Genotypes of Helicobacter pylori in patients with peptic ulcer bleeding

AIM: Helicobacter pylori causes chronic gastritis, peptic ulcer, gastric cancer and MALT-lymphoma. Different genotypes of Helicobacter pylori are confirmed from diverse geographic areas. Its association with bleeding peptic ulcer remains controversial. The aim of this study was to investigate the Helicobacter pylori vacA alleles, cagA and iceA in patients with bleeding peptic ulcer. METHODS: We enrolled patients with bleeding, non-bleeding peptic ulcers and chronic gastritis. Biopsy specimens were obtained from the antrum of the stomach for rapid urease test, bacterial culture and PCR assay. DNA extraction and polymerase chain reaction were used to detect the presence or absence of cagA and to assess the polymorphism of vacA and iceA. RESULTS: A total of 168 patients (60.4%) (25 patients with chronic gastritis, 26 patients with bleeding gastric ulcer, 51 patients with non-bleeding gastric ulcer, 26 patients with bleeding duodenal ulcer, and 40 patients with non-bleeding duodenal ulcer) were found to have positive PCR results between January 2001 and December 2002. Concerning genotypes, we found cagA (139/278, 50%), vacA s1a (127/278, 45.7%), and ice A1 (125/278, 45%) predominated in all studied patients. In patients with bleeding peptic ulcers, vacA s1a and m1T were fewer than those in patients with non-bleeding peptic ulcers (37/106 vs 69/135, P=0.017, and 4/106 vs 21/135, P =0.002). CONCLUSION: In patients with peptic ulcers, H pylori vacA s1a and m1T prevent bleeding complication.     

Is Helicobacter pylori eradication indicated in cirrhotic patients with peptic ulcer disease?

INTRODUCTION: The association between H. pylori infection and peptic ulcer disease (PUD) and the efficacy of eradication of H. pylori in treating ulcer disease in cirrhotic patients remains controversial. This study was carried out to ascertain the prevalence and significance of H. pylori in cirrhotic patients with PUD and to assess the need for anti H. pylori thrapy METHODS: Three groups of patients were studied . These were patients with (A) cirrhosis and PUD, (B) uncomplicated PUD and (C) cirrhosis without PUD. H. pylori status was determined by endoscopic urease test . Eradication therapy was given with a four drug regimen and repeat endoscopy was done three months later to detect ulcer healing as well as H. pylori status with PUD in groups A and B. RESULTS: Cirrhotic patients with PUD had a significantly lesser prevalence of H. pylori compared to uncomplicated ulcer patients (46.9 % vs 80 %; p = 0.04). While H. pylori eradication rates were similar between cirrhotic and non cirrhotic patients, ulcer healing rate was significantly lesser in cirrhotic patients ( 48 % vs 80.9 %) . Majority of residual ulcers in cirrhotic patients were negative for H. pylori. CONCLUSION: Eradication of H. pylori does not reduce the residual ulcer rate indicating that H. pylori infection might not be a significant risk factor for PUD in cirrhotic patients. Hence, routine H. pylori eradication might not be warranted in patients with cirrhosis and peptic ulcer disease.     

Changing rates of Helicobacter pylori testing and treatment in patients with peptic ulcer disease

OBJECTIVES: The aim of this study was to identify temporal trends in the rate of Helicobacter pylori (H. pylori) testing, prevalence, and treatment among patients with peptic ulcer disease in Olmsted County, MN, from 1984 through 1997. METHODS: All 3317 Olmsted County residents with a clinical diagnosis of peptic ulcer disease at the Mayo Clinic from 1984 through 1997 were identified. The complete medical records of an age-, sex-, and calendar year-stratified random sample were reviewed (n = 720); 298 patients (41%) had confirmed peptic ulcer disease. Changes in proportions of H. pylori testing, infection, and treatment over time were analyzed by logistic regression. RESULTS: Of the 298 patients with confirmed peptic ulcer disease, 32% were tested for H. pylori; 36% were positive for infection, of whom 66% received antibiotic therapy. The rate of testing for H. pylori increased from 0% in 1984 to 96% in 1997, but the prevalence of infection did not change (36.4% vs 36.5%). The rate of treatment of those infected increased from 0% to 95%. By logistic regression, calendar year was associated with H. pylori testing and treatment but not infection. Recent use of nonsteroidal anti-inflammatory drugs was reported by 58% of patients, and 44% presented with GI bleeding. CONCLUSIONS: Physicians' practice of testing and treating for H. pylori in patients with confirmed peptic ulcer disease has steadily increased over the past 14 yr. However, in our study, only 36% of these patients were infected with H. pylori, whereas the majority used nonsteroidal anti-inflammatory drugs (NSAIDs). Therefore, testing seems to be more appropriate than empiric treatment in patients with peptic ulcer disease.     

