Cure Helicobacter Pylori Infection Research Articles

Influence of Cytokine Genetic Polymorphisms in Helicobacter pylori-Associated Gastric Inflammation According to Sex in South Korea.

: The relationship between genetic polymorphisms and gastric inflammation remains unclear. This study aimed to evaluate the impact of genetic polymorphisms on Helicobacter pylori (HP)-associated gastritis according to sex. : Two hundred thirty-two male and 404 female subjects with current HP infection were prospectively enrolled. The genotyping of IL-1B-511 C/T, IL-1RN variable number of tandem repeats, IL-6-572 G/C, IL-8-251 A/T, IL-8-781 C/T, IL-10-1082 G/A, IL-10-592 C/A, TNF-A-308 G/A, and transforming growth factor (TGF)-B-509 C/T, was determined by polymerase chain reaction-restriction fragment length polymorphism. The degree of monocyte or neutrophil infiltration, atrophic gastritis, and intestinal metaplasia was evaluated using the updated Sydney system. : Among the male subjects, moderate/severe atrophic gastritis of the corpus was higher in IL-1B-511 CC carriers than in CT and TT carriers independent of age, alcohol consumption, and HP virulence factors (26.9% vs 10.4%; adjusted hazard ratio [HR], 4.377; 95% confidence interval, 1.387 to 13.814). In females, IL-8-251 AA carriers were independently and significantly associated with moderate/severe atrophic gastritis of the corpus compared with that in AT and TT carriers (21.4% vs 6.0%, adjusted HR=3.799). In males, the IL-8-251 TT genotype was associated with moderate/severe intestinal metaplasia of the corpus compared with the AT and AA genotypes (13.4% vs 5.6%, adjusted HR=3.128), while the IL-10-592 CA and CC genotypes were associated with moderate/severe monocyte infiltration of the antrum compared with AA genotype (83.6% vs 71.8%, adjusted HR=2.227). : Genetic polymorphisms in cytokines play different roles in HP-associated gastritis according to sex.

Preoperative H. pylori Eradication Therapy Facilitates Precise Delineation in Early Gastric Cancer with Current H. pylori Infection

Introduction: Early gastric cancer with current Helicobacter pylori infection (HpC-EGC) is common, but it is still unclear whether H. pylori eradication therapy (Hp-ET) or endoscopic submucosal dissection (ESD) should be performed first. We evaluated Hp-ETs short-term effects on horizontal boundary delineations of HpC-EGC in ESD. Methods: Prospectively enrolled HpC-EGC patients were randomly assigned to eradication or control groups. Operation scopes of HpC-EGC lesions were delineated with marking dots at 5 mm out of the endoscopic demarcation line by an independent endoscopist, unaware of eradication status, before formal circumferential incision. As representatives, precise delineation rate, the shortest distance of all marking dots to the pathological demarcation line in all slices of one intact resected specimen (D_min), and negative marking dot specimen rate were examined. Results: Twenty-three HpC-EGC patients (25 lesions) were allocated to eradication group and 26 patients (27 lesions) were allocated to the control group with similar eradication success rates and all were differentiated type. With improving background mucosa inflammation after Hp-ET and similar gastritis-like epithelium rates, 10 lesions (40.0%) in the eradication group were of precise delineation compared to control group with 2 lesions (7.4%) (relative risk = 5.40, 95% CI 1.31–22.28). D_min of eradication and control groups were 4.17 ± 2.52 mm and 2.67 ± 2.30 mm (p = 0.029), accompanied by 4 (14.8%) and none (0.0%) specimens that exhibited positive marking dots (p = 0.11), respectively. Conclusion: For HpC-EGC patients, administrating eradication medication before ESD is beneficial for the precise delineation of lesions and reducing the risk of positive horizontal resection margins.

Current Helicobacter pylori Infection Is Associated with Early Liver Injury: A Cross-Sectional Study in the General Population.

