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The CagA protein one of the key virulence factors of Helicobacter pylori plays an important role in the pathogenesis of peptic ulcer diseases. Unfortunately the cagA gene status can only be determined by PCR while serology is an alternative approach to detect antigens or antibodies. Our aim is to detect the CagA antigen in sera of infected subjects by the development of an in-house capture ELISA test. Gastric antral biopsies and serum samples were collected from 63 patients. PCR was used to determine the cagA status. Our previously developed recombinant CagA protein and monoclonal antibody were used for setting up the capture ELISA test. H. pylori positive [(38 gastritis, 14 duodenal ulcers (DU), 11 gastric ulcer (GU)] patients were determined by PCR. The cagA gene was detected in 21 (55%) of gastritis, 11 (78%) of DU and 7 (60%) of GU patients. The reagents used in setting up the capture ELISA test following optimization displayed high performance. This study showed that our developed in-house capture ELISA has the potential to detect the CagA antigen at very low concentrations even though not detected in our H. pylori infected patients sera but we are also intended to use it in saliva and stool samples., (Copyright © 2020. Published by Elsevier B.V.)

Objectives: To assess the concordance and performance characteristics of Helicobacter pylori laboratory tests compared with histopathology and to propose algorithms for the diagnosis of H pylori that minimize diagnostic error., Methods: H pylori diagnostics were reviewed from a 12-year period within a health system (2,560 cases). Analyses were performed to adjust diagnostic performance based on treatment and consensus histopathologic diagnoses among pathologists. Markers of access to care, including test cancellation frequency and turnaround time, were assessed. Costs and performance of candidate noninvasive testing algorithms were modeled as a function of disease prevalence., Results: Serum H pylori IgG demonstrated a higher sensitivity (0.94) than urea breath and stool antigen tests (0.64 and 0.61, respectively). Evidence of an advantage in access to care for serology included a lower cancellation rate. Interobserver variability was higher (κ = 0.34) among pathologists for cases with a discordant laboratory test than concordant cases (κ = 0.56). A model testing algorithm utilizing serology for first-time diagnoses minimizes diagnostic error., Conclusions: Although H pylori serology has modestly lower specificity than other noninvasive tests, the superior sensitivity and negative predictive value in our population support its use as a noninvasive test to rule out H pylori infection. Reflexive testing with positive serology followed by either stool antigen or urea breath test may optimize diagnostic accuracy in low-prevalence populations., (© American Society for Clinical Pathology, 2020. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Purpose: To evaluate serum levels of high-sensitivity C-reactive protein (hs-CRP) in chronic gastritis patients to predict Helicobacter pylori (HP) infection, inflammatory activity, and precancerous lesions., Methods: A total of 811 patients with upper gastrointestinal symptoms and histopathological diagnosis of chronic gastritis were enrolled in the study. On endoscopy, five gastric biopsies were taken according to Modified Sydney protocol, which were stained with hematoxylin & eosin and Giemsa., Results: HP infection was found in 28.6% of patients, being significantly more common in specimens with acute and chronic inflammatory activity. Mucosal atrophy, intestinal metaplasia, and dysplasia were found in 20.2%, 18.8% and 2.7% of biopsy specimens. Mean hs-CRP was 1.9±1.6 mg/dl for males and 2.2±1.9 mg/dl for females. hs-CRP average were significantly higher in patients with severe acute inflammation (p:0.049), in patients with severe chronic inflammation (p:0.015) and in those with HP (p: 0.001) . The severity of HP infection increased significantly with the increased degree of acute inflammation, chronic inflammation and hs-CRP level (p=0.001 for both)., Conclusion: Serum hs-CRP level increases in patients with chronic gastritis, it could be an indicator of severity of acute or chronic mucosal inflammation, and presence of HP infection. Therefore, hs-CRP may aid the diagnosis of chronic gastritis, but it is not associated with pre-cancerous lesions.

The association between gastroesophageal reflux disease (GERD) prevalence and its risk factors in an area with low Helicobacter pylori prevalence is important to clarify. We analyzed the prevalence of GERD and risk factors in an area of Indonesia with low prevalence of H. pylori infection. We recruited 104 dyspeptic patients who underwent endoscopy in Surabaya. Patients were diagnosed with GERD based on the Los Angeles classification. We evaluated gastric biopsy specimens and measured serum pepsinogen levels. Interleukin polymorphisms were evaluated by polymerase chain reaction-restriction fragment length polymorphism. Of 104 patients, 56 (53.8%) were endoscopically found to have GERD, with most categorized as grade A; 48 (46.2%) were classified as non-GERD. Higher economic status, smoking, and a history of proton-pump inhibitor use significantly increased the risk of GERD. GERD Questionnaire scores showed a positive correlation with GERD (P < 0.001). An association was found between antral atrophic gastritis and GERD (P = 0.030), and patients with GERD more frequently had severe antral atrophy than nonerosive reflux disease (P = 0.018). We found an association between pepsinogen I/II levels and GERD (P = 0.047), but with low accuracy. IL-1β -511 TT and CT were predominant among the IL-1β -511 genotypes, and IL-8-251 AT and TT were predominant among the IL-8-251 genotypes. In conclusion, we found a high prevalence of GERD in an area with low prevalence of H. pylori infection, which could be associated with acid reflux. Smoking, history of proton-pump inhibitor use, and higher economic group significantly increased the risk of GERD., Competing Interests: The authors have declared that no competing interests exist.

Strong evidence for an association between idiopathic thrombocytopenic purpura (ITP) and Helicobacter pylori (HP) infection has been reported in humans. Chronic ITP is known to be improved by the eradication of HP. The purpose of this study was to reproduce these events by the experimental infection of several strains of mice with HP. BALB/c, C57BL/6, and DBA/2 mice were untreated or orally inoculated with HP. Two months later, platelet counts were compared in samples from HP-infected and noninfected mice. Platelet counts (mean ± SD, × 10 4 cells/µl) in blood samples from HP-infected BALB/c, C57BL/6, and DBA/2 mice were 102.28 ± 14.71, 99.65 ± 17.00, and 111.57 ± 16.20, respectively; the respective counts from noninfected mice were 121.80 ± 13.30, 104.35 ± 18.20, and 107.84 ± 14.33. A significant difference in platelet counts between HP-infected and noninfected mice was observed in BALB/c mice (P≤0.01) but was not observed in DBA/2 mice, even though the histocompatibility (H)-2 type of the DBA/2 was the same as that of BALB/c mice. According to ELISA results, the optical density value for the anti-HP antibody in HP-infected BALB/c mice was not correlated with the number of platelets (P>0.50). These results suggest that the decrease in platelet count caused by HP infection is not related to antibody titer and histocompatibility-2 type. Experimental infection of BALB/c mice with HP can reproduce the relationship between HP and ITP and serves as a good model to investigate the mechanistic basis for the effectiveness of HP eradication therapy for ITP treatment.

BACKGROUND The bacterial pathogen Helicobacter pylori (H. pylori) can cause chronic gastritis. CA54/61 is a serum tumor marker that has been shown to be positive in the several types of human malignancy. However, the association of between chronic gastritis due to H. pylori and elevated serum levels of CA54/61 has not been previously reported. This report is of three cases of increased serum levels of CA54/61 associated with H. pylori chronic gastritis. CASE REPORT Case 1 was a 44-year-old Japanese woman with a serum CA54/61 level of 138 U/ml (normal level: 12 U/ml). Following treatment and eradication of H. pylori the serum CA54/61 level decreased to 14 U/ml. Case 2 was a 73-year-old Japanese man with a serum level of less than 2 U/ml before completion of successful eradication therapy of H. pylori with a small peak of 30 U/ml after therapy. Case 3 was a 54-year-old Japanese man who maintained a serum CA54/61 level of approximately 20 U/ml before and until 603 days after eradication therapy. None of the three patients had malignancy, which is usually suggested by this serum marker. CONCLUSIONS These three case reports suggest the possibility of an association between chronic gastritis involving H. pylori infection and an elevated serum level of CA54/61. It is possible that the inflammatory gastric mucosal cells supply CA54/61 to the bloodstream. However, further studies are required to confirm the association between serum levels of CA54/61 and H. pylori chronic gastritis and the underlying mechanisms of this association.

