The effects of eradication of Helicobacter pylori on the recurrence of duodenal ulcers in patients with cirrhosis

BACKGROUND: The role of Helicobacter pylori in patients with cirrhosis and increased prevalence of peptic ulcers is still poorly defined. The objective is to evaluate the effect of H pylori eradication on ulcer recurrence in patients with cirrhosis. METHODS: The study was conducted at a single, tertiary, referral hospital with 1200 beds. Patients with cirrhosis and duodenal ulcers were tested for H pylori and were enrolled in the study. Patients with positive H pylori received eradication therapy. Patients with duodenal ulcers received antisecretory therapy and regular endoscopic examinations. Main outcome measurements were the recurrence of duodenal ulcers within 1 year. RESULTS: A total of 104 patients with cirrhosis and duodenal ulcers were enrolled. Fifty-four patients (52%) were H pylori positive, and 50 patients (48%) were H pylori negative. Forty-four patients received antimicrobial treatment and 36 patients achieved eradication of H pylori. Recurrent duodenal ulcers within 1 year were noted in 21 of 36 patients (58%) who achieved H pylori eradication. Recurrent duodenal ulcers also were noted in 8 of the 18 patients (44%) who remained H pylori positive and in 24 of the patients (48%) who were H pylori negative since their enrollment in the study (p = 0.53). The limitation was a relatively small sample size. CONCLUSIONS: The results of our study showed that the prevalence of H pylori in patients with cirrhosis and duodenal ulcers was only 52%. Eradication of H pylori in patients with cirrhosis and duodenal ulcers did not effectively reduce the recurrence of ulcers.     

Role of Helicobacter pylori in ulcer healing and recurrence of gastric and duodenal ulcers in longterm NSAID users. Response to omeprazole dual therapy.

BACKGROUND: The relation between Helicobacter pylori infection and non-steroidal anti-inflammatory drug (NSAID)-associated peptic ulcers remains unclear; in particular, it is not known whether H pylori plays a part in the healing and recurrence of these ulcers. AIMS: To evaluate prospectively in a consecutive series of arthritis patients receiving longterm NSAID treatment the prevalence of peptic ulcer as well as the effect of H pylori eradication on the healing and recurrence of gastric and duodenal ulcer found. PATIENTS: Some 278 consecutive patients underwent gastroscopy with multiple biopsies of the gastric antrum and corpus for histological examination and rapid urease test. One hundred peptic ulcers (59 gastric ulcers, 39 duodenal ulcers, and two gastric ulcers concomitant with a duodenal ulcer) were found. Seventy per cent of these ulcers were H pylori positive. METHODS: According to their H pylori status, ulcer patients were randomised to one of the following treatments: H pylori negative ulcers received omeprazole 20 mg twice daily for four to eight weeks, whereas H pylori positive lesions were treated with omeprazole 20 mg twice daily plus amoxycillin 1 g twice daily (the second of these for the first two weeks) or omeprazole alone for four to eight weeks while continuing NSAID therapy. Patients with healed ulcers were endoscopically followed up for six months after stopping antiulcer therapy while continuing NSAIDs. RESULTS: Endoscopic healing rates for gastric and duodenal ulcers in the three different groups were similar both at four and eight weeks. H pylori eradication did not influence healing, which occurred in 14 of 20 (70%) of patients in whom H pylori was eradicated, compared with 14 of 17 (82%) of patients with persistent infection. Cumulative recurrence rates at six months did not statistically differ among the three different groups (27% in H pylori negative, 46% in H pylori positive, and 31% in those where H pylori was eradicated during the healing phase), although a numerical trend in favour of a higher recurrence rate in infected patients was evident. CONCLUSIONS: H pylori eradication does not confer any significant advantage on the healing of gastric and duodenal ulcers associated with longterm NSAID use. It remains to be established with certainty whether eradication may be helpful in the reduction of recurrence in a specific subset of NSAID associated ulcer.     

Peptic ulcer bleeding: is Helicobacter pylori a risk factor in an endemic area?