Persistence of Helicobacter pylori infection in patients with peptic ulcer perforation

OBJECTIVE: In patients with perforated peptic ulcer (PPU) the convergence between the high eradication rate of Helicobacter pylori infection and low rates of ulcer relapse after treatment has been associated with reinfection by non-virulent strains. The objective of this study was to evaluate the persistence of infection by virulent H. pylori strains and ulcer recurrence in 33 patients with PPU one year after surgery and antimicrobial treatment. MATERIAL AND METHODS: The histological evaluation and molecular detection of H. pylori cagA and ureA genes, vacA allelic types and the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analyses of the glmM gene products from antral mucosa specimens were performed initially, 2-5 months and 1 year after therapy. RESULTS: The density of H. pylori colonization was temporarily decreased (p<0.05) 2-5 months after therapy. After one year, complete eradication was achieved in only 7 patients (23%) at histological examination and recurrent ulcers were found in 3/33 (9%) patients. The vacA s1a allelic type of cagA-positive strains persisted in 19/33 (58%) PPU patients with identical PCR-RFLP fingerprints in 8/9 (89%) of the patients. CONCLUSIONS: In PPU patients with a low eradication rate of H. pylori infection after surgical and antimicrobial treatment, the frequent recrudescence of the infection is mostly caused by the persisting virulent strains of the cagA and vacA s1a subtypes. In the 1-year follow-up period the recurrent ulceration can be postponed just by the lowered colonization density of H. pylori after eradicative therapy.     

Diagnostics of Helicobacter pylori infection in patients with peptic ulcer bleeding

BACKGROUND: In peptic ulcer bleeding, the sensitivity of H. pylori tests, in particular of the rapid urease test (RUT), has been reported to be insufficient. AIM: To validate the RUT, serology and the urea breath test were carried out in patients with bleeding peptic ulcers, and to study the influence of H. pylori suppressive treatment (HpSuT), i. e., antibiotics and proton pump inhibitors. PATIENTS AND METHODS: 123 consecutive patients (mean age 65.5 years) with a relevant bleeding from gastric or duodenal ulcers were prospectively tested for H. pylori infection by directs tests (RUT, histology, culture, urea breath test) and by IgG serology as an indirect test. Positive H. pylori status was defined by positive histology or culture. RESULTS: In patients without HpSuT during the preceding four weeks (N = 83), the sensitivity and specificity of RUT was 94 and 84 %, that of serology 83 and 68 % respectively. The sensitivity of urea breath test decreased from 82 to 60 % after even one day of HpSuT. In the overall group, the duration of HpSuT and preceding hospitalization were independent factors linked with negative results of all direct tests. CONCLUSIONS: In peptic ulcer bleeding, RUT combined with histology is an adequate diagnostic approach. However, false negative results have to be considered following even short-term HpSuT or hospitalization. Non-invasive diagnosis based on serology alone is inaccurate and should be complemented by the urea breath test prior to starting HpSuT.     

Persistence of Helicobacter pylori infection in patients with peptic ulcer perforation

Objective. In patients with perforated peptic ulcer (PPU) the convergence between the high eradication rate of Helicobacter pylori infection and low rates of ulcer relapse after treatment has been associated with reinfection by non-virulent strains. The objective of this study was to evaluate the persistence of infection by virulent H. pylori strains and ulcer recurrence in 33 patients with PPU one year after surgery and antimicrobial treatment. Material and methods. The histological evaluation and molecular detection of H. pylori cagA and ureA genes, vacA allelic types and the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analyses of the glmM gene products from antral mucosa specimens were performed initially, 2–5 months and 1 year after therapy. Results. The density of H. pylori colonization was temporarily decreased (p<0.05) 2–5 months after therapy. After one year, complete eradication was achieved in only 7 patients (23%) at histological examination and recurrent ulcers were found in 3/33 (9%) patients. The vacA s1a allelic type of cagA-positive strains persisted in 19/33 (58%) PPU patients with identical PCR-RFLP fingerprints in 8/9 (89%) of the patients. Conclusions. In PPU patients with a low eradication rate of H. pylori infection after surgical and antimicrobial treatment, the frequent recrudescence of the infection is mostly caused by the persisting virulent strains of the cagA and vacA s1a subtypes. In the 1-year follow-up period the recurrent ulceration can be postponed just by the lowered colonization density of H. pylori after eradicative therapy.     