Aim: To investigate the clinicopathological features of the patients testing negative for high titer serum anti- Helicobacter pylori ( H. pylori ) antibody., Methods: The antibody titers were measured using antigens derived from Japanese individuals. 13 C-urea breath test-positive individuals were defined as having H. pylori infection. We investigated the demographic characteristics, laboratory data, endoscopic findings including Kyoto classification of gastritis, and histology in negative-high titer patients without H. pylori eradication therapy. Kyoto classification consisted of scores for gastric atrophy, intestinal metaplasia, enlarged folds, nodularity, and redness., Results: Of the 136 subjects enrolled, 23 (17%) had H. pylori infection. Kyoto classification had an excellent area under the receiver operating characteristics curve (0.886, 95% confidence interval: 0.803-0.968, P = 3.7 × 10 -20 ) for predicting H. pylori infection with a cut-off value of 2. Further, Kyoto classification, H. pylori density, and neutrophil activity had high accuracies (89.7%, 96.3%, and 94.1%, respectively). Kyoto classification was independent of the demographic and laboratory parameters in multivariate analysis., Conclusion: Endoscopic Kyoto classification of gastritis is a useful predictor of H. pylori infection in negative-high titer antibody patients., Competing Interests: Conflict-of-interest statement: During the last five years, Toyoshima O received personal fees from Otsuka Pharmaceutical Co., Ltd. and Takeda Pharmaceutical Co., Ltd. outside of the submitted work; Suzuki H received scholarship funds for the research from Astellas Pharma Inc., Astra-Zeneca K.K., Otsuka Pharmaceutical Co., Ltd., Takeda Pharmaceutical Co., Ltd., and Zeria Pharmaceutical Co., Ltd. and received service honoraria from Astellas Pharma, Inc., Astra-Zeneca K.K., Otsuka Pharmaceutical Co., Ltd., Takeda Pharmaceutical Co., Ltd., and Zeria Pharmaceutical Co., Ltd.

Background: Endothelial dysfunction is one of the early stages of vascular diseases., Objective: The aim of this study was to investigate the endothelial dysfunction markers in patients with chronic gastritis associated with Helicobacter pylori (H. pylori) infection., Methods: By a cross sectional study, basic and clinical information of 120 participants (40 patients with positive H. pylori infection, 40 patients with negative H. pylori infection and 40 healthy people) were analyzed. Carotid intima media thickness and flow-mediated dilation levels were measured in all patients and controls. Soluble vascular cell adhesion molecule-1 (sVCAM-1) and intercellular adhesion molecule-1 (ICAM-1) were measured with Elisa for all subjects. IgG level was assessed in chronic gastritis patients., Results: The flow-mediated dilation level in patients with positive H. pylori infection (0.17%±0.09) was significantly lower than those with negative H. pylori infection (0.21% ±0.10, P<0.05) and compared to the control group (0.27% ±0.11, P<0.05). Carotid intima media thickness level in patients with positive H. pylori infection (0.58±0.13 mm) was significantly higher than those with negative H. pylori infection (0.48±0.32 mm, P<0.05) and compared to the control group (0.36±0.44mm, P<0.05). The mean level of sICAM-1 in positive H. pylori infection group (352.16±7.54 pg/mL) was higher than negative H. pylori infection group (332.64±8.75 pg/mL =0.75) and compared to the control group (236.32±12.43 pg/mL, P<0.05). A direct relationship was revealed between flow-mediated dilation and carotid intima media thickness changes and between sICAM-1 and sVCAM-1 associated with the level of H. pylori IgG in chronic gastritis., Conclusion: The levels of flow-mediated dilation, carotid intima media thickness and sICAM-1 were higher among patients with positive H. pylori infection. Patients with chronic gastritis associated with H. pylori infection are at risk of endothelial dysfunction due to flow-mediated dilation and carotid intima media thickness abnormalities and increased level of sICAM-1 and sVCAM-1.

Background: Gastric cancer arises, mainly, on an inflammatory background. Helicobacter pylori neutrophil activating (HP-NAP) protein functions as a potent pro-inflammatory mediator. Similarly, IL-4 plays a critical role in the inflammation pathway, the levels of which are altered by C to T transition at position -590 in its promoter region. Here, we have aimed to assess the risk of gastritis and gastric cancer in the co-presence of these two inflammation modulating mediators., Methods: Gastritis (n=58) and gastric cancer (n=31) patients were evaluated and compared with H. pylori-positive asymptomatic controls (n=46), for serum antibodies against recombinant HP-NAP and IL-4 C-590T single nucleotide polymorphism using immunoblotting and PCR-RFLP, respectively. Multivariable logistic regression, adjusting for age, gender and ethnicity, was used for data analysis., Results: In terms of susceptibility to gastritis, seropositivity to HP-NAP projected a risk impact of 4.62 fold (OR=4.62, 95% CI=1.50-14.22), which when present in IL-4 -590 T carriers augmented the risk up to 9.7 fold (OR=9.70, 95% CI=2.06-45.69). A similar pattern, but of a stronger magnitude, occurred for the risk of gastric cancer, which was estimated at 9.07 fold (OR=9.07, 95% CI=1.99-42.0) for HP-NAP-seropositive subjects and was drastically amplified (OR=33.64, 95% CI=2.06-548.68), when double-positive (HP-NAP seropositive/IL-4 -590 T carrier) subjects were examined against double negatives (HP-NAP seronegative/IL-4 -590 CC)., Conclusion: Our preliminary data indicate that serum antibodies against HP-NAP represent a state of risk, which is further exacerbated in IL-4 -590 T carriers. These biomarkers, if validated in larger prospective studies, can be used to screen for gastric cancer susceptibility.

The significance of Helicobacter pylori (H. pylori) infection in pediatric abdominal pain remains poorly recognized. We examined associations of H. pylori infection and serum pepsinogens (PGs), as non-invasive markers of gastritis, with pediatric abdominal pain. A case-control study was conducted among 99 children aged 5-17 years admitted to one hospital for abdominal pain (cases) without an apparent organic reason. Using enzyme-linked immunosorbent assays, sera were tested and compared with 179 controls for anti-H. pylori immunoglobulin G (IgG) antibodies and PGI and PGII levels. Multivariable analysis was performed to adjust for potential confounders. H. pylori IgG sero-positivity was 34.3 and 36.3% in cases and controls, respectively, P = 0.7. H. pylori-infected children had higher median PGI and PGII levels and a lower PGI/PGII ratio than uninfected children. Cases infected with H. pylori had a higher median PGII level (P < 0.001) and lower PGI/PGII ratio (P = 0.036) than controls infected with H. pylori. The percentage of cases with PGII ≥7.5 μg/L, as indication for antral inflammation, was higher than in controls: 58.6 versus 44.7%, P = 0.027. Children with PGII levels ≥7.5 μg/L had increased risk for abdominal pain: adjusted prevalence ratio 1.73 [95% confidence intervals 1.02, 2.93], P = 0.039., Conclusion: Children with increased serum PGII levels, as an indication of gastritis, are more likely to have abdominal pain. Serum PGs can be a useful non-invasive marker for gastritis, in evaluating children with severe abdominal pain with no apparent organic reason. What is Known: • The significance of Helicobacter pylori infection in pediatric abdominal pain remains debated. • Serum pepsinogens (PGs), non-invasive markers of gastric inflammation, were rarely utilized in assessing the association between H. pylori in pediatric abdominal pain of unknown origin. What is New: • High serum PGII level, as an indication of gastritis, rather than H. pylori infection itself, was associated with increased risk for abdominal pain. • Serum PGs can be a useful biomarker for gastritis in evaluating children with severe abdominal pain with no apparent organic reason.