BACKGROUND/OBJECTIVE: A high prevalence of Helicobacter pylori infection has been reported in Iran. Although the importance of H. pylori in the induction of peptic ulcer disease is clearly defined, only few studies have addressed its role in bleeding from peptic ulcers. We evaluated the role of H. pylori in peptic ulcer bleeding. METHODS: Patients with acute peptic ulcer bleeding (PUB) and those with peptic ulcer disease without bleeding ('controls') were enrolled. Upper GI endoscopy and rapid urease test were performed in both groups. Histological study for detection of H. pylori was performed in patients with active bleeding, if RUT was negative. Other variables evaluated included sex, age, smoking, previous history of bleeding, non-steroidal anti-inflammatory drugs use, ulcer size, ulcer location, and duration of acid-peptic disease. Multivariate logistic regression analysis was performed to identify independent risk factors. RESULTS: 161 patients with PUB and 287 control patients were enrolled. H. pylori infection was seen more frequently in patients with duodenal ulcer than gastric ulcer (88.9% vs. 60.5%, p< 0.001). Univariate analysis showed that patients with PUB were more often male, older in age, used NSAID, had history of PUB in the past, had ulcer located in the stomach and not in the duodenum, and more often had large ulcer (>1 cm). Logistic regression analysis showed that H. pylori infection was protective in PUB after controlling for confounders (OR 0.41, 95% CI 0.21-0.79), when ulcer location was not entered in the model. A second model including ulcer location (to test for a residual effect) showed that H. pylori infection was not a significant risk factor in PUB (OR 0.61, 95% CI 0.30-1.24). CONCLUSIONS: H. pylori may not be an independent factor in bleeding from peptic ulcers. The lower frequency of this infection in these patients can be described by the higher frequency of bleeding from gastric ulcers, which are less H. pylori related compared with duodenal ulcer.     

Attributable Risk of H. pylori in Peptic Ulcer Disease

Recent reports in the United States have found that fewer peptic ulcers are due to Helicobacter pylori than previously believed. The aim of this study is to determine if the declining prevalence of H. pylori infection in the general population can account for the apparent increase in the frequency of non-H. pylori ulcers. A total of 396 patients with peptic ulcer or ulcer scar were enrolled in this study. The pre-1950 population consisted of 149 patients with gastric ulcers and with 44 duodenal ulcers. The post-1950 population consisted of 96 patients with gastric ulcers and 107 with duodenal ulcers. The frequency of H. pylori-negative gastric ulcers was 5.4% in patients born before 1950 and 4.2% in patients born after 1950, and the frequency of H. pylori-negative duodenal ulcers was 0% and 1.9%, respectively. There are no statistical differences between the two populations in gastric and duodenal ulcers. H. pylori seropositivity was 74.9% in asymptomatic volunteers born before 1950 and 20.7% in those born after 1950 (P < 0.01) in the general population. The attributable risk of H. pylori infection in peptic ulcer diseases was not affected by the prevalence of H. pylori infection in the general population in Japan. This suggests that the apparent increase in frequency of non-H. pylori ulcers in the United States is not simply due to the declining prevalence of infection. Other explanations for non-H. pylori ulcers should be sought.     

Maintenance treatment is not necessary after Helicobacter pylori eradication and healing of bleeding peptic ulcer: a 5-year prospective, randomized, controlled study

BACKGROUND: It is well accepted that in patients with uncomplicated peptic ulcers, Helicobacter pylori eradication therapy does not need to be followed by further antisecretory treatment. However, it is uncertain whether patients with bleeding peptic ulcers should receive maintenance antiulcer therapy after successful H pylori eradication and ulcer healing. The aim of this 5-year, prospective, randomized, controlled study was to investigate the role of long-term maintenance therapy after successful H pylori eradication and healing of bleeding ulcers. METHODS: A total of 82 consecutive patients with H pylori-associated bleeding peptic ulcers were enrolled in the study. After successful H pylori eradication with the 1-week proton pump inhibitor-based triple therapy and an additional 3-week treatment with 20 mg of omeprazole daily for ulcer healing, the patients were assigned to one of four 16-week maintenance treatment groups as follows: group A received 15 mL of an antacid suspension 4 times daily; group B received 300 mg of colloidal bismuth subcitrate 4 times daily; group C received 20 mg of famotidine twice daily; and group D, the control group, received placebo twice daily. Follow-up included an urea breath test labeled with carbon 13, biopsy-based tests, and repeated endoscopic examination. RESULTS: An analysis of variance revealed no difference in mean age and mean follow-up time among the groups. During a mean follow-up of 56 months, there was no peptic ulcer recurrence among the 3 treatment groups, and all of the patients remained free of H pylori infection during the study period. CONCLUSIONS: In patients with bleeding peptic ulcers, antiulcer maintenance treatment was not necessary to prevent ulcer recurrence after successful H pylori eradication and ulcer healing. In addition, the 1-week proton pump inhibitor-based triple therapy had the efficacy to ensure long-term eradication of H pylori in a region of high prevalence.     

