Role ofHelicobacter pylori in cirrhotic patients with peptic ulcer

Helicobacter pylori was found to be a promoter factor of peptic ulcer that has an incidence higher in patients with hepatic cirrhosis. To clarify the role betweenH. pylori and peptic ulcer in patients with hepatic cirrhosis, a serological test (ELISA test, HEL-p, AMRAD, Australia), was used to measure the presence ofH. pylori of patients with hepatic cirrhosis. Within two years, 108 cirrhotic patients who had received a panendoscopic examination were enrolled in this study. There were 79 males and 27 females with a mean age of 53.2 years. Sixty-four cases had positive serum HBsAg and 44 had negative serum. The results showed that the prevalence ofHelicobacter pylori in cirrhosis was 43.5% (47/108). There was no difference of HEL-p-positive rate between peptic ulcer and normal gastroduodenal mucosa (45.2% vs 46.1%,P>0.05). According to this study, there appears to be no relation between peptic ulcer andH. pylori in patients with hepatic cirrhosis. The etiology of peptic ulcer in cirrhotic patients need further study.     

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.     

Eradication rates of helicobacter pylori infection with second-line treatment: non-ulcer dyspepsia compared to peptic ulcer disease

BACKGROUND/AIMS: Initial proton pump inhibitor (PPI)-based triple therapy for Helicobacter pylori (H. pylori) infection is less effective in patients with nonulcer dyspepsia (NUD) than those with peptic ulcer disease (PUD). To date, there have been no studies on the difference in eradication rates in NUD compared to PUD with regard to second-line therapy. Therefore, we retrospectively analyzed the difference in eradication rates of a second-line quadruple therapy for NUD and PUD patients. METHODOLOGY: Between June 2003 and December 2005, patients who failed to respond to initial PPI-based triple therapy, received 7 days of quadruple therapy (PPI b.i.d., bismuth 300mg q.i.d., metronidazole 500mg t.i.d., tetracycline 500mg q.i.d.) as a second-line treatment regimen. Four weeks after the completion of the course of medication, a 13C-urea breath test was performed for detection of H. pylori. RESULTS: A total of 87 patients received second-line quadruple therapy. Of these, 43 patients had NUD and 44 patients had PUD (19 gastric ulcers, 23 duodenal ulcers, 2 both ulcers). The eradication rates were 76.7% (33/43) in the NUD group and 90.9% (40/44) in the PUD group by per-protocol analysis. Therefore, the eradication rates in the NUD group were significantly lower than those in the PUD group (p = 0.034). CONCLUSIONS: A 7-day bismuth-based second-line quadruple therapy for H. pylori infection was less effective in patients with NUD than those with PUD. Therefore, a more potent second-line treatment regimen or extension of treatment duration of quadruple therapy should be considered for the eradication of H. pylori in patients with NUD.     

Campylobacter pylori and its role in peptic ulcer disease

In almost all patients with genuine nondrug-induced duodenal or gastric ulcer there is evidence of gastric Campylobacter pylori colonization and concomitant inflammation. C. pylori is only demonstrable in the duodenal cap when there is "gastric mucus metaplasia." Suppression or eradication of C. pylori with antibiotic therapy may accelerate duodenal ulcer healing. The relapse rate of duodenal ulcer is less after temporary clearing or permanent eradication of C. pylori. As eradication of C. pylori reduces or eliminates gastric (and duodenal) inflammation, this renders the gastroduodenal mucosa less susceptible to reulceration. Interference with C. pylori status presumably explains the retardation of relapse of duodenal ulcer healing with colloidal bismuth subcitrate.     

Epidemiology of peptic ulcer disease

In the United States about four million people have active peptic ulcers and about 350,000 new cases are diagnosed each year. Four times as many duodenal ulcers as gastric ulcers are diagnosed. Approximately 3000 deaths per year in the United States are due to duodenal ulcer and 3000 to gastric ulcer. There has been a marked decrease in reported hospitalization and mortality rates for peptic ulcer in the United States. Changes in criteria for selecting the underlying cause of death might account for some of the apparent decrease in ulcer mortality rates. Hospitalization rates for duodenal ulcers decreased nearly 50 per cent from 1970 to 1978, but hospitalization rates for gastric ulcers did not decrease. Although this decrease in hospitalization rates may reflect a decrease in duodenal ulcer disease incidence, it appears that changes in coding practices, hospitalization criteria, and diagnostic procedures have contributed to the reported declines in peptic ulcer hospitalization and mortality rates. There is no good evidence to support the popular belief that peptic ulcer is most common in the spring and autumn. The most consistent pattern appears to be low ulcer rates in the summer. There is strong evidence that cigarette smoking, regular use of aspirin, and prolonged use of steroids are associated with the development of peptic ulcer. There is some evidence that coffee and aspirin substitutes may affect ulcers, but most studies do not implicate alcohol, food, or psychological stress as causes of ulcer disease. Genetic factors play a role in both duodenal and gastric ulcer. The first-degree relatives of patients with duodenal ulcer have a two- to threefold increase in risk of getting duodenal ulcer and relatives of gastric ulcer patients have a similarly increased risk of getting a gastric ulcer. About half of the patients with duodenal ulcer have elevated plasma pepsinogen I. A small increase in risk of duodenal ulcer is found in persons with blood group O and in subjects who fail to secrete blood group antigens into the saliva. In most Western countries, morbidity from duodenal ulcer is more common than from gastric ulcer, even though deaths from gastric ulcer exceed or equal those from duodenal ulcer. In Japan, both morbidity and mortality are higher for gastric ulcer than for duodenal ulcer.     