Early prevention of liver injury by controlling risk factors deserves concern because of the heavy liver disease burden. Helicobacter pylori (HP) infection affects half of the world's population and the relationship between it and early liver damage is unclear. This study focuses on assessing the correlation between them in the general population to provide clues to prevent liver disease. A total of 12,931 individuals underwent liver function and imaging tests as well as 13C/14C-urea breath tests. Results showed that the detection rate of HP was 35.9%, and the HP-positive group had a higher rate of liver injury (47.0% versus 44.5%, P = 0.007). Specifically, Fibrosis-4 (FIB-4) and alpha-fetoprotein levels in the HP-positive group were higher whereas the serum albumin level was lower. HP infection would raise the percentage of elevated aspartate aminotransferase (AST; 2.5% versus 1.7%, P = 0.006), elevated FIB-4 (20.2% versus 17.9%, P = 0.002), and abnormal liver imaging (31.0% versus 29.3%, P = 0.048). Most of these results remained stable after covariate adjustment but, for liver injury and liver imaging, the conclusions only held in young people (ORliver injury, odds ratio of liver injury, 1.127, P = 0.040; ORAST, 1.33, P = 0.034; ORFIB-4, 1.145, P = 0.032; ORimaging, 1.149, P = 0.043). Overall, HP infection might be associated with early liver injury, particularly in youth, suggesting that people with early liver injury should pay more attention to HP infection to prevent the occurrence of severe liver diseases.

Different Metabolites of the Gastric Mucosa between Patients with Current Helicobacter pylori Infection, Past Infection, and No Infection History.

Helicobacter pylori (H. pylori) alters metabolism during the gastric carcinogenesis process. This study aimed to determine the metabolites in the gastric mucosa according to the status of the H. pylori infection. Patients who visited the outpatient clinic for a gastroscopy and H. pylori tests were included. Gas chromatography–time-of-flight mass spectrometry (GC-TOF-MS) analysis was performed using gastric biopsied specimens from the corpus. Twenty-eight discriminative metabolites were found in the gastric mucosa of 10 patients with current H. pylori infection, in 15 with past infection, and in five with no infection history. The relative abundances (RAs) of amino acids and sugars/sugar alcohols were higher in patients with no infection history than in patients with current or past infection. The current infection group showed higher RAs of organic acids and lower RAs of fatty acids and lipids compared with the other groups. The RA of inosine was highest in the past infection group. Based on GC-TOF-MS analysis findings, metabolites differed not only between the infected and non-infected patients, but also between those with and without infection history. Amino acid and sugars/sugar alcohol metabolites decreased in patients with current or past infection, whereas fatty acid and lipid metabolites decreased only during current infection.

Enlarged folds on endoscopic gastritis as a predictor for submucosal invasion of gastric cancers.

BACKGROUNDAccurate diagnosis of the depth of gastric cancer invasion is crucial in clinical practice. The diagnosis of gastric cancer depth is often made using endoscopic characteristics of the tumor and its margins; however, evaluating invasion depth based on endoscopic background gastritis remains unclear.AIMTo investigate predicting submucosal invasion using the endoscopy-based Kyoto classification of gastritis.METHODSPatients with gastric cancer detected on esophagogastroduodenoscopy at Toyoshima Endoscopy Clinic were enrolled. We analyzed the effects of patient and tumor characteristics, including age, sex, body mass index, surveillance endoscopy within 2 years, current Helicobacter pylori infection, the Kyoto classification, and Lauren’s tumor type, on submucosal tumor invasion and curative endoscopic resection. The Kyoto classification included atrophy, intestinal metaplasia, enlarged folds, nodularity, and diffuse redness. Atrophy was characterized by non-reddish and low mucosa. Intestinal metaplasia was detected as patchy whitish or grayish-white flat elevations, forming an irregular uneven surface. An enlarged fold referred to a fold width ≥ 5 mm in the greater curvature of the corpus. Nodularity was characterized by goosebump-like multiple nodules in the antrum. Diffuse redness was characterized by uniform reddish non-atrophic mucosa in the greater curvature of the corpus.RESULTSA total of 266 gastric cancer patients (mean age, 66.7 years; male sex, 58.6%; mean body mass index, 22.8 kg/m2) were enrolled. Ninety-three patients underwent esophagogastroduodenoscopy for surveillance within 2 years, and 140 had current Helicobacter pylori infection. The mean Kyoto score was 4.54. Fifty-eight cancers were diffuse-type, and 87 cancers had invaded the submucosa. Multivariate analysis revealed that low body mass index (odds ratio 0.88, P = 0.02), no surveillance esophagogastroduodenoscopy within 2 years (odds ratio 0.15, P < 0.001), endoscopic enlarged folds of gastritis (odds ratio 3.39, P = 0.001), and Lauren’s diffuse-type (odds ratio 5.09, P < 0.001) were independently associated with submucosal invasion. Similar results were obtained with curative endoscopic resection. Among cancer patients with enlarged folds, severely enlarged folds (width ≥ 10 mm) were more related to submucosal invasion than mildly enlarged folds (width 5-9 mm, P < 0.001).CONCLUSIONEnlarged folds of gastritis were associated with submucosal invasion. Endoscopic observation of background gastritis as well as the lesion itself may help diagnose the depth of cancer invasion.

