Helicobacter pylori and perforated peptic ulcer. Prevalence of the infection and role of non-steroidal anti-inflammatory drugs

AIMS: To study the prevalence of Helicobacter pylori infection in patients with perforated peptic ulcer, to compare it with the prevalence in patients with uncomplicated ulcer, and to assess the role of non-steroidal anti-inflammatory drugs in this prevalence. METHODS: Consecutive patients with perforated peptic ulcer were included in this retrospective study. As a control group, patients undergoing elective outpatient evaluation for the investigation of dyspepsia during the same time period and found to have a peptic ulcer at endoscopy were included. A 13C-urea breath test was carried out in all patients to diagnose H. pylori infection. RESULTS: Sixteen patients with perforated peptic ulcer and 160 with non-complicated peptic ulcer were included. Sixty-two percent of the patients with perforated peptic ulcer were infected by H. pylori, while the microorganism was detected in 87% of the patients without this complication (P = 0.01). Non-steroidal anti-inflammatory drugs intake was more frequent (P = 0.012) in patients with perforated peptic ulcers (56%) than in those without perforation (26%). H. pylori prevalence in perforated peptic ulcers was of 44% in patients with non-steroidal anti-inflammatory drugs intake, but this figure increased up to 86% when only patients not taking non-steroidal anti-inflammatory drugs were considered (P = 0.09). In the multivariate analysis, non-steroidal anti-inflammatory drugs intake was the only variable that correlated with peptic ulcer perforation [odds ratio, 3.6 (95% confidence interval, 1.3-10); P = 0.016]. CONCLUSION: The mean prevalence of H. pylori infection in patients with perforated peptic ulcer is, overall, of only about 60%, which contrasts with the 90-100% figure usually reported in non-complicated ulcer disease. However, the most important factor associated with H. pylori-negative perforated peptic ulcer is non-steroidal anti-inflammatory drugs use, and if this factor is excluded, prevalence of infection is almost 90%, similar to that found in patients with non-perforating ulcer disease.     

The effect of chronic aspirin use on duodenal and gastric ulcer hospitalizations

Aspirin is commonly accepted as a risk factor for gastric ulcer; however, there is little published evidence linking aspirin consumption to duodenal ulcer. The effect of 1 g of aspirin per day on site-specific ulcer hospitalizations was examined using data from a 3-year randomized, double-blind, placebo-controlled trial of 4,524 subjects (Aspirin Myocardial Infarction Study). There were 23 duodenal ulcer and 14 gastric ulcer hospitalizations during the follow-up period. All but two were verified by endoscopy, radiogram, or biopsy/surgery. For males, a Cox-model survival analysis showed that the age- and smoking-adjusted relative risk for duodenal ulcer hospitalization was 10.7 times higher for the aspirin group than for the placebo group (95% confidence interval, 2.5 to 45.5; p less than 0.0001). The adjusted relative risk for gastric ulcer was 9.1 (95% confidence interval, 1.2 to 71.4; p = 0.04). Due to the small number of females in the study, the relationship between site-specific ulcer and aspirin consumption for females was not analyzed. However, for males and females combined, the age-, smoking-, and sex-adjusted relative risk for peptic ulcer hospitalization was 7.7 (95% confidence interval, 2.7 to 21.7; p less than 0.0001). We conclude that chronic aspirin use is a risk factor for hospitalization for both duodenal and gastric ulcer in males, and for peptic ulcer in males and females.     

Hypersecretory duodenal ulcer and Helicobacter pylori infection: a four-year follow-up study.

BACKGROUND: About 10% of duodenal ulcer patients are characterized by gastric acid hypersecretion with normal gastrin values. Relapsing duodenal ulcer after Helicobacter pylori cure has been related to high acid output and maintenance antisecretory therapy has been suggested in hypersecretory duodenal ulcer patients. The role of Helicobacter pylori infection and the effects of Helicobacter pylori cure in hypersecretory duodenal ulcer patients still remain to be fully studied. AIM: To study: a) whether gastric acid hypersecretion "per se" is a risk factor for duodenal ulcer recurrence; b) whether maintenance antisecretory therapy is necessary after eradication in hypersecretory duodenal ulcer patients. PATIENTS: The study population comprised 8 hypersecretory duodenal ulcer patients, selected from a population of 79 Helicobacter pylori-positive duodenal ulcer patients. METHODS: Hypersecretory duodenal ulcer patients were followed-up for at least 4 years after eradication. Gastric acid secretion was measured again 12 months after Helicobacter pylori eradication. Gastroscopy with histology was performed 3, 6, 12 and 36 months after treatment, 13C-urea breath test after 42 months; clinical questionnaires were completed every 6 months. RESULTS: After eradication, despite a not significantly reduced high acid output (median value of basal acid output and pentagastrin-stimulated acid output, respectively, 23.1 mEq/h and 64.1 mEq/h before treatment vs 16 mEq/h and 49.7 mEq/h 12 months after treatment), all patients were free from symptoms, none of them had duodenal ulcer relapse or complications (7/8 before treatment), or needed antisecretory maintenance therapy, except for one patient taking non-steroidal anti-inflammatory drugs. CONCLUSIONS: These findings, obtained in a selected population of hypersecretory duodenal ulcer patients with long-term follow-up, suggest that after successful Helicobacter pylori eradication gastric acid hypersecretion "per se" is not able to determine the recurrence of duodenal ulcer.     

