Helicobacter pylori infection and gastritis: the Systematic Investigation of gastrointestinaL diseases in China (SILC)

Background and Aim: Helicobacter pylori infection remains common in East Asia, though its prevalence is decreasing in Western countries. H. pylori‐related atrophic gastritis (AG) may reduce the likelihood of gastroesophageal reflux disease (GERD). We investigated the prevalence of H. pylori infection and AG and their association with endoscopic findings and symptom‐defined GERD in Shanghai. Methods: A representative random sample of 3600 Shanghai residents aged 18–80 years was invited to complete a general information questionnaire and a Chinese version of the Reflux Disease Questionnaire, to provide blood samples for H. pylori serology and pepsinogen (PG) I/II assay (to detect AG, defined as PGI < 70 µg/L and/or PGI/PGII < 7), and to undergo endoscopy. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by multivariate logistic regression. Results: A total of 1022 Shanghai residents underwent endoscopy and were valid for inclusion in the study. Of these, 71.7% tested positive for H. pylori, 63.8% had AG and 30.5% had moderate/severe AG (PGI < 50 µg/L and/or PGI/PGII < 5). Helicobacter pylori infection was equally common in all age groups. Severity of AG increased with age in women. Reflux esophagitis was inversely associated with AG (OR, 0.23 [CI, 0.09–0.55] for moderate/severe AG compared with no H. pylori or gastritis). However, symptom‐defined GERD showed no clear association with AG. Conclusions: Helicobacter pylori infection and AG are very common in Shanghai, and the infection is acquired early in life. Atrophic gastritis is inversely associated with reflux esophagitis but is not significantly associated with symptom‐defined GERD.     

Serum Pepsinogen and Gastrin Levels: Reliable Markers to Predict Small Intestinal Bacterial Overgrowth

BackgroundSerum pepsinogen, a useful indicator of gastric acidity, could reflect small intestinal bacterial overgrowth. The aim of this study is to evaluate the relationship between small intestinal bacterial overgrowth and profiles including pepsinogen or gastrin.MethodsWe conducted a prospective study with 62 patients with a functional gastrointestinal disorder. All patients underwent glucose breath test for small intestinal bacterial overgrowth, immediately followed by upper endoscopy to survey gastric injury and Campylobacter-like organism test for Helicobacter pylori and serum laboratory tests including gastrin, pepsinogen I and II.ResultsThe positivity to small intestinal bacterial overgrowth was 17.7%. Significantly, low total hydrogen concentration during a glucose breath test, low prevalence for gastric injury, and high H. pylori positivity rate were shown in groups with pepsinogen I/II ratio ≤ 3.5 compared to those with pepsinogen I/II ratio > 3.5 or in groups with serum gastrin > 35.4 pg/mL comparing to those with serum ≤ 35.4 pg/mL, respectively. A high gastrin level was independently associated with H. pylori infection. A proportionally correlated tendency between pepsinogen I/II ratio and total hydrogen concentration was shown, whereas that of inverse proportion between H₂ and gastrin was observed. Old age was solely independent predicting factor for small intestinal bacterial overgrowth (P = .03) in the multivariate analysis.ConclusionOld age was significantly related to the presence of small intestinal bacterial overgrowth in functional gastrointestinal disorder patients. Although pepsinogen and small intestinal bacterial overgrowth seem irrelevant, elevated gastrin level may cautiously indicate a decreased breath hydrogen concentration. Further studies should consider the function of intestinal motility and gastric acidity in patients with hydrogen-producing small intestinal bacterial overgrowth.     

Standard vs magnifying narrow-band imaging endoscopy for diagnosis of Helicobacter pylori infection and gastric precancerous conditions

BACKGROUNDAdvances in endoscopic imaging enable the identification of patients at high risk of gastric cancer. However, there are no comparative data on the utility of standard and magnifying narrow-band imaging (M-NBI) endoscopy for diagnosing Helicobacter pylori (H. pylori) infection, gastric atrophy, and intestinal metaplasia. AIMTo compare the diagnostic performance of standard and M-NBI endoscopy for H. pylori gastritis and precancerous conditions. METHODSIn 254 patients, standard endoscopy findings were classified into mosaic-like appearance (type A), diffuse homogenous redness (type B), and irregular redness with groove (type C). Gastric mucosal patterns visualized by M-NBI were classified as regular round pits with polygonal sulci (type Z-1), more dilated and linear pits without sulci (type Z-2), and loss of gastric pits with coiled vessels (type Z-3). RESULTSThe diagnostic accuracy of standard and M-NBI endoscopy for H. pylori gastritis was 93.3% and 96.1%, respectively. Regarding gastric precancerous conditions, the accuracy of standard and M-NBI endoscopy was 72.0% vs 72.6% for moderate to severe atrophy, and 61.7% vs. 61.1% for intestinal metaplasia in the corpus, respectively. Compared to type A and Z-1, types B+C and Z-2+Z-3 were significantly associated with moderate to severe atrophy [odds ratio (OR) = 5.56 and 8.67] and serum pepsinogen I/II ratio of ≤ 3 (OR = 4.48 and 5.69). CONCLUSIONClose observation of the gastric mucosa by standard and M-NBI endoscopy is useful for the diagnosis of H. pylori gastritis and precancerous conditions.     