Gastric hyperplastic polyps inversely associated with current Helicobacter pylori infection.

The incidence of gastric hyperplastic polyps (HPs) has been on the rise in recent years. The contribution of Helicobacter pylori infection to this trend has remained to be elucidated. The present study aimed to explore the association between HPs and H. pylori in China, an area with a high infection rate of H. pylori. In order to study trends of HPs and H. pylori infection over the past decades, cases encountered from 2009 to 2018 were assessed and a total of 109,150 consecutive patients who underwent esophagogastroduodenoscopy at Qingdao Municipal Hospital (Qingdao, China) were enrolled. The incidence of HPs and the prevalence of H. pylori were determined and their correlation was explored. Gastric HPs were detected in 1,497 patients (1.6%) who received gastric biopsies. The incidence of HPs exhibited a rising trend, with a ~4-fold increase in the annual detection rate from 2009 to 2018. The prevalence of H. pylori infection was inversely associated with the prevalence of HPs (adjusted odds ratio, 0.66). The prevalence of H. pylori in the examined cohort decreased with time (r=-0.76, P=0.011). The decreasing trend of H. pylori infection was negatively correlated with the rising trend of HPs (r=-0.64, P=0.048), further indicating an inverse association between them. The difference in the prevalence of HPs between H. pylori-negative and -positive patients increased with age (r=0.80, P=0.018). The age-associated increase was slower in H. pylori-infected patients. The decline in H. pylori infection with time appeared to not be associated with the birth cohort effect, suggesting the decline was not caused by exposure to environmental factors during an early period of life. The present results indicated that the incidence of gastric HPs increased with the decline in H. pylori infection, demonstrating an inverse association between the occurrence of HPs and the infection.

Current Helicobacter pylori infection is significantly associated with subclinical coronary atherosclerosis in healthy subjects: A cross-sectional study.

Helicobacter pylori is a gastrointestinal pathogen known to be associated with cardiovascular disease (CVD). However, most analyses about the effect of H. pylori infection have been done in patients with a history of CVD but not in healthy subjects. We evaluated the association between H. pylori infection and subclinical atherosclerosis by using cardiac multidetector computed tomography (MDCT) in healthy subjects without previous CVD. From December 2007 to February 2014, 463 subjects who underwent the rapid urease test (CLO test), pulse-wave velocity (PWV) measurement, and MDCT for a self-referred health check-up were enrolled to this study. Helicobacter pylori infection was defined on the basis of CLO test positivity on endoscopic gastric biopsy. Significant coronary artery stenosis was defined as ≥50% stenosis in any of the major epicardial coronary vessel on MDCT. The CLO-positive subjects had a lower high-density lipoprotein-cholesterol (HDL-cholesterol) level compared to the CLO-negative subjects. The incidence of significant coronary stenosis was higher in the CLO-positive group (7.6% vs. 2.9%, P = 0.01). Furthermore, the number of subjects with coronary artery calcium score >0 and log{(number of segments with plaque)+1} were also significantly higher in the CLO-positive group. However, there was no statistical difference in the number of subjects with coronary artery calcium score >100, the prevalence of any plaque nor the plaque characteristics (calcified, mixed, or soft). Pulse-wave velocity (PWV) was neither associated with CLO test positivity. The CLO-positive group was 3-fold more likely to have significant coronary artery stenosis even after adjusting for confounding factors (adjusted odds ratio 2.813, 95% confidence interval 1.051–7.528, P = 0.04). In a healthy population, current H. pylori infection was associated with subclinical but significant coronary artery stenosis. The causal relationship between H. pylori infection and subclinical atherosclerosis in a “healthy” population remains to be investigated in the future.