Interaction between Helicobacter pylori and non-steroidal anti-inflammatory drugs in peptic ulcer bleeding

BACKGROUND: Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs) are the two primary causes of peptic ulcer disease. How H. pylori and NSAIDs interact and influence the development of ulcer bleeding is still not clear. METHODS: A hospital-based, age- and sex-matched case-control study was conducted. Multivariate and stratified analyses were performed for further evaluation of the interaction between H. pylori and NSAIDs. RESULTS: Ninety-seven patients (52 gastric ulcers, 45 duodenal ulcers) and 97 non-ulcer controls were enrolled in the study. H. pylori and NSAIDs were both found to be independent risk factors for ulcer bleeding (H. pylori odds ratio, 2.22; 95% confidence interval (CI), 1.23-4.01; NSAIDs odds ratio, 4.57; 95% CI, 2.50-8.35). There was no synergistic effect. In contrast, a negative interaction was observed in the logistic regression and stratified analysis, although the difference was not significant (H. pylori adjusted odds ratio, 3.47; 95% CI, 1.73-6.95; NSAID adjusted odds ratio, 6.16; 95% CI, 3.14-12.09). CONCLUSION: H. pylori increases the risk of peptic ulcer bleeding but may play a protective role in NSAID users.     

Helicobacter pylori-induced duodenal ulcer frequently coincides with gastro-oesophageal reflux disease

BACKGROUND: The relationship between Helicobacter pylori infection and gastro-oesophageal reflux disease is complicated. Evidence does not support a causal link. There have been reports, which have implicated successful eradication of Helicobacter pylori, in patients with a duodenal ulcer, with the subsequent development of gastro-oesophageal reflux disease. However, eradication of Helicobacter pylori in these patients with improvement in their condition and a return to normal lifestyle, weight gain and discontinuation of antacids may unmask pre-existing gastro-oesophageal reflux disease. AIMS: To determine the true prevalence of gastro-oesophageal reflux disease in patients with Helicobacter pylori-related duodenal ulceration. METHOD: Dyspeptic patients undergoing endoscopy were prospectively screened for the presence of a duodenal ulcer. Concomitant oesophagitis, when present, was recorded. All subjects with a Helicobacter pylori-related duodenal ulcer without endoscopic evidence of gastro-oesophageal reflux disease were invited to undergo a 24-hr ambulatory oesophageal pH assessment prior to receiving treatment. RESULTS: A total of 97 patients with a duodenal ulcer were identified and 83.5% were Helicobacter pylori positive. Overall, 27.8% had associated endoscopic evidence of oesophagitis, 70% grade I-II and 30% grade III-IV. Of those without evidence of oesophagitis at endoscopy, 68% underwent a 24-hr pH assessment. An additional 17% were identified by this means as having gastro-oesophageal reflux disease. Overall, 44% of symptomatic subjects with Helicobacter pylori and a duodenal ulcer were found to have coexistent gastro-oesophageal reflux disease. CONCLUSION: Gastro-oesophageal reflux disease is frequently found to coexist with Helicobacter pylori-related duodenal ulcer. In addition, almost 20% of symptomatic patients without endoscopic evidence of oesophagitis will have an abnormal oesophageal pH exposure. It is plausible that the development of gastro-oesophageal reflux disease following successful eradication of Helicobacter pylori represents unmasking of existing disease rather than de novo development.     

Acute perforated duodenal ulcer is not associated with Helicobacter pylori infection.