Typical and atypical symptoms of gastro esophageal reflux disease: Does Helicobacter pylori infection matter?

AIM: To analyze whether the presence of Helicobacter pylori(H. pylori) infection could affect the quality of symptoms in gastro-esophageal reflux disease(GERD) patients. METHODS: one hundred and forty-four consecutive patients referred to our Unit for suspected GERD were recruited for the study. All patients underwent esophageal p H-metric recording. For those with a positive test, C13 urea breath test was then performed to assess the H. pylori status. GERD patients were stratified according to the quality of their symptoms and classified as typical, if affected by heartburn and regurgitation, and atypical if complaining of chest pain, respiratory and ears, nose, and throat features. H. pylori-negative patients were also asked whether they had a previous diagnosis of H. pylori infection. If a positive response was given, on the basis of the time period after successful eradication, patients were considered as "eradicated"(E) if H. pylori eradication occurred more than six months earlier or "recently eradicated" if the therapy had been administered within the last six months. Patients without history of infection were identified as "negative"(N). χ2 test was performed by combining the clinical aspects with the H. pylori status.RESULTS: one hundred and twenty-nine of the 144 patients, including 44 H. pylori-positive and 85 H. pylori-negative(41 negative, 21 recently eradicated, 23 eradicated more than 6 mo before), were eligible for the analysis. No difference has been found between H. pylori status and either the number of reflux episodes(138 ± 23 vs 146 ± 36, respectively, P = 0.2, not significant) or the percentage of time with pH values 4(6.8 ± 1.2 vs 7.4 ± 2.1, respectively, P = 0.3, not significant). The distribution of symptoms was as follows: 13 typical(30%) and 31 atypical(70%) among the 44 H. pylori-positive cases; 44 typical(52%) and 41 atypical(48%) among the 85 H. pylori-negative cases,(P = 0.017 vs H. pylori +; OR = 2.55, 95%CI: 1.17-5.55). Furthermore, clinical signs in patients with recent H. pylori eradication were similar to those of H. pylori-positive(P = 0.49; OR = 1.46, 95%CI: 0.49-4.37); on the other hand, patients with ancient H. pylori eradication showed a clinical behavior similar to that of H. pylori-negative subjects(P = 0.13; OR = 0.89, 95%CI: 0.77-6.51) but different as compared to the H. pylori-positive group(P 0.05; OR = 3.71, 95%CI: 0.83-16.47).CONCLUSION: Atypical symptoms of GERD occur more frequently in H. pylori-positive patients than in H. pylori-negative subjects. In addition, atypical symptoms tend to decrease after H. pylori eradication.     

Helicobacter pylori Infection with Atrophic Gastritis Is an Independent Risk Factor for Advanced Colonic Neoplasm

Background/AimsHelicobacter pylori is a major risk factor for atrophic gastritis (AG) and gastric cancer. The correlation between H. pylori, AG and colorectal neoplasm (CRN) has only been examined in a limited number of studies, and findings have been inconclusive. We aimed to investigate the association between H. pylori infection status, AG and advanced CRN.MethodsThis cross-sectional study investigated the relationship between the presence of serum anti-H. pylori IgG antibodies, AG, and advanced CRN in 6,351 consecutive asymptomatic subjects who underwent a screening colonoscopy.ResultsA total of 316 participants (5.0%) had advanced CRN. H. pylori seropositivity was 61.3%. In a univariate analysis, the presence of H. pylori infection was associated with advanced CRN (odds ratio [OR], 1.49; 95% confidence interval [CI], 1.17 to 1.91; p=0.001). H. pylori infection was associated with an increased risk of advanced CRN after adjusting for clinically relevant confounders (OR, 1.34; 95% CI, 1.04 to 1.72; p=0.023). H. pylori-related AG was significantly associated with the risk of advanced CRN (OR, 1.40; 95% CI, 1.03 to 1.91; p=0.030), whereas H. pylori infection without AG was not.ConclusionsH. pylori infection increased the risk of advanced CRN, especially when it was combined with AG. Strict colonoscopy screening and surveillance may be warranted in those with H. pylori-positive AG.     