Aim: To develop a novel Helicobacter pylori ( H. pylori ) CagA antibody enzyme-linked immunosorbent assay (ELISA) suitable for detecting serum anti-CagA antibodies with high sensitivity., Methods: Recombinant East Asian-type CagA protein was purified and immobilized for ELISA. Serum samples from 217 Vietnamese individuals (110 H. pylori -infected and 107 uninfected individuals) were applied. Conventional ELISA from Western-type CagA and our East Asian-type CagA ELISA were evaluated by comparing 38 subjects with the Western-type genotype and 72 subjects with the East Asian-type cagA genotype. Histological scores of the gastric mucosa were determined using the updated Sydney System to examine the relationship with anti-CagA antibody titers., Results: Recombinant 70-100 kDa fragments were immobilized on the ELISA plate. In ROC analysis, the area under the curve of our East Asian-type CagA ELISA was comparable to that of conventional CagA ELISA. The sensitivity of the two ELISAs differed depending on the cagA genotype. The sensitivity of East Asian-type CagA ELISA was higher for subjects infected with East Asian-type cagA H. pylori ( P < 0.001), and the sensitivity of the conventional CagA ELISA tended to be higher for subjects infected with Western cagA H. pylori ( P = 0.056). The titer of anti-CagA antibody tended to correlate with monocyte infiltration scores ( r = 0.25, P = 0.058) and was inversely correlated with H. pylori density ( r = -0.26, P = 0.043)., Conclusion: The novel ELISA is useful to detect anti-CagA antibodies in East Asian countries, and the titer may be a marker for predicting chronic gastritis.

Helicobacter pylori infection shows a worldwide prevalence of around 50%. However, only a minority of infected individuals develop clinical symptoms or diseases. The presence of H. pylori virulence factors, such as CagA and VacA, has been associated with disease development, but assessment of virulence factor presence requires gastric biopsies. Here, we evaluate the H. pylori recom Line test for risk stratification of infected patients by comparing the test score and immune recognition of type I or type II strains defined by the virulence factors CagA, VacA, GroEL, UreA, HcpC, and gGT with patient's disease status according to histology. Moreover, the immune responses of eradicated individuals from two different populations were analysed. Their immune response frequencies and intensities against all antigens except CagA declined below the detection limit. CagA was particularly long lasting in both independent populations. An isolated CagA band often represents past eradication with a likelihood of 88.7%. In addition, a high recom Line score was significantly associated with high-grade gastritis, atrophy, intestinal metaplasia, and gastric cancer. Thus, the recom Line is a sensitive and specific noninvasive test for detecting serum responses against H. pylori in actively infected and eradicated individuals. Moreover, it allows stratifying patients according to their disease state.

The present study is done to study different aspects of Helicobacter pylori (H. pylori) such as its prevalence, association with upper gastrointestinal pathology, diagnosis and treatment outcome. Gastric antral biopsy and serology for H. pylori was done for all dyspeptic patients. Histopathology, gram stain and biopsy urease test was done from the gastric biopsy specimen. The prevalence of H. pylori infection was 58.8%. The sensitivity, specificity, positive and negative predictive value for histopathology was 96.9%, 100%, 100% and 95.8%, respectively; for biopsy urease test 80.4%, 100%, 100% and 78.2%, respectively; for gram stain 85.6%, 97.1%, 97.6% and 82.5%, respectively, and for serology 94.8%, 77.9%, 86% and 91.4%, respectively. Mostly peptic ulcer and duodenitis cases followed by chronic active gastritis were associated with H. pylori infection. Repeat biopsy revealed eradication of H. pylori in 90.7% cases. In dyspeptic patients, endoscopic biopsy not only detects H. pylori infection, but also reveals different gastric pathologies., (© The Author(s) 2016.)

Endoscopic findings of the background gastric mucosa are important in the Helicobacter pylori-seroprevalent population. It is strongly correlated not only with the risk of gastric cancer, but also with the excretion ability of gastric mucosa cells. In noninfected subjects, common endoscopic findings are regular arrangement of collecting venules, chronic superficial gastritis, and erosive gastritis. In cases of active H. pylori infection, nodularity on the antrum, hemorrhagic spots on the fundus, and thickened gastric folds are common endoscopic findings. The secreting ability of the gastric mucosa cells is usually intact in both noninfected and actively infected stomachs, and the intragastric condition becomes hyperacidic upon inflammation. Increased serum pepsinogen II concentration correlates well with active H. pylori infection, and also indicates an increased risk of diffuse-type gastric cancer. In chronic inactive H. pylori infection, metaplastic gastritis and atrophic gastritis extending from the antrum (closed-type chronic atrophic gastritis) toward the corpus (open-type chronic atrophic gastritis) are common endoscopic findings. The intragastric environment is hypoacidic and the risk of intestinal-type gastric cancer is increased in such conditions. Furthermore, there is a decrease in serum pepsinogen I concentration when the secreting ability of the gastric mucosa cells is damaged. Serologic and endoscopic changes that occur upon H. pylori infection are important findings for estimating the secreting ability of the gastric mucosa cells, and could be applied for the secondary prevention of gastric cancer., Competing Interests: No potential conflict of interest relevant to this article was reported.

Background: Ghrelin has been indicated as one of the etiological factors in functional dyspepsia (FD)., Methods: We analyzed 179 patients with FD (based on the Rome III criteria) and 103 asymptomatic healthy individuals (controls) who had undergone endoscopy at Seoul National University Bundang Hospital from February 2011 to June 2014. FD patients were classified into three groups by means of a self-reported questionnaire: patients with postprandial distress syndrome (PDS; n = 49), patients with epigastric pain syndrome (EPS; n = 45), and patients with a combination of these two types (mixed group; n = 85). The fasting blood levels of acyl ghrelin and desacyl ghrelin and messenger RNA (mRNA) expression of preproghrelin in the fundic mucosa were measured by ELISAs and reverse transcription quantitative real-time PCR, respectively. One year after participant enrollment, they were measured again in 79 participants and the changes in the values were compared according to Helicobacter pylori eradication or symptom response., Results: Plasma acyl ghrelin level was lower in the PDS group than in the control and EPS groups (control group 14.1 fmol/mL, PDS group 8.9 fmol/mL, EPS group 13.8 fmol/mL, mixed group 11.3 fmol/mL; P = 0.003 and P = 0.012, respectively). One year after the eradication of H. pylori, plasma acyl ghrelin level was increased and gastric preproghrelin mRNA expression was upregulated (P = 0.004 and P < 0.001, respectively). Patients with abatement of symptoms demonstrated an increase in plasma acyl ghrelin level (from 11.51 to 21.00 fmol/L, P = 0.040)., Conclusions: Our results suggest that plasma acyl ghrelin plays a role in the development of PDS. H. pylori eradication upregulates preproghrelin mRNA expression and increases plasma acyl ghrelin level, contributing to the abatement of PDS symptoms.

Serum pepsinogen I and II are considered as indicators of changes in gastric morphology. Important publications from the last decades are reviewed with regard to the serum level of these biomarkers for the diagnosis of normal gastric mucosa, diffuse gastritis and its change to atrophic gastritis and intestinal metaplasia as well as gastric cancer. Due to the low sensitivity of serum biomarkers for diagnosis of gastric cancer, especially at its early stage and the poor prognosis of the tumor at the time of diagnosis, its prevention by eradication of H. pylori remains the mandatory strategy. On the other hand, the severity of regression and non-reversibility of precancerous lesions and intestinal metaplasia in gastric mucosa through eradication of H. pylori make it necessary to diagnose diffuse gastritis at its early stage. Increased serum pepsinogen II compared to normal serum pepsinogen I seems to indicate the presence of diffuse gastritis without precancerous lesions suitable for eradication of H. pylori infection, when it is serologically positive. A diagram illustrates the strategy of this therapeutic measure depending on the age of people and the level of serum biomarkers in areas with high gastric cancer prevalence.