Most patients with chronic duodenal ulcer disease have Helicobacter pylori infection and eradicating it considerably reduces the relapse rate. The prevalence of H pylori in 80 patients (mean age = 52 years, range 17-85) presenting with acute perforated duodenal ulcer was examined and compared with age and sex matched hospital control patients. H pylori state was assessed by serum anti-H pylori IgG (Helico-G kit, Porton) using a titre of 18 or less as negative with a specificity of 89% and sensitivity of 88%. Only 47% of the perforated duodenal ulcer patients were positive for H pylori and this was similar to the value of 50% in the controls. In 51 of the perforated duodenal ulcer patients 14C-urea breath tests were also performed 4-10 weeks after surgery and this confirmed that only 49% were positive for H pylori. None of these patients had received perioperative drugs that might have eradicated the infection. The H pylori positive and H pylori negative perforated duodenal ulcer patients were similar with respect to age (53, 51), smoking (84%, 83%), and consumption of more than 15 units of alcohol per week (42%, 38%). Duodenal ulcer disease had been diagnosed before acute perforation in only 24% of those with H pylori and also 24% of those without the infection. Regular non-steroidal anti-inflammatory drug (NSAID) use was common in both those with (44%) and without (45%) H pylori. In conclusion, the lack of association of acute perforated duodenal ulcer and H pylori infection suggests that perforated duodenal ulcer has a different pathogenesis from chronic duodenal ulcer disease, and that the first should not be regarded simply as a complication of the second.     

Patients with Helicobacter pylori positive and negative duodenal ulcers have distinct clinical characteristics

AIM: To assess the clinical characteristics of Helicobacter pylori (H pylori) negative duodenal ulcer. METHODS:Patients with an endoscopic diagnosis of duodenal ulcer between 1996 and 2002 were included in the present study. Patients were considered to be negative for H pylori, if both histological examination and rapid urease test of biopsy specimens were negative. A comparison was made between patients with H pylori positive and negative duodenal ulcers. RESULTS: A total of 1 343 patients were studied. Their mean age was 54.7±0.5 years. There was a male preponderance (M:F=2.5:1). Three hundred and ninety-eight patients (29.6%) did not have H pylori infection. The annual proportion of patients with H pylori negative duodenal ulcers increased progressively from 1996 to 2002. On multivariate analysis, patients with H pylori negative duodenal ulcer were more likely to be older, have concomitant medical problem, pre-existing malignancy, recent surgery, underlying sepsis, or taken non-steroidal anti-inflammatory drugs. In terms of clinical presentations, patients with H pylori negative duodenal ulcer were more likely to present with bleeding, multiple ulcers and larger ulcers. CONCLUSION:The proportion of patients with H pylori negative duodenal ulcers is on the rise because of a continued drop in incidence of H pyloripositive duodenal ulcers in recent years. Such patients have distinct clinical characteristics and it is important to ascertain the H pylori status before starting eradication therapy.     

Biopsy specimen acquisition in patients with newly diagnosed peptic ulcer disease as determined from a national endoscopic database

BACKGROUND: Eradication of Helicobacter pylori infection decreases peptic ulcer recurrence. Therefore, assessment of Helicobacter pylori status is recommended for patients with newly diagnosed peptic ulcer disease. METHODS: Data obtained from the Clinical Outcomes Research Initiative's national endoscopic database were analyzed to characterize the acquisition of biopsy specimens in patients with a non-bleeding gastric or duodenal ulcer newly diagnosed by EGD. RESULTS: Between January 2000 and June 2003, 8299 patients underwent EGD with identification of non-bleeding peptic ulcer disease in the stomach (5390) or the duodenum (2909). Overall, biopsy specimens were obtained from the gastric or duodenal ulcer in 5578 (67%) of these patients. Multivariate analysis identified male gender (odds ratio [OR] 0.75, 95% confidence interval (CI) [0.66-0.85] vs. female), age greater than 75 years (OR 0.67, 95% CI [0.57-0.77] vs. age <55 years), ulcer location (OR 0.53, 95% CI [0.48-0.59] for duodenal vs. gastric ulcers) and endoscopy setting (OR 0.35, 95% CI [0.31-0.39] for academic vs. community; OR 0.36, 95% CI [0.32-0.41] for Veterans Affairs medical centers vs. community) as independent predictors for the acquisition of biopsy specimens (p < 0.001 for all). CONCLUSIONS: The findings of this study suggest that there is variation in the rates of biopsy specimen acquisition among patients with ulcers who may be at risk for Helicobacter pylori infection. Given the established benefit of Helicobacter pylori eradication, further study is needed to determine whether physicians are diagnosing and treating Helicobacter pylori infection adequately in patients with peptic ulcer.     