Autoimmune thyroid diseases and Helicobacter pylori: the correlation is present only in Graves's disease

AIM: To investigate the correlation between autoimmune thyroid diseases (ATDs) and the prevalence of Cag-A positive strains of Helicobacter pylori (H. pylori) in stool samples.METHODS: Authors investigated 112 consecutive Caucasian patients (48 females and 4 males with Graves’ disease and 54 females and 6 males with Hashimoto’s thyroiditis HT), at their first diagnosis of ATDs. Authors tested for H. pylori in stool samples using an amplified enzyme immunoassay and Cag-A in serum samples using an enzyme-linked immunoassay method (ELISA). The results were analyzed using the two-sided Fisher’s exact test and the respective odds ratio (OR) was calculated.RESULTS: A marked correlation was found between the presence of H. pylori (P ≤ 0.0001, OR 6.3) and, in particular, Cag-A positive strains (P ≤ 0.005, OR 5.3) in Graves’ disease, but not in Hashimoto’s thyroiditis, where authors found only a correlation with Cag-A strains (P ≤ 0.005, OR 8.73) but not when H. pylori was present.CONCLUSION: The marked correlation between H. pylori and Cag-A, found in ATDs, could be dependent on the different expression of adhesion molecules in the gastric mucosa.     

Age, smoking and overweight contribute to the development of intestinal metaplasia of the cardia

AIM: To assess the role of Helicobacter pylori (H. pylori), gastroesophageal reflux disease (GERD), age, smoking and body weight on the development of intestinal metaplasia of the gastric cardia (IMC).METHODS: Two hundred and seventeen patients scheduled for esophagogastroduodenoscopy were enrolled in this study. Endoscopic biopsies from the esophagus, gastroesophageal junction and stomach were evaluated for inflammation, the presence of H. pylori and intestinal metaplasia. The correlation of these factors with the presence of IMC was assessed using logistic regression.RESULTS: IMC was observed in 42% of the patients. Patient age, smoking habit and body mass index (BMI) were found as potential contributors to IMC. The risk of developing IMC can be predicted in theory by combining these factors according to the following formula: Risk of IMC = a + s - 2B where a = 2,…6 decade of age, s = 0 for non-smokers or ex-smokers, 1 for < 10 cigarettes/d, 2 for > 10 cigarettes/d and B = 0 for BMI < 25 kg/m² (BMI < 27 kg/m² in females), 1 for BMI > 25 kg/m² (BMI > 27 kg/m² in females). Among potential factors associated with IMC, H. pylori had borderline significance (P = 0.07), while GERD showed no significance.CONCLUSION: Age, smoking and BMI are potential factors associated with IMC, while H. pylori and GERD show no significant association. IMC can be predicted in theory by logistic regression analysis.     

Correlation of serum pepsinogens and gastrin-17 with atrophic gastritis in gastroesophageal reflux patients: a matched-pairs study

Background and Aim: An algorithm (GastroPanel) for the non‐invasive diagnosis of atrophic gastritis has been previously proposed, based on serum pepsinogen‐I, gastrin‐17, and Helicobacter pylori (H. pylori) antibodies. The aim of the present study was to evaluate whether serum markers correlate with and predict gastric atrophy in gastroesophageal reflux disease (GERD) patients. Methods: The baseline data of the prospective ProGERD study, a study on the long‐term course of GERD (n = 6215 patients), served to select patients with atrophic gastritis diagnosed in biopsies from gastric antrum and corpus, and control cases without atrophy. A total of 208 pairs were matched for age, sex, GERD status (erosive vs non‐erosive), presence of Barrett's esophagus, and histological H. pylori status were retrieved. Serum pepsinogen‐I, gastrin‐17, and H. pylori antibodies were determined using specific enzyme immunoassays. Results: A significant negative correlation was found between the degree of corpus atrophy and the level of serum pepsinogen‐I. A previously‐reported negative correlation between the degree of antral atrophy and serum gastrin‐17 could not be confirmed. The low sensitivity (0.32) and specificity (0.70) of the GastroPanel algorithm were mainly due to over diagnosis and under diagnosis of advanced atrophy in the antrum. Conclusion: The diagnostic validity of the GastroPanel algorithm to diagnose gastric atrophy non‐invasively is not sufficient for general use in GERD patients.     