Objective: To assess the role of Helicobacter pylori infection and interleukin 6 polymorphism -174 (rs1800795) in dyslipidemia., Design: Case-control study comparing serum lipids between H. pylori positive and negative patients and controlling for IL-6 -174 polymorphism, age, sex and smoking., Setting: 3 hospitals performing outpatient endoscopies in the city of Oulu, Finland., Participants: 199 adult patients with dyspepsia symptoms fulfilling Rome criteria originating from ethnically Finnish population. Patients with an immunosuppressive disorder or malignant disease, treated H. pylori infection, immunosuppressive or anticoagulant medication, previous gastric surgery or ongoing antibiotic treatment were excluded., Primary Outcome Measures: Association of H. pylori infection and serum lipid concentrations in the whole group or in genotype-based subgroups. The associations between peptic ulcer, gastric mucosal inflammation and serum lipid concentrations were assessed as secondary outcomes., Results: The median high-density lipoprotein (HDL) serum concentration was significantly lower in the H. pylori positive group (0.81 mmol/L) than in the negative group (0.95 mmol/L; p<0.001). In the genotype subgroup analyses, a similar association between H. pylori infection and HDL serum levels was seen within the IL-6 -174 CC genotype group (HDL 0.72 vs 1.06 mmol/L, respectively; p<0.001), but no significant associations were seen in the GC or GG genotype groups. Additionally, patients with peptic ulcer demonstrated lower HDL levels (0.75 mmol/L) than H. pylori positive patients without ulcer (0.86 mmol/L; p=0.010)., Conclusions: H. pylori infection associated significantly with low serum levels of HDL in the IL-6 -174 CC genotype patients but not in the other genotypes. This suggests that the association between H. pylori infection and serum HDL could be transmitted through IL-6. We suggest that the role of IL-6 genotype should also be studied in relation to other associations between gastrointestinal microbiome and cardiovascular risk factors., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/)

Background: Recently, a great variety of studies aimed to investigate and even suggest Helicobacter pylori as an important key factor in gastrointestinal and non-gastrointestinal events development. The well-established relationship between bacterial virulence and increased risk for peptic ulcer or gastric carcinoma is not so clear when comparing inflammation markers alterations, such C-reactive protein, with the pathogen., Objective: The objective of this study was to evaluate the presence of H. pylori, bacterial virulence and C-reactive protein serum levels in individuals diagnosed with functional dyspepsia., Methods: Were prospectively included in this study 489 dyspeptic individuals. They fulfill Rome III clinical criteria for the diagnosis of functional dyspepsia with no organic disease at endoscopy. The bacterial infection was established by histology and urease rapid test. The levels of serum C-reactive protein were obtained by immunonefelometry and CagA status of H. pylori positive individuals was determined through an imunoenzimatic assay., Results: Prevalence rate of H. pylori was 66.3% and virulence factor CagA was detected in nearly 43% of positive samples. In addition, it has been noticed an association between Ilex paraguariensis (yerba maté) consumption and pathogen's prevalence. An important effect of bacterial infection on inflammation was only observed in gastric epithelium., Conclusion: No systemic response to the pathogen, measured through C-reactive protein levels, was observed, regardless of CagA status. Otherwise, the intake of yerba maté should be considered as a cultural factor possibly related to H. pylori's transmission.

Iron deficiency anemia (IDA) affects > 500 million people worldwide, and is linked to impaired cognitive development and function in children. Helicobacter pylori, a class 1 carcinogen, infects about half of the world's population, thus creating a high likelihood of overlapping risk. This study determined the effect of H. pylori infection on iron homeostasis in INS-GAS mice. Two replicates of INS-GAS/FVB male mice (n = 9-12/group) were dosed with H. pylori (Hp) strain SS1 or sham dosed at 6-9 weeks of age, and were necropsied at 27-29 weeks of age. Hematologic and serum iron parameters were evaluated, as was gene expression in gastric and brain tissues. Serum ferritin was lower in Hp SS1-infected mice than uninfected mice (p < 0.0001). Infected mice had a lower red blood cell count (p<0.0001), hematocrit (p < 0.001), and hemoglobin concentration (p <0.0001) than uninfected mice. Relative expression of gastric hepcidin antimicrobial peptide (Hamp) was downregulated in mice infected with Hp SS1 compared to sham-dosed controls (p<0.001). Expression of bone morphogenic protein 4 (Bmp4), a growth factor upstream of hepcidin, was downregulated in gastric tissue of Hp SS1-infected mice (p<0.001). Hp SS1-infected mice had downregulated brain expression of tyrosine hydroxylase (Th) (p = 0.02). Expression of iron-responsive genes involved in myelination (myelin basic protein (Mbp) and proteolipid protein 2 (Plp2)) was downregulated in infected mice (p = 0.001 and p = 0.02). Expression of synaptic plasticity markers (brain derived neurotrophic factor 3 (Bdnf3), Psd95 (a membrane associated guanylate kinase), and insulin-like growth factor 1 (Igf1)) was also downregulated in Hp SS1-infected mice (p = 0.09, p = 0.04, p = 0.02 respectively). Infection of male INS-GAS mice with Hp SS1, without concurrent dietary iron deficiency, depleted serum ferritin, deregulated gastric and hepatic expression of iron regulatory genes, and altered iron-dependent neural processes. The use of Hp SS1-infected INS-GAS mice will be an appropriate animal model for further study of the effects of concurrent H. pylori infection and anemia on iron homeostasis and adult iron-dependent brain gene expression.

Background: Chronic tissue damage induced by Helicobacter pylori (HP)-driven inflammation is considered the main risk of gastric carcinoma (GC). Epstein–Barr virus (EBV) infection has also been associated with GC. In this study, we aim to address the role of EBV in inflammatory GC precursor lesions and its added risk to HP infection., Methods: Antibodies against EBV, HP and the bacterial virulence factor CagA were measured in sera from 525 Mexican and Paraguayan patients with gastric disease. Gastric samples were characterised according to the updated Sydney classification and associations were estimated between antibody responses and severity of both tissue damage and inflammation., Results: We found significant associations (odd ratios and trends) between EBV and HP copositivity and premalignant lesions and intestinal-type GC. The EBV and HP coinfection was also significantly associated with increased infiltration of immune cells. No association was found between EBV and the less inflammation-driven diffuse-type GC., Conclusions: Our study suggests that EBV co-participates with HP to induce severe inflammation, increasing the risk of progression to intestinal-type GC.

The analysis of noninvasive diagnostics of a phenotype of gastritis among 1050 people aged from 18 till 80 years which consistently addressed to policlinic is presented in the article. The instrument of diagnostics was a <>, including a complex of biomarkers - so-called <> (pepsinogen I, pepsinogen II, gastrin-17 and IgG- antibodies to Helicobacter Pylori). High frequency of different variants of atrophic gastritis (25%) with a gastric cancer risk and conditions with a risk of erosive and ulcer damages of the stomach mucous (26 %) was shown. Clinical and economical expediency of noninvasive screening of a phenotype of gastritis is postulated.

Background: Helicobacter pylori (H.pylori) is associated with chronic gastritis, peptic ulcers, gastric adenocarcinomas and mucosa associated tissue lymphomas. Cytotoxin associated gene A (CagA) is one of the virulence factors of H.pylori. It is hypothesized that reactive oxygen species (ROS) play roles in H.pylori associated disease especially in development of gastric adenocarcinoma. Individuals infected with H.pylori bearing CagA produce more ROS than others. 8-hydroxydeoxyguanosine (8OHdG) is an in vitro marker of DNA damage and oxidative stress. The aim of this study was to investigate the relationship between 8OHdG level, H.pylori infection and CagA and alterations of serum 8OHdG level after H.pylori eradication., Materials and Methods: Patients admitted with dyspeptic complaints and upper gastrointestinal endoscopy were assessed. H.pylori was determined from histopathology of specimens. Serum 8OHdG levels of three groups (H.pylori negative, H. pylori positive CagA negative and H.pylori positive CagA positive) were compared. Patients with H.pylori infection received eradication therapy. Serum 8OHdG levels pretreatment and posttreatment were also compared., Results: In total, 129 patients (M/F, 57/72) were enrolled in the study. Serum 8OHdG level of H.pylori negative, H. pylori positive CagA negative and H.pylori positive CagA positive groups were significantly different (5.77±1.35 ng/ml, 5.43±1.14 ng/ml and 7.57±1.25 ng/ml respectively, p=0.05). Furthermore, eradication therapy reduced serum 8OHdG level (6.10±1.54 ng/ml vs 5.55±1.23 ng/ml, p=0.05)., Conclusions: Individuals infected with H.pylori bearing CagA strains have the highest serum 8OHdG level and eradication therapy decreases the serum 8OHdG level. To the best of our knowledge this is the first study that evaluated the effect of CagA virulence factor on serum 8OHdG level and the effect of eradication therapy on serum 8OHdG levels together. Eradication of CagA bearing H.pylori may prevent gastric adenocarcinoma by decreasing ROS. 8OHdG level may thus be a good marker for prevention from gastric adenocarcinoma.