Eradication therapy in Helicobacter pylori positive peptic ulcer disease: systematic review and economic analysis

BACKGROUND AND AIM: We conducted a systematic review and economic analysis to ascertain the efficacy of eradication therapy in the treatment of H. pylori positive peptic ulcer disease. METHODS: Comprehensive search of electronic databases, bibliographies of retrieved articles, contact with pharmaceutical companies, and experts in the field to identify published and unpublished literature from 1966 to the present. The data were incorporated into a Monte Carlo simulation Markov model that incorporated all the uncertainty in the estimates to evaluate cost-effectiveness. RESULTS: Fifty-two trials were included in the final metaanalysis. In duodenal ulcer healing, H. pylori eradication therapy was superior to ulcer healing drug (relative risk (RR) of ulcer persisting = 0.66; 95% confidence interval (CI) = 0.58 to 0.76) and no treatment (RR = 0.37; 95% CI 0.26 to 0.53). In gastric ulcer healing, H. pylori eradication therapy was not statistically superior to ulcer healing drug (RR = 1.32; 95% CI = 0.92 to 1.90). In preventing duodenal ulcer recurrence, H. pylori eradication therapy was not statistically superior to maintenance therapy with ulcer healing drug (RR of ulcer recurring = 0.73; 95% CI = 0.42 to 1.25), but was superior to no treatment (RR = 0.19; 95% CI = 0.15 to 0.26). In preventing gastric ulcer recurrence, H. pylori eradication was superior to no treatment (RR = 0.31; 95% CI 0.19 to 0.48). The Markov model suggested H. pylori eradication is cost-effective for duodenal ulcer over 1 year and gastric ulcer over 2 years with over 95% confidence despite the uncertainty in the data. CONCLUSIONS: H. pylori eradication therapy reduces the recurrence of peptic ulcer disease and is cost-effective.     

Observations on peptic ulcer in Shan Dong, China

The study consisted of 10 994 inpatients with peptic ulcer in Shan Dong province. The ratio of duodenal to gastric ulcer was 1.59 : 1. The ratio of males to females was 6.8 : 1 for duodenal ulcer and 4.6 : 1 for gastric ulcer. The highest incidence was in adolescence and young adults and the presentation occurred more commonly in winter. A study of blood groups revealed that there was no relationship between blood group and duodenal or gastric ulcer. The majority (71.9%) of patients with peptic ulcer had complications of upper gastrointestinal bleeding, perforation or gastric outlet obstruction. Bleeding and obstruction were equally common in gastric and duodenal ulcer, but perforation was more common in gastric ulcer.     

Two new treatment regimens for Helicobacter pylori eradication: a randomised study

BACKGROUND: Several studies have found a fairly low Helicobacter pylori eradication rate using a standard 7-day triple therapy in Italy. Recently, two new therapeutic schedules have been proposed with an eradication rate higher than 90%. This study compared the efficacy of these two treatment regimens. PATIENTS AND METHODS: A total of 131 patients with Helicobacter pylori infection and either non-ulcer dyspepsia (73 patients] or peptic ulcer (58 patients) were enrolled. Helicobacter pylori infection was assessed by rapid urease test and histology on gastric biopsies. Patients were randomised to receive either a 5-day course of ranitidine bismuth citrate 400 mg bid, clarithromycin 500 bid, and tinidazole 500 bid, or a 10-day course of omeprazole 20 mg bid plus amoxycillin 1 g bid for the first 5 days, and omeprazole 20 mg bid, clarithromycin 500 mg bid and tinidazole 500 mg bid for the remaining 5 days. Eradication was assessed by endoscopy 4-6 weeks after therapy. RESULTS: Overall, 4 patients (2 for each treatment group) were lost to follow-up. Helicobacter pylori eradication rates were 67.2% (95% confidence interval: 55.7-78.7) and 65.2% (95% confidence interval: 53.7-76.6) at per protocol and intention-to-treat analyses, respectively, after the 5-day regimen, and 96.8% (95% confidence interval: 92.5-100) and 93.8% (95% confidence interval: 88-99.7) after the 10-day regimen (p<0.05). Both treatments were well tolerated, and no major side-effects were reported. CONCLUSIONS: The 5-day regimen gave disappointing results, while the eradication rate after the 10-day regimen was very high.     

胃、十二指肠溃疡幽门螺杆菌感染及相关病因回顾性分析204例

目的:研究福建省立医院胃、十二指肠溃疡患者幽门螺杆菌(H.pylori)感染及其他致病因素对疾病发生的作用.方法:选取2003-2008年福建省立医院胃镜中心进行检查并确诊为消化性溃疡的患者204例,所有患者在胃镜检查前记录详细情况,包括H.pylori感染,胃黏膜活检尿素酶法(14C-UBT),吸烟史(每日>10支)...     