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.     

The effect of eradicating helicobacter pylori on the development of gastric cancer in patients with peptic ulcer disease

OBJECTIVES: Infection with Helicobacter pylori is a risk factor for the development of gastric cancer. However, it is not known whether eradication therapy can prevent the development of gastric cancer in persons in whom the cancer is not yet established. In the present study, we investigated whether the eradication of H. pylori in patients with peptic ulcer disease reduces the likelihood of their developing gastric cancer. METHODS: Prospective posteradication evaluations were conducted in 1,342 consecutive patients (1,191 men and 151 women; mean age: 50 yr) with peptic ulcer diseases who had received H. pylori eradication therapy. After confirmation of eradication, endoscopy and a urea breath test were performed yearly. RESULTS: A total of 1,120 patients completed more than 1-yr follow-up and were followed for up to 8.6 yr (a mean of 3.4 yr). Gastric cancer developed in 8 of 944 patients cured of infection and 4 of 176 who had persistent infection (p= 0.04; log-rank test). All the gastric cancer developed in patients with gastric ulcer, but none in patients with duodenal ulcer (p= 0.005; Fisher's exact test). In patients with gastric ulcer, persistent infection was identified as a significant factor for the risk of developing gastric cancer (hazard ratio: 3.35; 95% confidence interval: 1.00-11.22; p= 0.04; Cox's proportional-hazards model). CONCLUSION: H. pylori eradication may reduce their risk of developing gastric cancer in patients with gastric ulcer. Large-scale studies in additional populations of this important international public-health issue are warranted.     

Epidemiology of Helicobacter pylori and peptic ulcer in India

BACKGROUND: There is a wide variation in the prevalence of peptic ulcer in India both before and since the use of endoscopy. We studied the prevalence of peptic ulcer disease in a community in northern India and its relationship with Helicobacter pylori infection. METHODS: A house-to-house survey of residents aged 15 years or above in a sub-sector of Chandigarh was performed as part of a pilot survey. Subsequently, the study randomly covered all sectors of Chandigarh and we screened 2649 persons. A questionnaire was administered to each subject by trained staff. All individuals with history of peptic ulcer/dyspepsia and an equal number of asymptomatic individuals were asked to attend the outpatient department of the Institute. Diagnosis of peptic ulcer was based on endoscopy or history of previous ulcer surgery. RESULTS: Two hundred and fifty-four individuals attended the outpatient department at the Institute and 147 underwent endoscopy, biopsy for histology and rapid urease test, and blood was collected for H. pylori serology. There were 80 symptomatic and 67 asymptomatic individuals. Helicobacter pylori was positive in 38 (56.7%) asymptomatic and 49 (61.3%) symptomatic individuals (P > 0.05). The point prevalence of active peptic ulcer was 3.4% and the lifetime prevalence was 8.8%. The duodenal-to-gastric ulcer ratio was 12:1. Helicobacter pylori was present in 11/13 (84.6%) subjects with peptic ulcer. Peptic ulcer was more common in elderly and dyspeptic individuals and there was no effect of sex or socioeconomic status. Helicobacter pylori was associated with age only and did not depend on sex, socioeconomic status or dyspepsia. Of the 38 asymptomatic persons having H. pylori infection, none had active peptic ulcer. CONCLUSIONS: This study demonstrates frequent occurrence of peptic ulcer and H. pylori in this part of the country. Peptic ulcer was more prevalent in the elderly and dyspeptic subjects. Helicobacter pylori was not associated with dyspepsia, and was more prevalent in elderly subjects. There was a low prevalence of peptic ulcer in asymptomatic H. pylori-infected persons in this community.     