Ideology of Helicobacter pylori prevalence in peptic ulcer disease in an inner-city minority population

GOALS AND BACKGROUND: The prevalence of Helicobacter pylori infection among patients with peptic ulcer disease has been reported to range from 61 to 94%. Recent studies show a reduction in the prevalence of H. pylori infection in patients with peptic ulcer disease. This study was conducted to determine the prevalence of H. pylori infection in peptic ulcer disease in an inner-city hospital in Washington, DC. METHODS: Medical records of all patients who had undergone upper gastrointestinal endoscopy from July 1997 through June 1999 were reviewed. All patients who had gastric ulcer and/or duodenal ulcer on upper gastrointestinal endoscopy were studied. Demographic characteristics, history of nonsteroidal antiinflammatory drug ingestion, alcohol consumption, and associated diseases were studied. H. pylori was considered to be present if CLOtest and/or histopathology were positive for H. pylori. Patients with negative pathology for H. pylori or negative pathology and CLOtest were considered negative for H. pylori. RESULTS: One-hundred fifty-six patients were found to have gastric and/or duodenal ulcers. Fifty-one ulcer patients did not meet the inclusion criteria and were excluded. Among the 105 patients who were included in the study, gastric ulcers were found in 48 patients (45.7%), duodenal ulcers were found in 46 patients (43.8%), and both gastric and duodenal ulcers were found in 11 patients (10.5%). H. pylori was present in 66.7% of gastric ulcer patients and in 69.5% of duodenal ulcer patients. Antral histology and CLOtest were in agreement 96% of the time. CONCLUSIONS: At the District of Columbia General Hospital, an inner-city hospital serving predominantly an African-American community, the prevalence of H. pylori in ulcer patients compares similarly to other more recent studies that have found a decreased prevalence of this bacterial infection in ulcer patients. This suggests that the treatment of H. pylori in minority patients is reducing the proportion of ulcers due to this bacterium, as has been seen with the majority population.     

Cure of Helicobacter pylori-positive active duodenal ulcer patients: a double-blind, multicentre, 12-month study comparing a two-week dual vs a one-week triple therapy. GISU (Interdisciplinary Group for Ulcer Study).

AIMS: To compare a two-week dual therapy to a one-week triple therapy for the healing of duodenal ulcer and the eradication of the Helicobacter pylori infection. PATIENTS AND METHODS: A total of 165 patients with active duodenal ulcer were enrolled in the study. At entry, endoscopy, clinical examination and laboratory tests were performed. Histology and the rapid urease test were used to diagnose Helicobacter pylori infection. Patients received either lansoprazole 30 mg plus amoxycillin 1 g bid for two weeks (two-week, dual therapy) or lansoprazole 30 mg plus amoxycillin 1 g plus tinidazole 500 mg bid for one week plus lansoprazole qd for an additional week (one-week, triple therapy). Two and twelve months after cessation of therapy, endoscopy and clinical assessments were repeated. RESULTS: Duodenal ulcer healing and Helicobacter pylori eradication were both significantly greater (p<0.0001) in the triple therapy group (healing: 98.6%; Helicobacter pylori cure rate: 72.6%) than in the dual therapy group (healing: 77.3%; Helicobacter pylori cure rate: 33.3%). Ulcers healed more frequently in Helicobacter pyloricured than in Helicobacter pylori-not cured patients (94.9% vs. 77.2%; p<0.0022). After one year, Helicobacter pylori eradication was re-confirmed in 46/58 patients previously treated with the triple therapy and in 10/40 patients treated with the dual therapy [p<0.0001]. Only three duodenal ulcer relapses were observed throughout follow-up: all were in Helicobacter pylori-not cured patients. CONCLUSIONS: Triple therapy was more effective than dual both in curing Helicobacter pylori infection and healing active duodenal ulcers. The speed of ulcer healing obtained after only 7 days of antibiotics and 14 days of proton pump inhibitors confirmed that longer periods of anti ulcer therapy were not necessary. Helicobacter pylori -not cured patients had more slowly healing ulcers which were more apt to relapse when left untreated.     