Prevalência de infecção por Helicobacter pylori em uma comunidade indígena em São Paulo e fatores associados: estudo transversalPrevalence of Helicobacter pylori infection in an indigenous community in São Paulo and associated factors: cross-sectional study.

The prevalence of Helicobacter pylori infection is unevenly distributed among different populations. The aim here was to evaluate the factors associated with Helicobacter pylori infection among children up to five years of age living in a high-risk community. Cross-sectional study in an indigenous community of Guarani Mbya ethnicity, Tekoa Ytu and Tekoa Pyau villages, Jaraguá district, city of São Paulo (SP), Brazil. 74 children aged 0.4 to 4.9 years (mean 2.9 ± 1.3 years; median 3.1), and 145 family members (86 siblings, 43 mothers and 16 fathers) were evaluated for Helicobacter pylori infection using the validated 13C-urea breath test. Clinical and demographic data were collected. The prevalence was 8.3% among children aged 1-2 years and reached 64.3% among those aged 4-5 years (P = 0.018; overall 31.1%). The prevalence was 76.7% among siblings and 89.8% among parents. There was a negative association with previous use of antibiotics in multivariate analysis adjusted for age (odds ratio, OR: 0.07; 95% confidence interval, CI: 0.01 to 0.66; P = 0.02). The prevalence was higher among males (OR: 1.55), and was associated with maternal infection (OR: 1.81), infection of both parents (OR: 1.5), vomiting (OR: 1.28), intestinal parasitosis (OR: 2.25), previous hospitalization (OR: 0.69) and breastfeeding (OR: 1.87). The prevalence was high among subjects older than three years of age, thus suggesting that the incidence of infection was higher over the first three years of life. Previous use of antibiotics was inversely associated with current Helicobacter pylori infection.

Effect of early and current Helicobacter pylori infection on the risk of anaemia in 6.5-year-old Ethiopian children.

BackgroundEpidemiological and clinical studies in high income countries have suggested that Helicobacter pylori (H. pylori) may cause anaemia, but evidence is lacking from low income countries.We examined associations between H. pylori infection in early childhood and anaemia at the age of 6.5 years in an Ethiopian birth cohort.MethodsIn 2011/12, 856 children (85.1 % of the 1006 original singletons in a population-based birth cohort) were followed up at age six and half. An interviewer-led questionnaire administered to mothers provided information on demographic and lifestyle variables. Haemoglobin level and red cell indices were examined using an automated haematological analyzer (Cell Dyn 1800, Abbott, USA), and stool samples analyzed for H. pylori antigen. The independent effects of H. pylori infection (measured at age 3.5 and 6.5 years) on anaemia, haemoglobin level, and red cell indices (measured at age 6.5 years) were determined using multiple logistic and linear regression.ResultsThe prevalence of anemia was 34.8 % (257/739), and the mean (SD) haemoglobin concentration was 11.8 (1.1) gm/dl. Current H. pylori infection at age 6.5 years was positively, though not significantly related to prevalence of anaemia (adjusted OR, 95 % CI, 1.15; 0.69, 1.93, p = 0.59). Any H. pylori infection up to age 6.5 years was significantly associated with an increased risk of anaemia at age 6.5 (adjusted OR, 95 % CI, 1.68; 1.22, 2.32, p = 0.01). A significant reduction in haemoglobin concentration and red cell indices was also observed among children who had any H. pylori infection up to age 6.5 (Hb adjusted β = −0.19, 95 % CI, −0.35 to −0.03, p = 0.01; MCV adjusted β = −2.22, 95 % CI, −3.43 to −1.01, p = 0.01; MCH adjusted β = −0.63, 95 % CI, −1.15 to - 0.12, p = 0.01; and MCHC adjusted β = −0.67, 95 % CI, −1.21 to −0.14, p = 0.01), respectively.ConclusionThis study provides further evidence from a low income country that any H. pylori infection up to age 6.5 is associated with higher prevalence of anaemia, and reduction of haemoglobin level and red cell indices at age 6.5.Electronic supplementary materialThe online version of this article (doi:10.1186/s12879-015-1012-y) contains supplementary material, which is available to authorized users.