Objective: To study immunization procedures and preparation methods of specific IgY antibodies (IgY-Hp, IgY-IB) produced by hens immunized with Helicobacter pylori (Hp) bacterial antigen and recombinant Hp specific antigen IB, detect the inhibition effects on Hp growth and Hp urease activity, and study the effects of oral administration for treating Hp infection., Methods: By using recombinant cholera toxin subunit B (rCTB) as an adjuvant, hens received intramuscular injection immunization for continuous 7 times at an interval of 14 days. Then, the eggs were collected; IgY was purified., Results: On day 49 after hens were immunized, levels of two antibodies all reached 1:12800; after they were purified by Ammonium sulfate precipitation, their purity was over 80%. IgY-Hp could inhibit Hp growth and inhibit Hp urease activity; although in vitro, IgY-IB could not inhibit Hp growth but could inhibit Hp urease activity. The experiments in vivo found that when IgY-Hp or IgY-IB with sucralfate dual oral therapy was used to treat Hp infected mouse model, the cure rate all could reach 83.3%., Conclusion: According to immunization procedure, high titer specific IgY antibody (1:12800) can be obtained in 49 days and its titer remains stable. Oral administration of the specific IgY antibodies in Hp infected mice can reach a cure rate of 83.3%, and the antibodies are expected to become new drugs and therapeutic methods of targeted therapy against Hp infection.

OBJECTIVE. Clinical implications of serum anti-Helicobacter pylori immunoglobulin G (IgG) titer were unclear. This study investigated the associations of serum anti-H. pylori IgG titer with grade of histological gastritis, mucosal bacterial density and levels of serum biomarkers, including pepsinogen (PG) I, PGII, PGI/II ratio and gastrin-17. MATERIAL AND METHODS. Study participants were from a screening program in northern China. Serum anti-H. pylori IgG measurements were available for 5922 patients with superficial gastritis. Serum anti-H. pylori IgG titer and serum biomarkers were measured using ELISA, and gastric biopsies were evaluated using standardized criteria. RESULTS. In patients with mild, moderate or severe superficial gastritis, the mean serum anti-H. pylori IgG titers were 17.3, 33.4 and 54.4 EIU (p for trend < 0.0001), respectively. As mucosal H. pylori density score increased from 0 to 3, the mean serum anti-H. pylori IgG titers also increased from 24.7 to 44.8 EIU (p for trend < 0.0001). Serum anti-H. pylori IgG titer was associated positively with serum PGI, PGII and gastrin-17 concentrations and negatively with PGI/II ratio, and the association was the strongest for PGII. The mean PGII concentration of the patients in the highest quartile of IgG titer was twice the mean concentration of the patients in the lowest quartile (17.2 vs. 8.6 EIU, p < 0.0001). CONCLUSIONS. Our results suggest that serum anti-H. pylori IgG titer was associated positively with grade of histological gastritis, mucosal bacterial density and concentrations of serum PGI, PGII and gastrin-17, and negatively with PGI/II ratio.

Irrespective of its etiology, long-standing, non-self-limiting gastric inflammation (mostly in Helicobacter pylori-associated cases) is the cancerization ground on which epidemic (intestinal-type) gastric carcinoma (GC) can develop. The natural history of invasive gastric adenocarcinoma encompasses gastritis, atrophic mucosal changes, and intraepithelial neoplasia (IEN). The topography, the extent and the severity of the atrophic changes significantly correlate with the risk of developing both IEN and GC. In recent years, both noninvasive (serological) tests and invasive (endoscopy/biopsy) procedures have been proposed to stratify patients according to different classes of GC risk. As a consequence, different patient-tailored GC secondary prevention strategies have been put forward. This review summarizes the histological features of H. pylori-related gastritis and the natural history of the disease. Histological and serological strategies to assess GC risk as well as the clinical management of atrophic gastritis patients are also discussed., (© 2014 S. Karger AG, Basel.)

Background: Chronic inflammation triggered by Helicobacter pylori causes altered DNA methylation in stomach mucosae, which is deeply involved in gastric carcinogenesis. This study aimed to elucidate the correlation between altered mucosal DNA methylation levels and activity of H. pylori-related gastritis, because inflammatory activity shows particular correlations with the development of diffuse-type cancer., Methods: Methylation levels in stomach mucosae of 78 healthy volunteers were determined by real-time methylation-specific PCR or bisulfite pyrosequencing. Examined loci were the promoter CpG islands of six genes (FLNc, HAND1, THBD, p41ARC, HRASLS, and LOX) and the CpG sites of non-coding repetitive elements (Alu and Satα) that are reportedly altered by H. pylori infection. Activity of H. pylori-related gastritis was evaluated using two serum markers: H. pylori antibody titer and pepsinogen II., Results: Methylation levels of the six CpG islands were consistently increased, and those of the two repetitive elements were consistently decreased in a stepwise manner with the activity of gastric inflammation as represented by serum marker levels. Each serum marker level was well correlated with the overall DNA methylation status of stomach mucosa, and these two serologic markers were additive in the detection of the mucosa with severely altered DNA methylation., Conclusions: Alteration in mucosal DNA methylation level was closely correlated with activity of H. pylori-related gastritis as evaluated by serum markers. The observed correlation between altered DNA methylation levels and activity of H. pylori-related gastritis appears to be one of the relevant molecular mechanisms underlying the development of diffuse-type cancer.

Surveyed 119 men in flight personnel. All were performed esophagogastroduodenoscopy and morphological study of biopsy material. Level of specific antibodies to Helicobacter pylorus (Hp) by enzyme immunoassay was determined, performed breathing Helika-test; Hp was determined by cytological method. Performed acidogastrometry. In 8 patients revealed erosive antral gastritis, 99--chronic gastritis, 12 patients have no stomach or duodenal ulcers. All patients with erosive gastritis were infected with Hp. antibodies to Hp were detected in all patients with chronic gastritis, and Helika-test and cytology for Hp were negative in 18.2% of patients in this group.

Lymphocytic gastritis (LG) is a chronic inflammatory process of poorly understood pathogenesis. We report the case of a 12-year-old premenstrual girl with refractory iron deficiency anemia in which the oral iron absorption challenge suggested iron malabsorption. Laboratory studies ruled out celiac disease and autoimmune gastritis, and carbon-13 urea breath test for Helicobacter pylori was also negative. Upper endoscopy with gastric body and antral mucosa biopsies revealed a LG with focal intestinal metaplasia and H. pylori infection. H. pylori eradication was undertaken with success and 3 months later her hematologic parameters normalized. Histologic reevaluation showed disappearance of LG. This case shows that investigation of malabsorption disease in the presence of refractory iron deficiency anemia can lead to the diagnosis of important gastric diseases, even in the absence of gastrointestinal symptoms. This nonceliac child was diagnosed with a severe histopathologic pattern of LG, with potential risk of malignant transformation, which was completely reverted with adequate H. pylori eradication treatment.

There are conflicting views about the association between type A gastritis with pernicious anemia (PA) and infection with Helicobacter pylori, and currently, no definite conclusion has been reached. In this study, we evaluated H. pylori infection in patients with type A gastritis who developed PA. The study included a total of 25 Japanese patients (13 males and 12 females) who had been diagnosed with PA at our department, with a mean age of 71.2 years. We diagnosed infection with H. pylori by measuring serum H. pylori-IgG antibodies in all 25 patients, and we performed gastric biopsy in 17 patients. They were all negative for H. pylori-IgG antibody (0/25) and H. pylori on gastric biopsy (0/17). Although the prevalence of H. pylori infection (70-80 %) in our age-matched controls in Japan is higher than the prevalence in similar populations in western countries, we believe that type A gastritis with PA is very poorly associated with H. pylori infection.