Clinical significance of widespread gastric metaplasia in the duodenal bulb

BACKGROUND: All the risk factors of peptic ulcer disease are not thoroughly understood. GOALS: To assess duodenal gastric metaplasia (DGM) in relation to Helicobacter pylori status and endoscopy findings with special reference to the effects of highly selective vagotomy. STUDY: The study population consisted of 1056 adult patients and an additional 154 patients who had had a highly selective vagotomy. Their clinical and endoscopy records as well as the histology of gastric and duodenal biopsies were evaluated retrospectively. H. pylori infection had been determined by serology and culture. RESULTS: Widespread (more than 20%) DGM was strongly associated with H. pylori positive duodenal ulcer disease (in 59.7% of patients). The prevalence of DGM diminished progressively the more proximally the ulcer was located in the stomach, and was 2.5% in proximal gastric ulcers patients. In vagotomized patients, the prevalence of widespread DGM (8.4% of patients, median 14 years after operation and the majority still H. pylori positive) was close to that of patients with H. pylori gastritis without peptic ulcer disease (4.5%). CONCLUSIONS: Widespread DGM is an indicator for an increased risk of duodenal ulcer among H. pylori positive patients and it could be used to select patients for eradication therapy.     

Does Helicobacter pylori infection eradication modify peptic ulcer prevalence？ A 10 years＇ endoscopical survey

AIM: To compare peptic ulcer prevalence in patients referred for upper gastrointestinal endoscopy in two Italian hospitals in pre-Helicobacter era and ten years after the progressive diffusion of eradication therapy. METHODS: We checked all the endoscopic examinations consecutively performed in the Gastroenterology Unit of Padova during 1986-87 and 1995-96, and in the Gastroenterology Unit of Parma during 1992 and 2002. Chi Square test was used for statistic analysis. RESULTS: Data from both the endoscopic centers showed a statistically significant decrease in the prevalence of ulcers: from 12.7% to 6.3% (P< 0.001) in Padova and from 15.6% to 12% (P< 0.001) in Parma. The decrease was significant both for duodenal (from 8.8% to 4.8%, P< 0.001) and gastric ulcer (3.9% to 1.5%, P< 0.001) in Padova, and only for duodenal ulcer in Parma (9.2% to 6.1%, P< 0.001; gastric ulcer: 6.3% to 5.8%, NS). CONCLUSION: Ten years of extensive Helicobacter pylori (H pylori) eradication in symptomatic patients led to a significant reduction in peptic ulcer prevalence. This reduction was particularly evident in Padova, where a project for the sensibilization of H pylori eradication among general practioners was carried out between 1990 and 1992. Should our hypothesis be true, H pylori eradication might in the future lead to peptic ulcer as a rare endoscopic finding.     

4-day triple therapy with rabeprazole, amoxicillin and clarithromycin in the eradication of Helicobacter pylori in patients with peptic ulcer disease--A pilot study

BACKGROUND: It is well established that a 7-day triple therapy achieves eradication rates of Helicobacter pylori between 90% and 95%. Due to a lack of highly effective short-term eradication studies the aim of the present pilot study was to investigate the effect of a 4-day triple therapy with the new proton pump inhibitor rabeprazole (20 mg b. i. d.) in combination with clarithromycin (500 mg b. i. d.) and amoxicillin (1 g b. i. d.) without acid-suppressive pre-treatment in patients with H. pylori-related peptic ulcer disease. METHODS: 20 patients (11 men, 9 women) with endoscopically diagnosed peptic ulcers (gastric ulcer: n = 5; duodenal ulcer: n = 9; combined gastric and duodenal ulcer: n = 2, gastric or duodenal ulcer scars: n = 4) and H. pylori infection were consecutively recruited. The Helicobacter pylori status was assessed by means of histology, CLO (urea-) test and C13-urea breath test (C13-UBT) at entry. Treatment success was determined by C13-UBT 35-42 days after end of treatment. RESULTS: In 18 out of the 20 patients (90%) [77-100%, 95%-CI] a negative test result was found in C13-UBT 35-42 days after treatment. The 2 patients who remained H. pylori-positive had a duodenal ulcer. CONCLUSION: A 4-day triple therapy of rabeprazole in combination with clarithromycin and amoxicillin seems to be highly effective in eradicating H. pylori and well tolerated in patients with gastric and duodenal ulcer disease. The achieved eradication rate of 90% is comparable with the established 7-day triple therapy regimens. On the basis of these results and considering costs, side effects and compliance a large number of patients should be enrolled in a confirmatory 4-day eradication trial.     