Second Cancers and Residual Disease in Patients Treated for Gastric Mucosa-Associated Lymphoid Tissue Lymphoma by Helicobacter pylori Eradication and Followed for 10 Years

Cure of Helicobacter pylori infection induces remission in most patients with gastric mucosa-associated lymphoid tissue lymphoma (GML) that is associated with these bacteria. We determined the long-term outcomes of these patients in a prospective multicenter trial and investigated whether they developed second cancers or had histologic residual disease. We followed 120 patients with stage EI1 GML for a median of 122 months after H pylori eradication (range, 1-171 months). Remission was determined by histology analysis and development of second cancers was documented. Of the patients, 80% (96 of 120) achieved complete remission from GML, and 80% of those (77 of 96) remained disease free. Estimated mean survival time in the Kaplan-Meier analysis was 147 months (95% confidence interval: 138-156 months). Of the patients that achieved complete remission, 17% (16 of 96) had histologic residual disease after a median of 32 months (range, 3-68 months). Disease did not progress in any of these patients, and all but 1 achieved a second complete remission (median duration, 46 months). Standardized morbidity ratios revealed a significantly higher incidence of gastric cancer (8.567; 95% confidence interval, 3.566-20.582) or non-Hodgkin lymphoma (18.621; 95% confidence interval: 8.365-41.448) in the 96 patients that achieved a complete remission, compared with the general German population. Cure of H pylori infection leads to continuous complete remission in most patients with H pylori-associated GML. Patients are at risk for development of secondary cancers (ie, gastric cancer and non-Hodgkin lymphoma).

Efficacy, Tolerability, and Factors Affecting the Efficacy of the Sequential Therapy in Curing Helicobacter Pylori Infection in Clinical Setting

BackgroundSequential therapy is currently suggested as first-line therapy in curing Helicobacter pylori infection, but results coming from its use in clinical practice are scarce. We evaluated the efficacy of this...

Use of tobacco products and gastrointestinal morbidity: an endoscopic population-based study (the Kalixanda study)

The impact of snus (smokeless tobacco or snuff) on gastrointestinal symptoms and pathological findings is largely unknown. The authors aimed to investigate whether the exposure to different forms of tobacco influences upper gastrointestinal symptoms, histology and frequency of Helicobacter pylori infection. A random sample (n = 2,860) of the adult population of two northern Swedish municipalities Kalix and Haparanda (n = 21,610) was surveyed between December 1998 and June 2001 using a validated postal questionnaire assessing gastrointestinal symptoms (response rate 74.2%, n = 2,122) (The Kalixanda Study). A random sub-sample (n = 1,001) of the responders was invited to undergo an esophagogastroduodenoscopy (participation rate 73.3%) including biopsies, Helicobacter pylori culture and serology and symptom assessment and exploration of present and past use of tobacco products. No symptom groups were associated with snus use. Snus users had a significantly higher prevalence of macroscopic esophagitis univariately but snus use was not associated with esophagitis in multivariate analysis. Snus use was associated with basal cell hyperplasia (OR = 1.74, 95% CI: 1.02, 3.00) and with elongation of papillae (OR = 1.79, 95% CI: 1.05-3.05) of the squamous epithelium at the esophago-gastric junction. Current smoking cigarettes was associated with overall peptic ulcer disease (OR = 2.32, 95% CI: 1.04, 5.19) whereas snus use was not. There were no significant association between current Helicobacter pylori infection and different tobacco product user groups. Snus significantly alters the histology of the distal esophagus but does not impact on gastrointestinal symptoms or peptic ulcer disease.

Effect of Helicobacter pylori Infection and Its Eradication on Reflux Esophagitis and Reflux Symptoms

We evaluated the association between current Helicobacter pylori infection and reflux esophagitis and the effect of H. pylori eradication on reflux esophagitis in a healthy screening population. A total of 10,102 subjects in a comprehensive screening cohort were enrolled, and 4,007 subjects had follow-up after a median of 2 years. Effects of H. pylori infection on reflux esophagitis were estimated with odds ratios (ORs) and 95% confidence intervals (CIs) using multiple logistic regression analysis. We evaluated the change in prevalence of reflux esophagitis and reflux symptoms after H. pylori eradication vs. persistence. The prevalence of reflux esophagitis (as classified by the Los Angeles system) was 4.9% (490/10,102). Whereas the prevalence of reflux esophagitis was 6.4% (319/4,971) in subjects without H. pylori infection, it was 3.3% (171/5,131) in subjects with infection (P<0.001). H. pylori infection had a strong negative association with reflux esophagitis in multivariate analysis (OR 0.42; 95% CI, 0.34-0.51). Compared with the prevalence of reflux esophagitis in the persistent infection group, the prevalence of reflux esophagitis increased after successful H. pylori eradication (OR 2.34; 95% CI, 1.45-3.76; P<0.001), which was comparable to that of the H. pylori-negative group (OR 2.42; 95% CI, 1.73-3.36; P<0.001). However, reflux symptoms had no association with H. pylori infection or eradication. In a healthy screening population, H. pylori infection had a strong negative association with reflux esophagitis, but H. pylori eradication increased the prevalence of erosive esophagitis to the level of H. pylori-negative individuals. Long-term clinical significance of newly developed erosive esophagitis after H. pylori eradication should be evaluated prospectively.