Changing patterns of antibiotic resistance of Helicobacter pylori in patients with peptic ulcer disease]

BACKGROUND/AIMS: Antibiotic resistance of Helicobacter pylori (H. pylori) is a significant clinical problem because it reduces the efficacy of eradication therapy. The aims of this study were to assess the changing patterns of antibiotic resistance of H. pylori in patients with peptic ulcer diseases and to evaluate the eradication rate in antibiotic resistant H. pylori strains. METHODS: One hundred forty four H. pylori isolates obtained from 466 patients with peptic ulcer disease between June 2001 and December 2005 were examined for antimicrobial resistance. The minimum inhibitory concentration (MIC) of metronidazole was determined by modified broth microdilution method (mBMD) and E test. MICs of clarithromycin and amoxicillin were determined by mBMD, E test, and disc diffusion test. The breakpoints for metronidazole, clarithromycin, and amoxicillin resistance were defined as >8 microg/mL, >1 microg/mL, and > or =1 microg/mL, respectively. RESULTS: Resistance to metronidazole and clarithromycin was detected in 34.7% and 16.7% of H. pylori isolates, respectively. During the recent 5-year study period, amoxicillin-resistant rate of H. pylori was 11.8%, and multi-drug resistance rate of H. pylori was 16.7%. The eradication rate of clarithromycin containing triple therapies was low (7.8%) in clarithromycin-resistant H. pylori strains. CONCLUSIONS: The proportions of clarithromycin-resistant H. pylori strains have increased significantly over the last 5-years. There is an increasing tendency for the emergence of strains with multi-drug resistance. The increase in clarithromycin-resistant strains results in a decrease in eradication rate for H. pylori. In areas with high clarithromycin resistance, new alternative first-line treatment combination should be considered.     

Helicobacter pylori and gastric acid output in peptic ulcer disease

Helicobacter pylori is associated with peptic ulcer, and a causal relationship has been postulated. We investigated the association betweenHelicobacter pylori and gastric acid output. Two hundred forty-one patients were studied: 173 with duodenal ulcer, 51 with gastric ulcer (41 corpus, 10 prepyloric), and 17 with combined gastric and duodenal ulcer. In 194 patients (80%),Helicobacter pylori could be demonstrated histologically from gastric antral biopsies. The presence or absence ofHelicobacter pylori was not influenced by age, sex, or use of tobacco or analgesics. Patients with duodenal ulcer or combined gastric and duodenal ulcer had similar gastric acid outputs irrespective of the presence or absence ofHelicobacter pylori. However, gastric ulcer patients withHelicobacter had higher basal and maximal acid outputs when compared to patients withoutHelicobacter (mean basal output: 4.1 mmol/hr vs 2.4,P<0.05; mean maximal output 19.5 mmol/hr vs 14.4,P<0.05). AlthoughHelicobacter pylori is associated with both gastric ulcer and duodenal ulcer, its significance may be different in the two diseases.     

Six-year follow-up after successful triple therapy for Helicobacter pylori infection in patients with peptic ulcer disease.

OBJECTIVE & DESIGN: We question whether Helicobacter pylori eradication in peptic ulcer disease patients leads to a decrease in symptoms and reduced use of anti-dyspeptic drugs. Therefore, the recurrence rate of H. pylori, upper abdominal symptoms and the use of acid-suppressive drugs were determined 6 years after successful triple therapy. METHODS: Peptic ulcer disease patients successfully treated in 1990-1993 with 'classic' triple therapy were eligible. Patients were asked about symptoms and invited for a 13C-urea breath test or endoscopy in 1997-1998. Data on the use of anti-dyspeptic drugs were obtained from the pharmacy or general practitioner. RESULTS: Of the 113 eligible patients, 90 could be included in the study. The mean follow-up time was 6 years (range 4.6-7.6 years). H. pylori infection recurred in one patient (recurrence rate: 0.19% per patient-year; 95% confidence interval: 0.01-1.1%). Moderate or severe symptoms were experienced before therapy by 79% of the patients and after therapy by 18% of the patients (P< 10(-7)). Before triple therapy, 98% of the patients used H2-receptor antagonists and 54% were on maintenance treatment. After treatment, 30% used anti-dyspeptic medication and only 13% were on maintenance treatment (P < 10(-7)). CONCLUSIONS: Six years after successful triple therapy in peptic ulcer disease patients, the recurrence rate of H. pylori infection is low and both symptoms and the use of anti-dyspeptic drugs have decreased significantly.     