Atrophic gastritis and gastric cancer tissue miRNome analysis reveals hsa-miR-129-1 and hsa-miR-196a as potential early diagnostic biomarkers

BACKGROUNDGastric cancer (GC) is one of the most frequently diagnosed tumor globally. In most cases, GC develops in a stepwise manner from chronic gastritis or atrophic gastritis (AG) to cancer. One of the major issues in clinical settings of GC is diagnosis at advanced disease stages resulting in poor prognosis. MicroRNAs (miRNAs) are small noncoding molecules that play an essential role in a variety of fundamental biological processes. However, clinical potential of miRNA profiling in the gastric cancerogenesis, especially in premalignant GC cases, remains unclear.AIMTo evaluate the AG and GC tissue miRNomes and identify specific miRNAs’ potential for clinical applications (e.g., non-invasive diagnostics).METHODSStudy included a total of 125 subjects: Controls (CON), AG, and GC patients. All study subjects were recruited at the Departments of Surgery or Gastroenterology, Hospital of Lithuanian University of Health Sciences and divided into the profiling (n = 60) and validation (n = 65) cohorts. Total RNA isolated from tissue samples was used for preparation of small RNA sequencing libraries and profiled using next-generation sequencing (NGS). Based on NGS data, deregulated miRNAs hsa-miR-129-1-3p and hsa-miR-196a-5p were analyzed in plasma samples of independent cohort consisting of CON, AG, and GC patients. Expression level of hsa-miR-129-1-3p and hsa-miR-196a-5p was determined using the quantitative real-time polymerase chain reaction and 2^-ΔΔCt method.RESULTSResults of tissue analysis revealed 20 differentially expressed miRNAs in AG group compared to CON group, 129 deregulated miRNAs in GC compared to CON, and 99 altered miRNAs comparing GC and AG groups. Only 2 miRNAs (hsa-miR-129-1-3p and hsa-miR-196a-5p) were identified to be step-wise deregulated in healthy-premalignant-malignant sequence. Area under the curve (AUC)-receiver operating characteristic analysis revealed that expression level of hsa-miR-196a-5p is significant for discrimination of CON vs AG, CON vs GC and AG vs GC and resulted in AUCs: 88.0%, 93.1% and 66.3%, respectively. Compar-ing results in tissue and plasma samples, hsa-miR-129-1-3p was significantly down-regulated in GC compared to AG (P = 0.0021 and P = 0.024, tissue and plasma, respectively). Moreover, analysis revealed that hsa-miR-215-3p/5p and hsa-miR-934 were significantly deregulated in GC based on Helicobacter pylori (H. pylori) infection status [log2 fold change (FC) = -4.52, P-adjusted = 0.02; log2FC = -4.00, P-adjusted = 0.02; log2FC = 6.09, P-adjusted = 0.02, respectively].CONCLUSIONComprehensive miRNome study provides evidence for gradual deregulation of hsa-miR-196a-5p and hsa-miR-129-1-3p in gastric carcinogenesis and found hsa-miR-215-3p/5p and hsa-miR-934 to be significantly deregulated in H. pylori carrying GC patients.     

Potential mechanism of corpus-predominant gastritis after PPI therapy in Helicobacter pylori-positive patients with GERD

The long-term use of proton pump inhibitors (PPIs) exacerbates corpus atrophic gastritis in patients with Helicobacter pylori (H. pylori) infection. To identify a potential mechanism for this change, we discuss interactions between pH, bile acids, and H. pylori. Duodenogastric reflux, which includes bile, occurs in healthy individuals, and bile reflux is increased in patients with gastroesophageal reflux disease (GERD). Diluted human plasma and bile acids have been found to be significant chemoattractants and chemorepellents, respectively, for the bacillus H. pylori. Although only taurine conjugates, with a pKa of 1.8-1.9, are soluble in an acidic environment, glycine conjugates, with a pKa of 4.3-5.2, as well as taurine-conjugated bile acids are soluble in the presence of PPI therapy. Thus, the soluble bile acid concentrations in the gastric contents of patients with GERD after continuous PPI therapy are considerably higher than that in those with intact acid production. In the distal stomach, the high concentration of soluble bile acids is likely to act as a bactericide or chemorepellent for H. pylori. In contrast, the mucous layer in the proximal stomach has an optimal bile concentration that forms chemotactic gradients with plasma components required to direct H. pylori to the epithelial surface. H. pylori may then colonize in the stomach body rather than in the pyloric antrum, which may explain the occurrence of corpus-predominant gastritis after PPI therapy in H. pylori-positive patients with GERD.     