The role of Helicobacter pylori status and serum zinc value in gastric disease patients and healthy controls were investigated. Cases used in this work were 45 gastric cancer patients, 44 with peptic ulcers, 52 suffering gastritis and 64 healthy controls, all diagnosed histologically with the controls undergoing medical checkups. Helicobacter pylori status and serum levels of Zn were determined by 13C-urea breath test and flame atomic absorption spectrophotometer, respectively. Our study showed that Helicobacter pylori infection has no change in gastritis, peptic ulcer and gastric cancer group, on the contrast, serum levels of Zn were significantly reduced in gastritis, peptic ulcer and gastric cancer group, compared with healthy controls, and the higher the Zn levels are, the more increased risk of gastric cancer. Helicobacter pylori infection is a cause of gastritis, peptic ulcers and even gastric cancer, while serum zinc level is an indicator of protection of gastric membranes against damage.

Background/aims: Autoimmune gastritis (AIG) may predispose to gastric carcinoid tumors or adenocarcinomas and may also cause unexplained iron and/or vitamin B(12) deficiency. The aims of this study were to explore clinical manifestations, endoscopic findings and laboratory features of patients with AIG., Methods: 109 patients with AIG were enrolled into the study. In addition to demographic and clinical data, gastric lesions, serum gastrin, vitamin B(12), antiparietal cell antibody (APA), current Helicobacter pylori status, and anti-H. pylori IgG were also investigated., Results: The mean age of the patients was 53.06 ± 12.7 years (range 24-81; 72 (66.1%) women). The most common main presenting symptom was abdominal symptoms in 51 patients, consultation for iron and/or vitamin B(12) deficiency in 36, and non-specific symptoms including intermittent diarrhea in 15 patients. Endoscopic lesions were detected in 17 patients, hyperplastic polyps in 8, gastric carcinoid tumor in 4, fundic gland polyps in 3, and adenomatous polyps in 2 patients. H. pylori was negative in all patients in biopsy specimens; however, anti-H. pylori IgG was positive in 30 (27.5%) patients. 91 patients (83.4%) were positive for APA., Conclusion: In patients with AIG, the main symptoms prompted for clinical investigation were: abdominal symptoms, iron/B(12) deficiency and non-specific symptoms. 20% of patients with AIG had various gastric lesions including type I gastric carcinoids. None of the patients were positive for H. pylori by means of invasive tests; however, anti-H. pylori IgG was found in 27.5% of patients. Patients referring with non-specific abdominal symptoms such as bloating, diarrhea and iron/B(12) deficiency should be investigated for the presence of AIG., (Copyright © 2012 S. Karger AG, Basel.)

Objective: To evaluate the clinical manifestations, endoscopic, and radiological characteristics, histological features, and treatment of eosinophilic gastroenteritis in adult patients., Methods: The clinical records of 34 patients diagnosed as eosinophilic gastroenteritis and eight patients who had abdominal symptoms and unexplained peripheral eosinophilia but no evidence of tissue eosinophilic infiltration were reviewed and analyzed., Results: Thirteen patients had a history of asthma or allergic rhinitis, while 10 had an allergic history. Peripheral eosinophilia occurred in 83.3% of patients, IgE was elevated in half, and α2-macroglobulin was elevated in 92.8% of patients. The small intestine(82.4%)was the most common site involved. Erythema was the predominate feature seen on endoscopy. Radiographic study generally revealed thickening of the small intestinal wall. Eosinophilia generally involved the lamina propria of mucosa, but any layer of the gut could be affected, even in sites which had normal endoscopic or radiographic appearance. In all, 15.4% (6/39) of patients had Helicobacter pylori infection. Symptom remission within 1 week was found in 80% (20/25) of patients treated with steroids and in 58.8% (10/17) of patients treated with symptomatic treatment. In all, 85.7% (18/21) of patients had their eosinophil counts return to normal within 2 weeks in the steroid treatment group, but none (0/13) in the other group., Conclusion: Eosinophilic gastroenteritis may be more common than previously recognized. Multiple biopsies obtained from the both normal and abnormal appearing areas in the second part of the duodenum are highly recommended. Steroids are effective in relieving symptoms and improving eosinophilia.

Objective: Gastritis induced by Helicobacter pylori can cause the onset of gastric cancer, and H. pylori cytotoxin associated gene A (cagA) is considered to be an important factor for its development. We investigated the relationship between the grades of gastritis and cagA phenotype in Japanese and Brazilian patients., Material and Methods: We studied 47 Brazilian and 47 age-, gender-matched Japanese patients. Status of H. pylori infection, the degree of histologic gastritis, and the levels of serum pepsinogen levels were evaluated. DNA was extracted from paraffin-embedded sections and a portion of the cagA gene was amplified using the polymerase chain reaction, followed by direct sequencing of the fragment. We investigated the cagA subtype using a newly developed restriction fragment length polymorphism (RFLP) system., Results: In H. pylori-positive patients, the grades of histological and serological gastritis were more prominent in the Japanese subjects than their Brazilian counterparts, although no difference was detected in the H. pylori-negative subjects. According to cagA phenotype analysis, our RFLP system was helpful for evaluating cagA phenotype, and we found that the prevalence of the East Asia subtype was significantly higher in the Japanese subjects than in the Brazilian., Conclusion: Infection with H. pylori possessing the East Asian cagA gene contributes to the progression of gastritis.

Background: Helicobacter pylori causes gastritis and is the most important risk factor of peptic ulcer disease and gastric cancer. In chronic adulthood H. pylori infection some matrix metalloproteinases (MMPs), which are proteolytic metalloendopeptidases regulated by tissue inhibitors of metalloproteinases (TIMPs), are upregulated. Our aim was to determine circulating levels of MMPs and their regulators TIMP-1, human neutrophil elastase (HNE) and myeloperoxidase (MPO) in childhood H. pylori infection., Design and Methods: Twenty-six H. pylori positive and 34 H. pylori negative children whose H. pylori status was verified by histological examination of gastric biopsies were included. Serum samples were analysed by enzyme-linked immunosorbent assay., Results: Significantly decreased serum levels of TIMP-1 were detected in H. pylori-infected children (median, 97.50 ng/mL) as compared to H. pylori-negative children (median, 118.5 ng/mL, p = 0.003). However, there were no significant differences in serum levels of MMP-2, -7, -8, -9, and their regulators HNE and MPO between H. pylori-positive and -negative children., Conclusions: Differing from the recent findings in adulthood H. pylori infection, only circulating TIMP-1 levels were significantly different between H. pylori-positive and -negative children. Whether this reflects the first sign of a proteolytic cascade later leading to increased levels of MMPs remains to be shown.

Objective: Helicobacter pylori (HP) is a cause of chronic gastritis. Beta-2 microglobulin has been used as a simple inflammatory indicator in some diseases. We investigate the usability of beta-2 microglobulin as a simple marker that may reflect the severity of inflammation and intensity of HP in gastric mucosa., Materials and Methods: A total of 114 patients was included in the study, who applied to an outpatient gastroenterology clinic with complaint of dyspepsia. Serum beta-2 microglobulin levels were evaluated in 109 patients. Esophagogastroduodenoscopy was performed on patients included in the study, and histological analysis was performed by obtaining two specimens from each of antrum, corpus, and incisura angularis. All specimens were evaluated according to the updated Sydney System., Results: No statistically significant result was found between serum beta-2 microglobulin levels and the intensity of HP and the severity of inflammation of gastric mucosa. However, it was observed that the serum beta-2 microglobulin level in specimens taken from corpus was found to be higher in patients with moderate-severe HP intensities compared to those with lower HP intensities., Conclusions: Although HP is the cause of the chronic active gastritis characterized with the infiltration of lymphocytes, plasma cells, and neutrophils, it is accompanied by local involvement apart from diseases with a course of systemic involvement. We suggest that the serum beta-2 microglobulin level cannot be used as a simple marker of HP intensity and severity of inflammation in gastric endoscopic biopsies.