幽门螺杆菌感染根除与老年消化性溃疡发生、复发关系的研究

目的　探讨老年消化性溃疡发生、复发与幽门螺杆菌 (Hp)感染的关系。方法　应用 PCR法对 78例老年性消化性溃疡幽门螺杆菌感染及幽门螺杆菌感染根除治疗后半年、 1年幽门螺杆菌再感染者进行了测定。结果　幽门螺杆菌检出率老年组明显高于青年组 ,Hp根治率青年组明显高于老年组 ,经 Hp根除治疗组溃疡愈合率明显高于未根除治疗组。结论　老年消化性溃疡发生与幽门螺杆菌感染密切相关 ,在溃疡治疗中 ,根除 Hp感染对减少溃疡复发具有重要临床意义     

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.     

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.     

老年消化性溃疡患者幽门螺杆菌、生长激素释放肽和生长抑素相关性分析

目的 通过检测抑酸药物治疗前老年消化性溃疡(PU)患者循环血中生长激素释放肽(ghrelin)和生长抑素(SST)的含量及幽门螺杆菌(Hp)感染情况,探讨老年性PU患者ghrelin和SST及Hp三者之间的关系.方法 选取Gu患者36例,其中老年组13例,中青年组23例;DU患者33例,其中老年10例,中青年23例;正常对照组15例;采用ELISA和BIA法检测血液中ghrelin和SST的水平,快速尿素酶联合血清抗体法检测Hp感染情况.结果 ①老年DU和GU组血清中ghrelin的水平与中青年组相同且明显高于正常对照组(P<0.05,P<0.01);②老年GU和DU组血浆中SST水平与中青年组相同且明显高于正常对照组(P<0.05,P<0.01),且GU组高于DU组(P<0.05);③Hp感染对循环血中ghrelin与SST水平无明显影响;④Ghrelin与SST之间的相关系数为GU:r=0.445(P<0.05),DU:r=0.462(P<0.05).结论 老年PU患者循环血中gIIrelin及SST的水平显著增高可能与溃疡的发病有关.Hp感染对循环血中ghrelin及SST水平无明显影响.ghrelin及SST在PU循环血中的表达成正相关.     

Helicobacter pylori infection in peptic ulcer disease: the importance of smoking and ethnicity

This study was conducted to determine the prevalence of Helicobacter pylori (H. pylori) and its associated factors among patients with peptic ulcer disease in Taiping Hospital. Consecutive peptic ulcer disease patients who had undergone esophagogastro-duodenoscopy were included. The H. pylori status was assessed by the rapid urease test. We excluded those who had active bleeding, a perforated peptic ulcer, severe vomiting, a history of gastric surgery, peptic ulcer disease or renal or liver diseases, carcinoma of the stomach, and recent use of antibiotics or proton pump inhibitors. Socio-demography, H. pylori status, medication history and other relevant clinical data were collected from case notes. A total of 416 subjects were selected, 49.7% were positive and 50.3% were negative for H. pylori infection. There were significant associations between H. pylori and age, ethnicity, smoking status and NSAID usage. However, there were no significant relationships between H. pylori status and gender or type of peptic ulcer. Multiple logistic regression showed that other ethnicities than Malays and smokers had a higher risk of H. pylori. Our prevalence rate was low and the identified risk factors were consistent with previous studies. Ethnic differences may be related to genetic and sociocultural behaviors. Quitting smoking may benefit peptic ulcer patients with H. pylori infection.     

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.     

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.     

Active peptic ulcer disease in patients with hepatitis C virus-related cirrhosis: the role of Helicobacter pylori infection and portal hypertensive gastropathy.

BACKGROUND & AIM: The relationship between Helicobacter pylori infection and peptic ulcer disease in cirrhosis remains controversial. The purpose of the present study was to investigate the role of H pylori infection and portal hypertension gastropathy in the prevalence of active peptic ulcer among dyspeptic patients with compensated hepatitis C virus (HCV)-related cirrhosis. METHODS: Patients undergoing upper endoscopy with compensated HCV-related cirrhosis were enrolled. Child-Pugh's score was determined at the entry. Variceal size was measured endoscopically and the severity of portal hypertensive gastropathy was graded. H pylori infection status was determined by urea breath testing and/or histology. RESULTS: A total of 178 patients positive for HCV (A and B Child-Pugh's score) were prospectively included. The prevalence of H pylori infection was 43%. An active peptic ulcer was found in 14 patients (8%) and was significantly more common among those with H pylori infection (16% versus 2% in H pylori uninfected patients, odds ratio: 8.0). No association was observed between H pylori infection and variceal size, or hypertensive gastropathy. CONCLUSIONS: Patients with compensated cirrhosis and H pylori infection showed higher risk of developing a peptic ulcer. Clinical relevance of this result would be that dyspeptic patients with HCV-related cirrhosis may benefit from preventive screening and eradication of H pylori, especially those with features of insufficient hemostasis.