Optimal initiation of Helicobacter pylori eradication in patients with peptic ulcer bleeding

AIM:To evaluate when Helicobacter pylori(H.pylori)eradication therapy(ET)should be started in patients with peptic ulcer bleeding(PUB).METHODS:Clinical data concerning adults hospitalizedwith PUB were retrospectively collected and analyzed.Age,sex,type and stage of peptic ulcer,whether endoscopic therapy was performed or not,methods of H.pylori detection,duration of hospitalization,and specialty of the attending physician were investigated.Factors influencing the confirmation of H.pylori infection prior to discharge were determined using multiple logistic regression analysis.The H.pylori eradication rates of patients who received ET during hospitalization and those who commenced ET as outpatients were compared.RESULTS:A total of 232 patients with PUB were evaluated for H.pylori infection by histology and/or rapid urease testing.Of these patients,53.7%(127/232)had confirmed results of H.pylori infection prior to discharge.In multivariate analysis,duration of hospitalization and ulcer stage were factors independently influencing whether H.pylori infection was confirmed before or after discharge.Among the patients discharged before confirmation of H.pylori infection,13.3%(14/105)were lost to follow-up.Among the patients found to be H.pylori-positive after discharge,41.4%(12/29)did not receive ET.There was no significant difference in the H.pylori eradication rate between patients who received ET during hospitalization a n d t h o s e w h o c o m m e n c e d E T a s o u t p a t i e n t s[intention-to-treat:68.8%(53/77)vs 60%(12/20),P=0.594;per-protocol:82.8%(53/64)vs 80%(12/15),P=0.723].CONCLUSION:Because many patients with PUB who were discharged before H.pylori infection status was confirmed lost an opportunity to receive ET,we should confirm H.pylori infection and start ET prior to discharge.     

Characteristics of gastric cancer in peptic ulcer patients with Helicobacter pylori infection

AIM:To evaluate the incidence and clinical characteristics of gastric cancer(GC) in peptic ulcer patients with Helicobacter pylori(H.pylori) infection.METHODS:Between January 2003 and December 2013, the medical records of patients diagnosed with GC were retrospectively reviewed.Those with previous gastric ulcer(GU) and H.pylori infection were assigned to the Hp GU-GC group(n = 86) and those with previous duodenal ulcer(DU) disease and H.pylori infection were assigned to the Hp DUGC group(n = 35).The incidence rates of GC in the Hp GU-GC and Hp DU-GC groups were analyzed.Data on demographics(age, gender, peptic ulcer complications and cancer treatment), GC clinical characteristics [location, pathological diagnosis, differentiation, T stage, Lauren's classification, atrophy of surrounding mucosa and intestinal metaplasia(IM)], outcome of eradication therapy for H.pylori infection, esophagogastroduodenoscopy number and the duration until GC onset were reviewed.Univariate and multivariate analyses were performed to identify factors influencing GC development.The relative risk of GC was evaluated using a Cox proportional hazards model.RESULTS:The incidence rates of GC were 3.60%(86/2387) in the Hp GU-GC group and 1.66%(35/2098) in the Hp DU-GC group.The annual incidence was 0.41% in the Hp GU-GC group and 0.11% in the Hp DUGC group.The rates of moderate-to-severe atrophy of the surrounding mucosa and IM were higher in the Hp GU-GC group than in the Hp DU-GC group(86% vs 34.3%, respectively, and 61.6% vs 14.3%, respectively, P 0.05).In the univariate analysis, atrophy of surrounding mucosa, IM and eradication therapy for H.pylori infection were significantly associated with the development of GC(P 0.05).There was no significant difference in the prognosis of GC patients between the Hp GU-GC and Hp DU-GC groups(P = 0.347).The relative risk of GC development in the Hp GUGC group compared to that of the Hp DU-GC group,after correction for age and gender,was 1.71(95%CI:1.09-2.70;P=0.02).CONCLUSION:GU patients with H.pylori infection had higher GC incidence rates and relative risks.Atrophy of surrounding mucosa,IM and eradication therapy were associated with GC.     