High incidence of newly-developed gastroesophageal reflux disease in the Japanese community: a 6-year follow-up study

Background and Aim: We conducted a community‐based study to assess the incidence of newly‐developed gastroesophageal reflux disease (GERD). We also analyzed the risk factors of GERD occurrence. Methods: A total of 322 patients without acid suppression therapy (135 men, mean age: 59.8 years), who lived in the Japanese community, took a QUEST questionnaire (a self‐administered questionnaire for the screening of GERD) in 1998. Blood samples were taken for the measurement of an anti‐Helicobacter pylori antibody and pepsinogen (PG) I/II to assess the grade of gastric atrophy. Of these patients, 289 scored less than six points and were diagnosed as non‐GERD. Two‐hundred‐and‐forty‐one patients (95 men, mean age: 67.0 years) took the QUEST questionnaire again in 2004 (after 6 years). The incidence of newly‐developed GERD was analyzed. These patients were categorized into three groups based on their initial PG I/II (group A: less than three, group B: three to six, and group C: more than six). The risk factors of GERD occurrence were evaluated. Results: Of the 241 non‐GERD patients, 37 patients (15.4%) developed GERD after 6 years. The incidence of newly‐developed GERD in group C was significantly higher than both groups A and B (group A: 3.8% [three of 79], group B: 11.8% (11/93), group C: 33.3% (26/69), P < 0.01, respectively). The prevalence of H. pylori negativity, constipation, and medication of Ca antagonists in newly‐developed GERD were significantly higher than in those who did not develop GERD. [Correction added after online publication on 1 July 2007: the preceding sentence has replaced one that read ‘The prevalence of H. pylori negativity, constipation, and medication of Ca antagonists in newly‐developed GERD were significantly higher than in those who did develop GERD.’] Conclusion: The incidence of newly‐developed GERD in the Japanese community was 16.5% for 6 years. The incidence of newly‐developed GERD patients who scored a PG I/II over six was significantly higher than those who scored lower. H. pylori negativity, constipation, and medication of Ca antagonists might be risk factors of GERD occurrence.     

Long-term follow-up of pepsinogen I/II ratio after eradication of Helicobacter pylori in patients who underwent endoscopic mucosal resection for gastric cancer

BackgroundAlthough the pepsinogen I/II (PGI/II) ratio after Helicobacter pylori eradication is recovered at short-term follow-up, long-term follow-up studies of PGI/II are rare.MethodsA total of 773 patients with gastric cancer who underwent endoscopic resection and pepsinogen and H. pylori tests were enrolled. H. pylori was eradicated in these patients. Endoscopic and pepsinogen tests were performed every year. A low PGI/II ratio was defined as ≤3.ResultsThe PGI/II ratio was higher in non-infected patients (n = 275, 4.99) than infected patients (n = 498, 3.53). After H. pylori eradication, the PGI/II ratio increased to 5.81 and 5.63 after 1 and 2 years (each p < 0.05). The PGI/II ratio in the non-eradication group decreased to 3.94 and 2.75 after 1 and 2 years. The PGI/II ratio in the H. pylori eradication group became similar to that of the H. pylori-negative group at 3 (4.48 vs. 4.34), 4 (4.88 vs. 4.34), and 5 years (4.89 vs. 4.23). The adjusted odds ratios for a lower PG I/II ratio in the non-eradication group compared to the eradication group were 4.78 (95% CI 2.15–10.67) after 1 year and 8.13 (95% CI 2.56–25.83) after 2 years.ConclusionsAfter H. pylori eradication, the PGI/II ratio increased and was similar to that of H. pylori-negative controls for up to 5 years of follow-up.     

