P < 0.001). The age of onset of IBD showed unimodal distribution in H. pylori seronegative patients, with a peak between 30 and 40 years, although there was some evidence of bimodality in CD. In contrast, H. pylori seropositive patients had clear bimodal pattern with peaks at 20-40 and 50-60 years of age. Conclusions: Our results confirm the low prevalence of H. pylori infection in IBD, and in particular in CD. The significantly higher age of onset and bimodal pattern of age-specific incidence in seropositive IBD patients suggest that H. pylori infection significantly modifies the development of IBD and may have a protective effect.

Serum anti-Lewis X antibody is not elevated in patients with gastric cancer infected with Helicobacter pylori.

Lipopolysaccharides of Helicobacter pylori express Lewis X similar to that occurring in gastric mucosa. Patients infected with H. pylori produce anti-Lewis X antibodies. The aim of this study was to examine whether anti-Lewis X antibody was associated with the development of gastric cancer, particularly intestinal type cancer. Serum sample was collected from 98 patients with early gastric cancer and 98 gender- and age-matched control subjects who underwent endoscopy. Histologically, 77 cancers were of the intestinal type. Titers of anti-H. pylori and anti-Lewis X immunoglobulin G (IgG) antibodies were assayed by enzyme-linked immunosorbent assay. The mean titer of Lewis X antibody was 0.097 in patients with gastric cancer and 0.110 in matched control subjects (not significant). In 72 H. pylori-seropositive patients with intestinal type cancer and their matched H. pylori-seropositive controls, mean titer was 0.115 and 0.107, respectively (not significant). The odds ratio for the risk of gastric cancer if Lewis X antibody was high titer was 0.93 (95% CI 0.43-2.00). The odds ratio for the risk of intestinal type gastric cancer in patients with H. pylori infection if Lewis X antibody was high titer was 1.10 (95(% CI, 0.46-2.62). Anti-Lewis X antibody does not seem to be associated with the development of gastric cancer, even the intestinal type cancer.