Phenotypic and genotypic characterization of Helicobacter pylori from patients with and without peptic ulcer disease

BACKGROUND: Helicobacter pylori plays an important role in peptic ulcer disease, although not all H. pylori-infected persons will develop a peptic ulcer. Currently, H. pylori strains cannot be divided into commensals and pathogens. METHODS: Fifty H. pylori strains were cultured from patients divided into five groups on the basis of upper endoscopic findings: gastric ulcer, duodenal ulcer, gastritis, esophagitis, or normal. The ultrastructural adherence pattern in vivo, autoagglutination, hemagglutination, adhesion to human gastric adenocarcinoma (AGS) cells, and the lipopolysaccharide (LPS) profile of H. pylori strains were recorded; randomly amplified polymorphic DNA (RAPD) and urease gene typing were performed and correlated with diagnostic groups. RESULTS: Electron micrographs showed that H. pylori strains from patients with gastric ulcers adhered more frequently through filamentous strands and were less frequently found free in mucus than any other diagnostic group (P < 0.0001). Neither median hemagglutination titer nor median adhesion capacity to a human gastric adenocarcinoma cell line was related to endoscopic findings. Nevertheless, H. pylori strains from patients with gastric ulcers were more prone to autoagglutinate than were strains from the other diagnostic groups (P = 0.03). H. pylori strains from gastric ulcer patients were found to be more homogeneous, as determined by RAPD and urease gene typing, than strains from the other diagnostic groups (P < 0.01). In addition, a positive correlation was found between a patient's age and the adhesion to AGS cells of the patient's H. pylori strain (P = 0.006). CONCLUSION: A combination of an H. pylori autoagglutination test, RAPD, and urease gene typing may be useful in separating gastric ulcer-related strains from duodenal ulcer-related and non-ulcer dyspepsia-related strains.     

Evaluation of Helicobacter pylori infection and other risk factors in patients with benign peptic ulcer disease

ObjectiveTo assess and compare the risk factors in patients with benign gastric and duodenal ulcers and to correlate the prevalence of Helicobacter pylori (H. pylori) infection in benign peptic ulcer disease.MethodsA total of 30 consecutive patients with peptic ulcer disease were included in this study after upper gastrointestinal endoscopy. Their clinical profile and endoscopic findings were noted. Antral biopsies were subjected to histopathological examination and urease test for detection of H. pylori. Results were correlated. The study was cleared by the Institute Research Council and the Ethics committee.ResultsThe male: female ratio was 11:4. Overall, H. pylori infection was prevalent in 93.3% of the patients. Patients who took spicy food had a significantly higher rate of H. pylori positivity (P=0.04). Smoking, alcohol intake and NSAIDs did not affect H. pylori status in patients. There was no significant association between the site of the ulcer and H. pylori infection.ConclusionsBased on our observations we conclude that prevalence of H. pylori infection is similar in duodenal and gastric ulcers and intake of spicy food is a significant risk factor.     

Helicobacter pylori is a risk factor for peptic ulcer disease in cirrhotic patients. A meta-analysis

BACKGROUND : Peptic ulcer disease is highly prevalent in cirrhosis, and ulcer complications are a major cause of morbidity in these patients. Helicobacter pylori infection is considered the chief aetiological factor of ulcer disease. However, in cirrhotic patients the role of H. pylori in the pathogenesis of peptic ulcer remains uncertain. AIM : To evaluate the evidence of the pathogenic role of H. pylori infection in peptic ulcer disease in patients with cirrhosis. MATERIALS AND METHODS : An extensive MEDLINE search of the literature was performed. Studies reporting the prevalence of H. pylori infection in cirrhotic patients with and without ulcers were selected. Meta-analysis was conducted using RevMan 4.0.3. Pooled odds ratios were calculated for each comparison, using a fixed model analysis. RESULTS : The search identified seven studies with a total of 976 patients with cirrhosis (275 cases with ulcer disease and 701 controls). The prevalence of H. pylori infection in patients with peptic ulcer disease was higher than in those without. The pooled odds ratio was 2.70 (95% CI, 1.91-3.82). H. pylori infection was associated more or less equally with duodenal and gastric ulcers. CONCLUSION: H. pylori infection increases the risk of peptic ulcer disease in patients with cirrhosis.