Size of the peptic ulcer in Helicobacter pylori-positive patients: association with the clinical and histological characteristics

OBJECTIVE: Based on a large trial of Helicobacter pylori-positive peptic ulcer patients, we studied whether the size of the ulcer, along with other clinical and histological characteristics, has any effect on healing. We also studied the clinical and endoscopic characteristics associated with size of the peptic ulcer. MATERIAL AND METHODS: A total of 333 consecutive patients with H. pylori infection and peptic ulcer were enrolled (mean age 54.8+/-12.7 years). Location of the ulcer was recorded by gastroscopy and the presence of H. pylori was assured by rapid urease test, histology and by serum H. pylori IgG and IgA antibody measurement. The diameter of the ulcer was measured by placing the opened biopsy forceps (7 mm) beside it. Biopsy specimens were examined in accordance with the Sydney system. RESULTS: Mean size of the peptic ulcer was 13.2+/-8.3 in corpus, 11.3+/-5.3 in antrum, 13.8+/-7.8 in angulus, 9.5+/-5.3 in prepylorus and 9.2+/-4.7 mm in duodenum (duodenal versus gastric type; p<0.05). Average size of the ulcers was 9.4+/-5.3 mm in patients with Forrest III type and 11.5+/-6.8 in other types (p<0.05). Patients who were >or=50 years of age, currently smoking, or who had corpus-predominant chronic gastritis or atrophic gastritis, had larger ulcers than others. Size of index ulcers, successful eradication of H. pylori and the presence of atrophic gastritis were independent factors for healing. The odds ratio was 11.5 (95% CI 3.3-40.5; p<0.01) for eradication of H. pylori, 3.5 (95% CI 1.1-11.2; p<0.05) for size of the index ulcer (10 mm) and 3.4 (95% CI 1.2-9.8; p<0.05) for atrophic gastritis versus no atrophy. CONCLUSIONS: Size of the peptic ulcer, successful H. pylori eradication and atrophic gastritis were independent factors for the healing of peptic ulcers. A number of clinical and endoscopic variables (age, current smoking, corpus-predominant gastritis, Forrest classification) were associated with size of the peptic ulcer in H. pylori-positive patients.     

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.     

Helicobacter pylori, non-steroidal anti-inflammatory drugs and smoking in risk pattern of gastroduodenal ulcers

BACKGROUND: Helicobacter pylori, NSAID and cigarette smoking are major risk factors for gastroduodenal ulcers. However, the results of studies on the interaction between these factors on ulcerogenesis are controversial. This study was designed to examine the association between gastroduodenal ulcers and H. pylori infection, NSAID use, smoking and age. METHODS: 5967 dyspeptic patients underwent 13C-urea breath test (UBT) and upper endoscopy, while age and dyspeptic symptoms were reported. RESULTS: Out of 5967 patients, 31.8% were ulcerated; 9.2% had gastric, 17.2% duodenal and 5.4% both gastric and duodenal ulcers. H. pylori was found in 72.5% of gastric ulcer patients, in 83.6% of duodenal ulcer patients, in 76.9% of gastroduodenal ulcer patients and in 64.8% of dyspeptic patients. The gastric, duodenal and gastroduodenal ulcers were related to H. pylori significantly and the respective ORs were: 1.44, 2.77 and 1.81. NSAID alone was used by 6.2%-12.7% of ulcer patients, tending to raise only the risk of gastric ulcer but reducing that of duodenal and gastroduodenal ulcers. The H. pylori prevalence was significantly higher in smokers (76%) than in non-smokers (67%) and the ulcer risk was also significantly higher in smokers than in non-smokers. About 20% of ulcers were 'idiopathic', i.e. without NSAID and H. pylori and the ratio of these ulcers to all ulcers significantly increased during the 5 years of the study. CONCLUSIONS: Based on multivariable logistic regression analysis we conclude that: 1) H. pylori infection, NSAID use, smoking and age play major roles in the pathogenesis of peptic ulcerations; 2) there is a negative interaction between H. pylori and NSAID on duodenal ulcers, suggesting that H. pylori reduces the development of these ulcers in NSAID users, and 3) about 20% of peptic ulcers in the Polish population are unrelated to H. pylori and NSAID use (idiopathic ulcers).     