Is Furazolidone Therapy for Helicobacter pylori Effective and Safe?

We have read with great interest the study performed in Pakistan by Abbas et al. [1] on the efficacy and safety of a ‘‘rescue’’ therapy to cure Helicobacter pylori infection. Briefly, following a quadruple therapy including high-dose esomeprazole, bismuth salts, amoxicillin-clavulanic acid, and furazolidone, an 81% eradication rate was achieved at ITT analysis, with a side-effects incidence as high as 50%. The authors concluded that ‘‘it is reasonably well tolerated and is an effective second-line regimen’’ and even suggested it could be used as a first-line therapy. We have some concerns about these conclusions. First, following the first-line therapy, H. pylori eradication was achieved in 119 (67.6%) out of 176 enrolled patients. Consequently, 57 eradication failure patients were available instead of 52, as was reported. If all these patients received a second-line therapy, then both ITT and PP analysis should be accordingly calculated. Second, the reported side-effects incidence (up to 50%) would appear much higher than that observed following a simpler, 10-day levofloxacin-based second-line triple therapy, which is 18% in near 1,000 patients, with an 81% eradication rate [2]. Third, it has been claimed that drug cost is a cause for concern in developing countries [1]. However, esomeprazole is the most expensive proton pump inhibitor, and the dose used (40 mg b.i.d.) in this study was twice that widely suggested in the literature [3]. This markedly increased the overall therapeutic cost of eradication therapy, contrasting one of the aims of the study. In addition, when bismuth salts are administered with a high-dose of the proton pump inhibitor, bismuth toxicity may also be a cause for concern, since very high blood bismuth concentrations within the Hillemand alarm levels have been found in 9% of patients receiving a quadruple therapy, suggesting there should be more caution in prescribing bismuth salt with proton pump inhibitors [4]. Finally, some relevant ethical concerns arise with the use of furazolidone. This is an antibiotic that was used in the 1980s for parasitic infections, and some studies described its use in human subjects to treat H. pylori infection. In the 1990s, studies were published that raised several concerns about this agent and its potential for causing tumors. At the same time, the company that made the agent in the United States (Roberts Pharmaceuticals) was sold to Shire Pharmaceuticals, and the FDA withdrew its approval for furazolidone in March 2005. The drug was ordered removed even from animals as an antibiotic by the FDA in 2002. The FDA has subsequently sued companies that illegally imported the drug from Mexico for use in animals. Simultaneously, the European Medicinal Agency (EMEA; the equivalent of the FDA in the European Union) banned the drug in Europe. Although the drug continues to be available in some developing countries such as Iran, Pakistan, India, Mexico, and Brazil, a number of public and press campaigns from concerned individuals have urged governments to ban the drug in some of those countries. Therefore, can we consider a therapy including furazolidone as the authors declared as ‘‘safe’’? Although it has been stated that the study was approved by the Ethical Committee, were patients informed of the possible genotoxic and carcinogenetic effects [5, 6] for which furazolidone is not currently approved by the FDA and EMEA? V. De Francesco E. Ierardi Gastroenterology Unit, ‘‘Riuniti’’ Hospital, Foggia, Italy

The Association Between Current Helicobacter pylori Infection and Coronary Artery Disease