Helicobacter pylori seropositivity in diabetic patients is associated with microalbuminuria

AIM:To investigate the relationship between Helicobacter pylori(H.pylori) seropositivity and the presence of microalbuminuria.METHODS:Between December 2003 and February 2010,asymptomatic individuals who visited the Seoul National University Healthcare System Gangnam Center for a routine check-up and underwent tests for H.pylori immunoglobulin G antibodies and urinary albumin to creatinine ratio(UACR) were included.All study subjects completed a structured questionnaire,anthropometric measurements and laboratory tests.Anti-H.pylori immunoglobulin G was identified using an enzyme-linked immunosorbent assay kit.A random single-void urine sample,collected using a clean-catch technique,was obtained to determine the UACR.The presence of microalbuminuria was defined as a UACR from 30 to 300 μg/mg.The presence of diabetes mellitus(DM) was defined as either a fasting serum glucose level greater than or equal to 126 mg/dL or taking anti-diabetic medication.Multiple logistic regression analysis was performed to identify the risk factors.The dependent variable was microalbuminuria,and the independent variables were the other study variables.RESULTS:A total of 2716 subjects(male,71.8%;mean age,54.9 years) were included.Among them,224 subjects(8.2%) had microalbuminuria and 324 subjects(11.9%) had been diagnosed with DM.Subjects with microalbuminuria had a significantly higher H.pylori seropositivity rate than subjects without microalbuminuria(60.7% vs 52.8%,P = 0.024).Multivariate analysis after adjustment for age,body mass index(BMI),waist circumference,and glucose and triglyceride levels showed that H.pylori seropositivity was significantly associated with microalbuminuria [odds ratio(OR),1.40,95% CI,1.05-1.89,P = 0.024].After the data were stratified into cohorts by glucose levels(≤ 100 mg/dL,100 mg/dL < glucose < 126 mg/dL,and ≥ 126 mg/dL or history of DM),H.pylori seropositivity was found to be significantly associated with microalbuminuria in diabetic subjects after adjusting for age,BMI and serum creatinine     

Helicobacter pylori infection, chronic atrophic gastritis and major cardiovascular events: a population-based cohort study

ObjectiveThere is debate whether infection with Helicobacter (H.) pylori, the main inducer of chronic atrophic gastritis (CAG), is a risk factor for cardiovascular disease and premature mortality.MethodsSerological measurements of H. pylori infection and pepsinogen (PG) I and II were obtained in a population-based German cohort of 9953 older adults (50–74 years). Cox regression was employed to estimate hazard ratios (HR) and 95% confidence intervals (CI) for myocardial infarction, stroke, cardiovascular and all-cause mortality during five-year follow-up.ResultsAccording to serology, 4977 participants (51.9%) were infected with H. pylori (2604 with cytotoxin-associated gene A (cagA) strains) and 541 (5.7%) had CAG (PGI < 70 ng/mL and PGI/PGII < 3). During follow-up, 540 participants died (163 from cardiovascular causes), 170 experienced a primary myocardial infarction and 241 had a stroke. Neither cytotoxin-associated gene A (cagA) negative nor cagA positive H. pylori infections were associated with an increased risk for myocardial infarction, stroke or all-cause mortality. Intriguingly, infection with cagA positive H. pylori strains was inversely associated with cardiovascular mortality (HR, 0.62; CI: 0.41–0.94). No statistically significant associations were observed for the small group of participants with CAG, but point estimates of adjusted HRs for myocardial infarction, stroke and cardiovascular mortality were all below 1 (0.71, 0.59 and 0.65, respectively).ConclusionsOur results do not support the hypothesis that H. pylori infection or CAG are risk factors for cardiovascular disease or mortality and instead suggest an inverse relationship of cagA positive H. pylori infection with fatal cardiovascular events.     

Costo-beneficio de cribado de adenocarcinoma gástrico por pepsinógeno sérico en la población mexicana

Introduction and aimHelicobacter pylori (H. pylori) is known to be capable of causing chronic inflammation of the gastric mucosa that slowly progresses through the premalignant stages, reaching localized gastric adenocarcinoma (GAC). Its outcome is closely related to the stage at which diagnosis is made. The aim of the present study was to determine cost-benefit by comparing esophagogastroduodenoscopy, serum pepsinogen detection, and no screening at all.Material and methodsUtilizing Markov chains and Monte Carlo simulation, the costs and effects of various detection modalities were simulated to analyze the cost-benefit of each strategy. For our population, we used the published data of patients with gastric cancer, applicable to the Mexican population.ResultsThe results were reported as incremental cost-effectiveness ratios. The best strategy was serum pepsinogen determination, followed by the strategy of endoscopic examination with continued monitoring every 3 years.ConclusionsThe performance of serum pepsinogen serology and directed endoscopic examination (and continued monitoring, if necessary) for GAC screening could be a cost-effective intervention in Mexico, despite the low-to-moderate general prevalence of the disease.     

Risk of gastric cancer in Helicobacter pylori infection in a 15-year follow-up

Objective: We investigated the risk of gastric cancer among men with Helicobacter pylori (H. pylori) infection or atrophic gastritis (AG) in a 15-year follow-up.