Prevalence of Peptic Ulcer in Dyspeptic Patients and the Influence of Age,Sex, and <Emphasis Type="Italic">Helicobacter pylori</Emphasis> Infection

We investigated the prevalence of peptic ulcer in dyspeptic patients in China to analyze the influence of age, sex, and Helicobacter pylori (H. pylori) infection. The results showed that the prevalence of gastric and duodenal ulcer increased with age. In patients under 60 years old, the prevalence of duodenal and gastric ulcers in females was markedly lower than that in males, especially the prevalence of duodenal ulcer. The prevalence of duodenal ulcer and gastric ulcer in H. pylori-infected patients was markedly higher than in patients without H. pylori infection. In the patients under 60 years old, sex differences were still seen in both H. pylori-positive and H. pylori-negative patients. The prevalence of gastric and duodenal ulcers was markedly increased with age in both H. pylori-positive and H. pylori-negative patients. Multivariate logistic regression analysis showed that age, male sex, and H. pylori infection were three independent risk factors for gastric and duodenal ulcers.     

What consideration should be given to Helicobacter pylori in treating nonsteroidal anti-inflammatory drug ulcers?

Although Helicobacter pylori and nonsteroidal anti-inflammatory drugs (NSAIDs) both cause peptic ulcers, they do so by different mechanisms so any interaction is not necessarily harmful. H. pylori has been shown to enhance gastric mucosal prostaglandin synthesis, while NSAIDs suppress it Pragmatically, there is no compelling evidence in favour of H. pylori eradication in all patients who take NSAIDs. As a broad generalisation, in therapeutic studies of NSAID users, those who have no ulcer at trial entry are more prone to ulcer development if they are H. pylori-positive. By contrast, in those who have ulcers at baseline, H. pylori-positive individuals are less likely to develop ulcers, particularly if taking acid-suppressive therapy. Trials of H. pylori eradication therapy tend to replicate this dichotomy. In one study of patients starting NSAIDs for the first time, with no ulcer history and no baseline ulcer, use of bismuth-based eradication therapy was associated with a lower incidence of gastric ulcer at 2 months. Conversely, in a study of patients with endoscopically proven ulcers and/or troublesome dyspepsia, proton pump inhibitor based eradication treatment had no effect on outcome (of acid suppression) over 6 months. H. pylori eradication has been associated with significantly slower healing of gastric ulcers compared with patients who did not undergo eradication. However, the effect of H. pylori eradication on healing of NSAID-associated duodenal ulcers does not appear to be so dramatic, and limited evidence suggests that it may be possible to prevent H. pylori-associated duodenal ulcer by eradicating the infection. An evidence-based approach to treatment would suggest that NSAID users should undergo H. pylori eradication therapy if they have a duodenal ulcer, whether or not they continue NSAIDs. Because COX-2 inhibitors appear not to be ulcerogenic, management of H. pylori in patients taking these drugs can be based upon the same risk assessment as in patients not taking anti-arthritis drugs. H. pylori eradication should not be used universally or in high-risk gastric ulcer patients who require management with acid suppression.     