Helicobacter pylori is a cause of chronic gastritis. Mean platelet volume (MPV) has been started to be used as a simple inflammatory indicator in some diseases. We have aimed especially to investigate the usability of MPV as a simple indicator that may reflect severity of inflammation in gastric mucosa. Included in the study were a total of 114 patients who visited the outpatient clinic of gastroenterology with complaint of dyspepsia. Blood MPV levels in hemogram results were evaluated. Esophagogastroduodenoscopy was performed on patients included in the study, and histological analysis was performed by obtaining 2 specimens from each of antrum, corpus, and incisura angularis. All specimens were evaluated according to the updated Sydney System. No statistically significant result was found among blood MPV levels, the intensity of H pylori, and the severity of inflammation of gastric mucosa. However, it is interesting that mean MPV levels in cases with lymphoid follicle were lower. We suggest that MPV level cannot be used as a simple marker to reflect H pylori intensity and severity of inflammation in gastric endoscopic biopsies.

Helicobacter pylori (HP) chronic gastritis can lead to precursor stages of gastric cancer. New biological markers have been proposed to study the gastric mucosal state. We evaluate biological results in comparison with histological ones in a dyspeptic population. Forty nine dyspeptic patients underwent endoscopy with gastric biopsies for histological examination. Blood samples were obtained to measure levels of gastrin 17 (G17), pepsinogen 1 (PG1), pepsinogen 2 (PG2) and the rate of anti-HP IgG antibodies. Four patients have a healthy gastric mucosa and 45 have a gastritis (32 have a nonatrophic gastritis and 13 an atrophic one). An increase in the level of PG2 and a decrease of the PG1/PG2 ratio were noticed in the group of subjects with a nonatrophic gastritis compared to the healthy mucosa group. The decrease of the PG1/PG2 ratio was more important in the corpus atrophic gastritis group than in the antrum restricted atrophic gastritis one. In conclusion, in front of dyspeptic patients, we advice to practice in first intention the measurement of the serological level of G17, PG1, PG2 and anti-HP IgG antibodies.

Aim: to find out biomarker as diagnostic tool of H. pylori chronic gastritis., Methods: the design of present study was a diagnostic test and there were 104 subjects with H. pylori chronic gastritis who fulfilled the inclusion and exclusion criteria. The diagnosis of H. pylori chronic gastritis was based on histopathological examination and PCR with ureC primer of the gastric biopsy specimen. In addition, we also performed the examination of serum gastrin, pepsinogen (PG) I and PG (pepsinogen) II level. By using analysis of receiver operating characteristic (ROC), an optimal cut off point of serum gastrin, PGI and PGII level as well as PGI/PGII ratio was determined. Analysis of bivariate logistic regression was used to determine the involved independent variables and possibilities as biomarkers. Significance level was determined by p value <0.05., Results: we found optimal cut off points on serum gastrin, PGI and PGII level as well as the PGI/PGII ratio at 5.89 pmol/L; 82.5 µg/L; 6.48 µg/L and 13.6 respectively. By using the analysis of bivariate logistic regression, we found gastrin level with p = 0.078 (OR 2.75;95%CI 0.89-8.45) and PGI/PGII ratio with p = 0.000 (OR 14.63;95%CI 3.55-60.63). The opportunity of gastrin level and PGI/PGII ratio as biomarkers was 0.8 with 47% sensitivity, 83% specificity, 74% PPV, 61% NPV, 65% accuracy, LR+ = 2.76 and LR- = 0.64., Conclusion: gastrin level of >5.89 pmol/L and PGI/PGII ratio ≤13.6 can be utilized as biomarkers of H. pylori chronic gastritis.

Persistent infection with Helicobacter pylori confers an increased risk of peptic ulceration and gastric adenocarcinoma. Reactive oxygen and nitrogen species play a crucial role in the progression from normal gastric mucosa to cancer. The aim of the present study was to investigate the plasma malondialdehyde and nitric oxide levels in H. pylori related gastroduodenal diseases and associate their levels with gastric pathology and genotypes of H. pylori. Malondialdehyde and nitric oxide levels in plasma samples of 250 subjects were spectrophotometrically determined. Subsequently, genotypic and histopathological assessment was performed in gastric biopsies obtained during endoscopy. The levels of MDA and NO exceeded in subjects infected with genotype-1 of Hp than those with other genotypes suggesting more precise interaction of highly virulent strains of Hp in eliciting severe tissue damage. In conclusion, the study demonstrates close relationship between the plasma malondialdehyde and nitric oxide levels, gastric histopathology and genotypes of H. pylori.

31 bioptates in the antral mucosa of 24 patients with a chronic gastritis and a body of a stomach for revealing H. pylori were being analysed and for the further studying morpho-immunology communications. The presence of H. pylori in bioptates, gastrits's activity (leukocytic infiltration), gastrits's degree evidence, also eosinophilus's presence and IgE containing plasmocytus had correlated with antibodies titre to H. pylori. After inspection, at the majority of patients serum antibodies to H. pylori correlated with positive respiratory-test. Considering that high sensitivity and specificity of immune-enzyme detection of antibodies to H. pylori in theirs blood serum, this method side by side with respiratory-test can be used at the primary screening H. pylori infections. The Biotates morphological examination is the "golden standard" of H. pylori gastritis' diagnostic by it's informatively and diagnostic's importance.

The metabolism of the trace elements is altered in infection or inflammation. Helicobacter pylori infection is a causative in chronic gastritis, duodenal ulcer disease and gastric cancer. It is not known whether H. pylori infection is associated with the changes in the serum levels of trace elements. The aim of this study was to determine serum concentrations of zinc and copper, using atomic absorption spectrophotometer, in patients with H. pylori positive chronic gastritis, patients with H. pylori negative chronic gastritis and healthy individuals. Serum Zn was significantly higher in patients with H. pylori positive chronic gastritis compared to both patients with H. pylori negative chronic gastritis and to healthy individuals, while serum Cu and Cu/Zn ratio was not significantly different in any study group. The serum zinc and copper concentrations were not altered in patients with chronic gastritis.

Unlabelled: H. pylori is considered to be a major etiological agent of chronic gastritis. Mannan-binding lectin (MBL) is one of the key factors of the innate immunity. It belongs to collectins binding to saccharides on the surface of a variety of pathogenic microorganisms, H. pylori including. MBL after coating the bacteria is recognized by the receptor on macrophages, facilitates phagocytosis by direct opsonization and activates complement via the lectin pathway which protects the host against infection. Single nucleotide polymorphisms of MBL2 gene affect both MBL concentration and biological activity., Aim: Evaluation of the correlation between the occurrence of MBL2 gene mutations, MBL concentration in serum, and prevalence of duodenal ulcer and chronic gastritis with or without H. pylori infection., Material and Methods: The study comprised 174 children aged 6-17 years (mean 13.1 x 4.2), among them 74 children with H. pylori infection-associated chronic gastritis (group Hp+), 41 with H. pylori infection excluded (group Hp-), and 11 children with duodenal ulcer (DU). The control group consisted of 46 healthy children without gastritis, endoscopically checked. Determination of serum MBL concentration was performed using ELISA. Polymorphisms of the promoter region as well as mutations of exon 1 MBL2 gene were identified with polymerase chain reaction methods. H. pylori was detected with both urease test and histopathology Giemsa staining., Results: MBL serum concentration was significantly lower in children with both Hp+ (1809 ng/ml) and Hp-gastritis (1439 ng/ml) when compared to the control group (2545 ng/ml) (p < 0.05 and p < 0.01, respectively). The same trend (however the difference was insignificant) was observed in the case of DU group (1643 ng/ml). The frequency of MBL2 gene mutations did not differ between any group of patients as compared to controls., Conclusions: No influence of MBL2 genotype on the incidence of duodenal ulcer or gastritis was found. MBL serum concentrations are lower in chronic gastritis patients (with or without H. pylori infection) when compared to the age-matched healthy individuals.