Materials and methods: Study population consists of 12,016 men aged 50–65 years at the beginning of the follow-up in 1994–1996. Serum levels of pepsinogen I (SPGI) and antibodies (IgG) to H. pylori (HpAb) were assayed from serums collected in 1994–1996. Incidence of gastric cancer in the study population was assessed in follow-up from 1994 to 2011 by data from the nationwide cancer registry. Based on SPGI and HpAb values, standardized incidence ratios (SIRs) of gastric cancer were calculated in three subgroups, that is, in those with a healthy stomach, those with H. pylori infection but without AG and those with AG. Risk ratios (RR) of gastric cancer were calculated using SIR of subgroups.

Results: During 15 years, seven gastric cancers appeared per 79,928 person years among men with healthy stomachs, 50 cancers per 92,533 person years in men with H. pylori infection but without AG, and 8 per 8658 person years in men with AG. Risk ratio (RR) of stomach cancer in men with H. pylori infection was 5.8 (95%CI: 2.7–15.3) compared to men with healthy stomachs, and 9.1 (95%CI: 2.9–30.0) in men with AG. There were no differences in cancer risk between cardia and distal stomach.

Conclusions: Risk of gastric cancer is low in men with healthy stomachs. It is significantly increased in those with H. pylori infection and more in those with AG.     

Effect of Helicobacter pylori Eradication on the Development of Reflux Esophagitis and Gastroesophageal Reflux Symptoms: A Nationwide Multi-Center Prospective Study

Background/Aims

A two-year, prospective, nationwide multicenter study was undertaken to evaluate the effect of Helicobacter pylori eradication on the development of reflux esophagitis (RE) and gastroesophageal reflux disease (GERD) symptoms in the Korean population.

Methods

In total, 1,489 subjects without RE were enrolled at the outpatient clinics of 12 tertiary hospitals nationwide, and 452 subjects underwent follow-up (F/U) for 2 years to evaluate the development of RE and GERD symptoms.

Results

RE was found in 33 subjects (7.3% of 452 subjects) and 14 subjects (7.3% of 192 subjects) during the first and second year of F/U, respectively. H. pylori status was not associated with the development of RE. RE was found in six (9.0%) of 67 H. pylori-negative patients, in 26 (11.2%) of 233 eradicated subjects and in eight (7.0%) of 114 noneradicated subjects (p=0.532). Multivariate analysis showed that age ≥60 years (odds ratio [OR], 7.11; 95% confidence interval [CI], 1.92 to 26.41), alcohol consumption (OR, 4.43; 95% CI, 1.03 to 19.19) and F/U cholesterol levels ≥200 mg/dL (OR, 5.03; 95% CI, 1.32 to 19.17) were significant risk factors for the development of RE. There was no significant difference in the development of GERD symptoms or weight according to H. pylori status during the 2-year F/U.

Conclusions

Eradication of H. pylori did not affect the development of reflux esophagitis or GERD symptoms among patients in outpatient gastroenterology clinics in South Korea.     

Antibiotic Susceptibility Profile of Helicobacter pylori Isolated from the Dyspepsia Patients in Tehran, Iran

Background/Aim:

Helicobacter pylori is an important pathogen for gastroduodenal diseases. Infection with H. pylori can be limited by regimens of multiple antimicrobial agents. However, antibiotic resistance is a leading cause of treatment failure. The aim of this study has been to determine the resistance patterns of H. pylori strains isolated from gastric biopsies of patients with dyspepsia by agar dilution method, in Tehran, Iran

Patients and Methods:

H. pylori isolates from patients with gastrointestinal diseases were evaluated for susceptibility testing by agar dilution method. Susceptibility testing was performed to commonly used antibiotics including clarithromycin, tetracycline, amoxicillin, metronidazole and ciprofloxacin.

Results:

Among 92 patients with dyspepsia, H. pylori strains were isolated from 42 patients. Seventeen (40.5%) of the isolates were resistant to metronidazole (MICs ≥ 8 μg/l), whereas one isolate (2.4%) was resistant to amoxicillin (MICs ≤ 0. 5 μg/ml) and ciprofloxacin (MICs ≤ 1μg/ml). The resistance rates to other antibiotics in H. pylori isolates are recorded as follows: clarithromycin 6 (14.3 %), tetracycline 2 (4.8%). In 5 of 42 resistant cases, combined resistance was found.

Conclusions:

These data suggest that metronidazole should be used among Iranian patients in first-line therapy with caution, and ciprofloxacin in association with amoxicillin and a proton pump inhibitor is more recommended.     