Prevalence of non-Helicobacter pylori duodenal ulcer in Karachi, Pakistan

AIM:To determine the prevalence of non-Helicobacter pylori (H pylori)-related duodenal ulcer in patients with acid-peptic diseases. METHODS: Medical records of patients who attended the Gastroenterology Department at Aga Khan University Hospital from 1999 to 2001 and had endoscopic diagnosis of duodenal ulcers were reviewed. Duodenal ulcer associated with H pylori was diagnosed on the basis of endoscopy, rapid urease test and histopathology whereas histories of aspirin or other non-steroidal anti-inflammatory drugs (NSAIDs) related duodenal ulcers. Non-H pylori, non-NSAID duodenal ulcers were those without H pylori infection and history of NSAID intake. Co-morbid conditions associated were noted. RESULTS: Of 2 260 patients, 10% (217/2 260) had duodenal ulcer. Duodenal ulcer related to H pylori infection accounted for 53% (116/217), NSAID-related 10% (22/217), non-H pylori non-NSAID 29% (62/217), and 8% (17/217) had both H pylori infection and histories of NSAID intake. Fifteen percent (18/116)_patients had past histories of peptic ulcer disease in H pylori infection, while 8% (5/62) in non-H pylori non-NSAID ulcer. Co-morbid conditions in H pylori infection were seen in 23% (27/116) and 34% (21/62) in non-H pylori non-NSAID ulcer. CONCLUSION: Incidence of H pylori infection related with duodenai ulcer is common. In the presence of co-morbids, non-H pylori and non-NSAID duodenal ulcer is likely to be present.     

中国上消化道疾病患者幽门螺杆菌感染根除前后胃粘膜病理改变与空泡毒素活性的关系

目的：观察幽门螺杆菌（H.pylori)阳性消化性溃疡病和慢性胃炎患者H.pylori根除前后胃粘膜病理改变与空泡毒素（VacA)活性的关系。方法：功能性消化不良伴H.pylori感染的中国患者74例,于H.pylori根除前和4－6周后作胃镜检查,根据新悉尼病理分级法按半定量记分对治疗前后的胃粘膜病理变化程度进行分级。结果：VacA^ 菌检出率为80％（59／74）,消化性溃疡病患者的检出率与慢性胃炎患者无明显差别;VacA^ 和VacA^-组患者的H.pylori根除率亦无明显差别。根除治疗前,VacA^ 和VacA^-组患者的胃粘膜慢性炎症、活动性、表面上皮损伤、萎缩、肠化和淋巴滤泡数量无显著差别;治疗后4－6周,两组患者的胃窦粘膜炎症活动性、表面上皮损伤和慢性炎症程度均明显减轻,尤以前者为著（P＜0．0001）,VacA^ 组患者的胃窦部淋巴滤泡数量减少亦稍较VacA^-组明显（P＝0．051）,两组患者的胃粘膜萎缩和肠化程度均无明显好转。结论：中国上消化道疾病患者H.pylori感染根除前后的胃粘膜病理改变与VacA活性无明显关系。成功根除H.pylori感染并不引起萎缩和肠化的逆转。     

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.     

A low prevalence of H pylori and endoscopic findings in HIV-positive Chinese patients with gastrointestinal symptoms

AIM： To compare the prevalence of H pylori infection, peptic ulcer, cytomegalovirus （CNV） infection and Candida esophagitis in human immunodeficiency virus （HIV）- positive and HIV-negative patients, and evaluate the impact of CD4 lymphocyte on H pylori and opportunistic infections.
METHODS： A total of 151 patients （122 HIV-positive and 29 HIV-negative） with gastrointestinal symptoms were examined by upper endoscopy and biopsy. Samples were assessed to determine the prevalence of Hpylori infection, CMV, candida esophagitis and histologic chronic gastritis.
RESULTS： The prevalence of Hpylori was less common in HIV-positive patients （22.1%） than in HIV-negative controls （44.8%; P 〈 0.05）, and the prevalence of H pylori displayed a direct correlation with CD4 count stratification in HIV-positive patients. In comparison with HIV-negative group, HIV-positive patients had a lower incidence of peptic ulcer （20.7% vs 4.1%; P 〈 0.01）, but a higher prevalence of chronic atrophy gastritis （6.9% vs 24.6%; P 〈 0.05）, Candida esophagitis and CMV infection. Unlike HIV-negative group, H pylori infection had a close relationship to chronic active gastritis （P 〈 0.05）. In HIV-positive patients, chronic active gastritis was not significantly different between those with Hpylori infection and those without.
CONCLUSION： The lower prevalence of H pylori infection and peptic ulcer in HIV-positive patients with gastrointestinal symptoms suggests a different mechanism of peptic ulcerogenesis and a different role of H pylori infection in chronic active gastritis and peptic ulcer. The pathogen of chronic active gastritis in HIV-positive patients may be different from the general population that is closely related to Hpylori infection.     

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.