BackgroundThe role of Helicobacter pylori (H. pylori) in the pathogenesis of coronary artery disease (CAD) is still controversial, and the relation between current H. pylori infection and CAD has not been fully examined. This study evaluated the relation between H. pylori infection as confirmed by gastroduodenoscopic biopsy and CAD.MethodsWe determined the presence of H. pylori infections, via gastroduodenoscopy, in 88 patients of the normal coronary angiographic group and also in 175 patients of the CAD group, and the latter patients had more than 50% coronary stenosis angiographically demonstrated. We excluded those patients with a history of previous H. pylori eradication and/or malignancy. A small piece of tissue from the antrum, which was obtained by gastroduodenoscopic biopsy, was stained by Warthin-starry silver stain. We defined a negative staining result that there was no stained tissue in the sample and the stained tissue was also positive for H. pylori infection.ResultsThere was no significant difference, except for gender, age, smoking and high density lipoprotein cholesterol (HDL-c), of the demographic and laboratory characteristics between the groups. Twenty seven (30.7%) patients of the normal control group and 71 (40.6%) patients of the CAD group were positive of H. pylori infection, yet there was no statistical difference. We angiographically followed up the 80 patients of the CAD group who were treated by percutaneous coronary intervention (PCI) at 6 to 9 months after their primary intervention. Twenty two (37.9%) of the 58 patients of the H. pylori negative group and 10 (45.5%) of the 22 patients of the H. pylori positive group were treated with reintervention, but reintervention was also not significantly different between the group with H. pylori infection and the group without the infection.ConclusionsThese data indicated that H. pylori infection had a modest influence on CAD and progressive atheroma, but the showed a tendency to increase. Further studies are needed to evaluate the relationship between H. pylori infection and CAD.

CagA status and Helicobacter pylori eradication among dyspeptic patients

Aim Triple therapy seems more effective in curing Helicobacter pylori infection in patients with peptic ulcer than in those with non-ulcer dyspepsia. It has been suggested that this difference depends on the expression of CagA protein that is more frequent in the former. The objective of this study was to investigate a potential association between serum CagA positivity, severity of gastric mucosal inflammation and eradication success among peptic ulcer and non-ulcer dyspepsia patients. Material and method Patients undergoing upper gastrointestinal endoscopy for investigation of dyspepsia at the Department of Gastroenterology, Hospital Vera Cruz, between March, 2000 and March 2001 were screened. H. pylori positive patients, as diagnosed by rapid urease test and histology were included. Severity of gastric mucosal inflammation was determined and serum CagA positivity was assessed using a commercially available ELISA assay prior to H. pylori 7-day eradication therapy with lansoprazole, clarithromycin and amoxicillin (30 mg, 500 mg and 1 g b.i.d., respectively). Eradication success was determined 8-24 weeks following completion of therapy. Results Seventy-four patients were included in the study (mean age 40.8, range 18-67, female = 28). CagA positivity was observed in 48% of patients. Gastroduodenal peptic ulceration was found in 54% of patients. Serum CagA positivity was significantly higher among peptic ulcer patients (62.5%), while CagA negativity was significantly higher among non-ulcer dyspepsia patients (67.7%). Lymphocyte and eosinophil infiltration was significantly higher among CagA + patients, despite being comparable when distributed among peptic ulcer and non-ulcer dyspepsia patients. Eradication was successful in 93.2% of patients, regardless of CagA status on a per protocol analysis. Based on a per protocol analysis, eradication success was comparable among peptic ulcer and non-ulcer dyspepsia patients, regardless of CagA status. Conclusion Our results support the concept that CagA positivity is associated to peptic ulcer disease and to a higher severity of lymphocyte and eosinophil infiltration. Efficacy of treatment eradication of H. pylori may not be affected by serum CagA status.

Helicobacter pylori–Specific Immune Response in Maternal Serum, Cord Blood, and Human Milk Among Mothers With and Without Current Helicobacter pylori Infection

We assessed the patterns of Helicobacter pylori (H. pylori) specific maternal antibodies in maternal serum, cord blood, and milk, which might play a role in prevention of H. pylori infection because transferred to the infant. Between November 2000 and November 2001, mothers were recruited after delivery of their offspring. H. pylori infection status was determined by 13C-urea breath test (UBT). Specific H. pylori antibody profiles were analysed using commercial H. pylori-specific enzyme-linked immunosorbent assay and Western blots. Among 898 mothers, 23% had a current H. pylori infection. Median H. pylori IgG antibody titers in serum and cord blood of UBT-positive mothers were 23.8 U/mL and 24.0 U/mL, respectively. Whereas prevalences of H. pylori-specific antibodies in serum of UBT-negative mothers were clearly lower than those among UBT-positive mothers, patterns of H. pylori-specific IgA antibodies in milk were similar among UBT-positive and UBT-negative mothers. Neonates born from H. pylori-infected women are provided with large amounts of transplacentally transferred specific IgG H. pylori antibodies. Breast-fed neonates are additionally provided with specific IgA antibodies in human milk. Notably, the latter may also be activated if exposure of the mother to H. pylori might have been long time ago and been cleared in the meantime.