Microbiome changes in the gastric mucosa and gastric juice in different histological stages of Helicobacter pylori-negative gastric cancers

BACKGROUND The gastric microbiota in patients with gastric cancer(GC)has received increasing attention,but the profiling of the gastric microbiome through the histological stages of gastric tumorigenesis remains poorly understood,especially for patients with Helicobacter pylori-negative GC(HPNGC).AIM To characterize microbial profiles of gastric mucosa and juice for HPNGC carcinogenesis and identify distinct taxa in precancerous lesions.METHODS The 16S rRNA gene analysis was performed on gastric mucosa from 134 Helicobacter pylori-negative cases,including 56 superficial gastritis(SG),9 atrophic gastritis(AG),27 intestinal metaplasia(IM),29 dysplasia(Dys),and 13 GC cases,to investigate differences in gastric microbial diversity and composition across the disease stages.In addition,paired gastric mucosa and juice samples from 18 SG,18 IM,and 18 Dys samples were analyzed.α-Diversity was measured by Shannon and Chao1 indexes,andβ-diversity was calculated using partial least squares discrimination analysis(PLS-DA).Differences in the microbial composition across disease stages in different sample types were assessed using the linear discriminant analysis effect size.RESULTS The diversity and composition of the bacterial microbiota in the gastric mucosa changed progressively across stages of gastric carcinogenesis.The diversity of the gastric mucosa microbiota was found to be significantly lower in the IM and Dys groups than in the SG group,and the patients with GC had the lowest bacterial community richness(P<0.05).Patients with IM and those with Dys had similar gastric mucosa microbiota profiles with Ralstonia and Rhodococcus as the predominant genera.Microbial network analysis showed that there was increasing correlation strength between IM and Dys(|correlation threshold|≥0.5,P<0.05).GC and its precancerous lesions have distinguishable bacterial taxa;our results identified HPNGC-associated bacteria Streptococcaceae and Lactobacillaceae(P<0.05).Additionally,across precancerous lesion stages from AG to Dys in Helicobacter pylori-negative patients,Burkholderiaceae abundance continuously increased,while Streptococcaceae and Prevotellaceae abundance presented a continuous downward trend.Furthermore,the microbial diversity was higher in gastric juice(P<0.001)than in the mucosa,while PLS-DA revealed a statistically significant difference between the two groups(ANOSIM,P=0.001).A significant difference in the microbial structure was identified,with Proteobacteria being more prevalent in the gastric mucosa and Firmicutes being more abundant in gastric juice.CONCLUSION Our results provide insights into potential taxonomic biomarkers for HPNGC and its precancerous stages and assist in predicting the prognosis of IM and Dys based on the mucosal microbiota profile.     

Severe gastric mucosal damage induced by NSAIDs in healthy subjects is associated withHelicobacter pylori infection and high levels of serum pepsinogens

Helicobacter pylori infection and NSAIDs are considered the two most important exogenous factors in ulcer disease. The interrelation between the two factors is not, however, clear. Moreover, serum pepsinogen has been suggested as a risk marker for the development of NSAID-induced gastrointestinal lesions. Fifty-one healthy volunteers, enrolled in a prospective, double-blind study carried out to evaluate gastrointestinal side effects of meloxicam and piroxicam, were analyzed to determine whether: (1) the prevalence ofH. pylori correlates with the occurrence and severity of NSAID-induced gastrointestinal lesions, and (2) serum pepsinogen A and C levels could be used as markers of NSAID-induced mucosal damage. Upper endoscopy was performed by the same investigator before and after 28 days of treatment with placebo, meloxicam (7.5 mg/day and 15 mg/day), or piroxicam (20 mg/day). NSAID-induced damage was graded separately for hemorrhages and erosion ulcers according to Lanza's scale. There were no statistically significant differences in the prevalence ofH. pylori in subjects with and without NSAID-induced mucosal lesions. However, there was a positive association betweenH. pylori infection and the severity of mucosal damage: total mean endoscopic score was 2.9±0.3 inH. pylori-positive subjects versus 1.6±0.5 inH. pylori-negative subjects (P<0.05). Pepsinogen A and C levels increased from 55.3±3 to 149.4±15 and from 6.3±0.5 to 11.5±2.2, respectively (P<0.05) in subjects who developed severe endoscopic injury. It is concluded thatH. pylori increases the severity of NSAID-induced gastrotoxicity and that pepsinogen A and C levels are valid markers of severe NSAID-induced mucosal lesions.