Background: Helicobacter pylori is one of the most common causes of peptic ulcer disease worldwide and a major cause of chronic superficial gastritis leading to atrophy of gastric glands., Methodology: A total of 60 patients suffering from gastric disease due to H. pylori infection were evaluated. Endoscopy was performed and gastric biopsies were obtained for histopathology and urease test. Blood was simultaneously collected for the determination of the levels of vitamin B12 and the MCV. Vitamin B12 levels were determined by chemiluminescent assay., Results: Our results indicate that the mean vitamin B12 level +/- SEM for the total population, the H.pylori infected and non-infected patients were 264.5+/-22.9, 207.7+/-21.9 and 419.7+/-39.8 respectively. H. pylori was found in 71.7% (43/60) of the patients tested. The level of vitamin B12 was lower than 200pg/ml (deficient) in 67.4% (29/43) of patients tested positive for H. pylori., Conclusion: H. pylori appears to be implicated in causing vitamin B12 deficiency.

Objective: The course of Helicobacter pylori infection and antibody response to CagA in patients with preneoplastic lesions and gastric cancer has not been thoroughly studied. We aimed to study H. pylori infection and antibody response to CagA in patients with non-atrophic gastritis, preneoplastic lesions, and gastric cancer., Methods: We studied patients attending one Oncology Hospital and one General Hospital in Mexico City. Diagnosis was based on endoscopy and histopathology in biopsies from six stomach regions. H. pylori infection was assessed by histology and serology, and antibodies against CagA were measured with immunoassay., Results: We included 618 patients, 368 with non-atrophic gastritis, 126 with precancerous lesions, and 65 with gastric cancer; in addition, 59 patients with duodenal ulcer were studied. Detection of infection and IgG against CagA had a significant increase from non-atrophic gastritis to mild and up to advanced stages of metaplasia (P < 0.05), followed by decreased infection and IgG to CagA in patients with gastric cancer (P < 0.05). However, infection and CagA antibodies were associated with young gastric cancer cases. Duodenal ulcer showed a significant association with infection detected by histology and serology, particularly among women, and a trend to associate with IgG to CagA., Conclusions: This study shows that H. pylori infection and CagA are risk markers for intestinal metaplasia. The prevalence of these risk markers decreases in gastric cancer, probably reflecting that infection decreases after advanced atrophy and metaplasia in the gastric mucosa. State of the disease, age, and sex influence the association of H. pylori infection and IgG response to CagA with gastroduodenal diseases.

Background/aims: Immune response against Helicobacter pylori is important for the course and outcome of infection. We conducted study looking for the difference in anti H. pylori IgG and IgA between patients with intestinal type of gastric cancer, superficial and atrophic gastritis., Methodology: For this study, 133 patients infected with H. pylori were enrolled: 50 with superficial gastritis, 42 with atrophic gastritis and 41 with gastric cancer. Anti H. pylori IgG and IgA ELISA tests were performed. The difference in antibody titers of IgG and IgA, frequency of IgA > IgG ratio and combination of low IgG and IgA > IgG ratio were analyzed., Results: The patients with gastritis had higher titer of IgG that the patients with gastric cancer (p < 0.01). The patients with superficial gastritis had higher titer of IgA than the patients with gastric cancer (p < 0.05). IgA > IgG ratio is more frequent in patients with gastric cancer than in the patients with superficial gastritis (p < 0.01). Low IgG and IgA > IgG is more frequent in the patients with gastric cancer than in the patients with gastritis (p < 0.01)., Conclusions: The patients with gastric cancer elicit different anti H. pylori IgG and IgA response than the patients with superficial and atrophic gastritis. Low IgG and IgA predominance seems characteristic for gastric cancer.

Background and Aim: Beta-2 microglobulin (beta2-m) is a minor plasma protein, secreted from the plasma membranes as a result of the continuous regeneration of membrane proteins in the cell surface of all nucleated cells. The relationship between Helicobacter pylori and beta2-m has not been adequately established in studies. In this study, we aimed to compare the levels of serum and tissue beta2-m in patients with and without H. pylori infection, and to examine the relationship between levels of serum and tissue beta2-m., Material and Methods: About 30 patients with H. pylori gastritis and 22 healthy persons were enrolled in this study. Gastric biopsies were histologically analyzed and compared according to tissue and serum beta2-m levels., Results: Serum beta2-m levels were comparable in H. pylori and control groups. There was no significant link between tissue H. pylori grade and serum beta2-m levels. Subendothelial beta2-m was detected in 19 (63.3%) cases with H. pylori and none of the control group with immunohistochemical staining (P < 0.001). There was no correlation between serum and tissue levels of beta2-m., Conclusion: beta2-m accumulates in the majority of gastric tissues of patients with active chronic gastritis who were H. pylori (+), whereas no accumulation was found in H. pylori (-) control subjects.

Background: Matrix metalloproteinases (MMPs) have roles in inflammation and other processes relevant to the architectural disturbances seen in the gastric mucosa in response to Helicobacter pylori infection. Upregulation of MMPs has been reported in H pylori infection, but there are no detailed reports regarding altered production of their inhibitors, the tissue inhibitors of metalloproteinases (TIMPs)., Aims: To investigate changes in the abundance of TIMPs in human gastric corpus mucosa and murine stomach in Helicobacter infection, and to study cellular sources in man., Methods: Gastric corpus biopsy samples were assessed for abundance of mRNA or protein for TIMP-1 to -4 by real-time quantitative PCR or western blotting, respectively. Antral and corpus biopsies were processed for histology, H pylori status and inflammatory scoring. Cellular sources of TIMP-1, -3 and -4 were examined by indirect immunohistochemistry. Circulating gastrin was measured by radioimmunoassay. Also, abundance of TIMP-1, -3 and -4 mRNA in the stomach of Helicobacter felis infected mice post-infection was compared with that of uninfected control animals., Results: Compared with uninfected patients, mRNA and protein for TIMP-1, -3 and -4 were significantly more abundant in the gastric corpus of H pylori infected subjects. Gastric TIMP expression did not differ significantly between hyper- and normogastrinaemic subjects within the H pylori negative and positive groups. There was no difference in mRNA abundance for MMP-3 or -8. Immunohistochemistry showed TIMP proteins localised to gastric epithelial, stromal cells and inflammatory cells. Murine H felis infection was associated with upregulation of TIMP-1 and -3 mRNA., Conclusions: Helicobacter infection is associated with upregulation of specific TIMPs (TIMP-1 and -3) in glandular epithelium and stroma. It is suggested that increased expression of specific protease inhibitors in the corpus mucosa may exert important effects on extracellular matrix remodelling and influence the outcome of H pylori infection.

Eradication of Helicobacter pylori may lead to improvement of chronic immune thrombocytopenic purpura (ITP), although its efficacy over time is uncertain. We report the results of H pylori screening and eradication in 75 consecutive adult patients with ITP. We also used molecular methods to investigate lymphocyte clonality and H pylori genotypes in the gastric biopsies from 10 H pylori-positive patients with ITP and 19 H pylori-positive patients without ITP with chronic gastritis. Active H pylori infection was documented in 38 (51%) patients and successfully eradicated in 34 (89%) patients. After a median follow-up of 60 months, a persistent platelet response in 23 (68%) of patients with eradicated infection was observed; 1 relapse occurred. No differences in mucosal B- or T-cell clonalities were observed between patients with ITP and control participants. Of note, the frequency of the H pylori cagA gene (P = .02) and the frequency of concomitant H pylori cagA, vacAs1, and iceA genes (triple-positive strains; P = .015) resulted statistically higher in patients with ITP than in control participants. All asymptomatic H pylori-positive patients with ITP were suffering from chronic gastritis. Our data suggest a sustained platelet recovery in a proportion of patients with ITP by H pylori eradication alone. Overrepresentation of specific H pylori genotypes in ITP suggests a possible role for bacterium-related factors in the disease pathogenesis.