Implications of corpus gastritis, atrophy and cyclooxygenase in the development of gastric erosions after curing Helicobacter pylori infection

Background. Helicobacter pylori eradication decreases recurrence of peptic ulcers with marked improvement in histological inflammation, but gastric mucosal injuries may be developed even after eradication. Purpose. To investigate the mechanisms responsible for the development of gastric erosions after eradication, we analysed the relationship between clinicopathological risk factors and the occurrence of gastric erosion after curing H. pylori infection. Patients. Sixty patients underwent endoscopy before, and 3, 6 and 12 months after the completion of H. pylori eradication. Methods. Risk factors associated with the development of gastric erosions after eradication were assessed by multivariate analysis, and cyclooxygenase-1 and -2 immunoreactivity was histologically examined in the gastric mucosa before and after eradication. Results. The cumulative prevalence of gastric erosions after H. pylori eradication was 38.3% within 1 year. Using multivariate analysis, corpus gastritis scores (inflammation score + activity score), corpus atrophy scores and an age of more than 50 years were found to be independent factors associated with the development of gastric erosion after eradication with odds ratios of 7.39, 0.13 and 5.00, respectively. Cyclooxygenase-2 immunoreactivity of the corpus was decreased for the non-erosion group after eradication, but not for the erosion group. Conclusions. Severe gastritis or less severe atrophy in oxyntic glands but not in pyloric glands before eradication may be involved in the development of gastric erosions after curing H. pylori infection.

Treatment options for patients with Helicobacter pylori infection resistant to one or more eradication attempts

Proton pump inhibitor-based triple regimens fail to cure Helicobacter pylori infection in at least 10-23% of treated patients. Re-treatment strategies after initial failure remain poorly defined. Of the factors leading to eradication failure, patients' compliance, gender, primary resistance to clarithromycin and metronidazole, and intragastric bacterial load appear to be the most important in determining treatment outcome. Empirical re-treatment should depend mainly upon the antibiotics initially used, as re-administration of the same compound (namely, metronidazole and clarithromycin) is not recommended. Quadruple therapy is usually suggested in this situation, but there is some reluctance to use it in clinical practice on account of the high number of tablets to be taken and concern about side-effects. The use of ranitidine bismuth citrate instead of a proton pump inhibitor plus a bismuth compound in triple second-line regimens has recently proven to be highly effective. Finally, rifabutin-based triple therapies have been shown to be a promising rescue strategy in patients who have failed two or more eradication attempts.

Omeprazole Plus Azithromycin and Either Amoxicillin or Tinidazole for Eradication of Helicobacter pylori Infection

To establish whether omeprazole plus azithromycin in association with either amoxicillin or tinidazole is effective in curing Helicobacter pylori infection in dyspeptic patients. Many antibiotics in combination with antisecretory drugs have been used in an attempt to find the optimal regimen for eradication of H. pylori. Azithromycin is a macrolide that achieves high concentrations in gastric tissue after a single 500-mg oral dose. A total of 160 consecutive symptomatic patients with H. pylori received omeprazole 20 mg twice daily for 1 week, azithromycin 500 mg/d for 3 days, and were randomly assigned to either amoxicillin 1 g twice daily (OAzAm group, n = 80) for 1 week or tinidazole 500 mg twice daily for 3 days (OAzT group, n = 80). H. pylori status was assessed by rapid urease test and histology at entry and by histology and (13)C-urea breath test after the end of the therapy. H. pylori was eradicated in 62.5% of patients in the OAzAm group (intention to treat [ITT] 62.5%) and in 71.2% of patients in the OAzT group (ITT 71.2%). Although the compliance was excellent and the side effects negligible, the regimens used were partially effective for the eradication of H. pylori.