Helicobacter pylori infection rates in duodenal ulcer patients in the United States may be lower than previously estimated

OBJECTIVE: Published studies have estimated the rate of Helicobacter pylori (H. pylori) infection in patients with duodenal ulcer disease to be as high as 95%; the majority of remaining duodenal ulcers have been attributed to the use of ulcerogenic drugs such as nonsteroidal antiinflammatory drugs (NSAIDs). We aimed to assess the H. pylori prevalence rates of U.S. duodenal ulcer patients in large, well-controlled studies. METHODS: More than 2900 patients with endoscopically diagnosed non-NSAID duodenal ulcers were enrolled in a series of six placebo-controlled, double-blind studies conducted in the United States that assessed H. pylori using a combination of tests. Patients were considered infected with H. pylori only if culture growth was observed, or both histological and CLOtest results were positive. Patients were considered uninfected if the results of at least two tests were negative. Patients with missing test results, results of only a single test, or conflicting test results were not evaluable for H. pylori assessment. RESULTS: Of the 2394 endoscopically diagnosed evaluable duodenal ulcer patients, 73% (1737) were confirmed infected with H. pylori at study entry. CONCLUSIONS: The results of six carefully designed and controlled studies suggest that an assumed H. pylori infection rate of approximately 95% may overestimate the actual rate of H. pylori infection in duodenal ulcer patients in the United States. Although H. pylori infection is an important factor in the etiology of noniatrogenic duodenal ulcer disease, other factors may predominate in some patients and should not be overlooked in determining an appropriate course of treatment. The empiric use of antibiotic therapy for ulcer patients without confirmation of the presence of H. pylori cannot be recommended.     

Recurrence of H. pylori infection and dyspeptic symptoms after successful eradication in patients cured of duodenal ulcer disease

BACKGROUND/AIMS: To evaluate the recurrence of Helicobacter pylori (H. pylori) infection and dyspeptic symptoms in patients previously cured of active duodenal ulcers followed by successful eradication with bismuth-based triple therapy. METHODOLOGY: Patients who remained H. pylori-negative by repeat endoscopy for 1 year were invited back and had their H. pylori status checked with a 13C-urea breath test. Those found positive for H. pylori underwent endoscopic confirmation by urease testing and histology. RESULTS: Thirty-four (69%) patients, 30 males/4 females, with a mean age of 56.4 years and a mean follow-up period of 4.8 years, were eligible for study. Five patients were considered recurrent with H. pylori infection, giving us a recurrence rate of 3% per patient per year. Sixty percent (3/5) of the patients with recurrence experienced typical ulcer symptoms, whereas none of the H. pylori-negative patients experienced typical ulcer symptoms if non-steroidal antiinflammatory drug (NSAID) use is excluded. CONCLUSIONS: Recurrence of H. pylori infection is low in Taiwan. Gender, age, smoking, alcohol consumption, and blood grouping do not appear to be significant risk factors for H. pylori recurrence. Reappearance of typical ulcer symptoms is suggestive of recurrence of H. pylori infection in patients cured of duodenal ulcer disease if the use of NSAID is excluded.     

Helicobacter pylori and upper gastrointestinal disease: a survey of gastroenterologists in the United Kingdom.

The objective of this study was to conduct a survey of the opinions and practices of gastroenterologists in the United Kingdom concerning the impact of Helicobacter pylori infection on the management of upper gastrointestinal diseases. A postal questionnaire was sent to all medically qualified members of the British Society of Gastroenterology working in the UK. Replies were received from 670 of 1037 eligible BSG members (65%). Of these, 73% thought that H pylori was a cause of duodenal ulcer and 84% thought that eradication of H pylori decreased ulcer recurrence in comparison with acid suppression. While 80% used anti-H pylori therapy for a chronic relapsing duodenal ulcer, only 25% used such therapy for an ulcer at first presentation and 17% never used anti-H pylori therapy for patients with duodenal ulcer. Although 75% of respondents did not agree that H pylori was a cause of non-ulcer dyspepsia, 69% used anti-H pylori therapy to treat a patient with this condition. At the time of the survey, 69% of those who used anti-H pylori therapy adopted some variant of standard triple therapy. Only 7% routinely tested for bacterial sensitivity to antibiotics and only 22% assessed their patients for eradication after treatment. There was a lack of consensus about whether H pylori was a cause of gastric ulcer or gastric cancer with only 47% and 17% respectively believing in these associations. In conclusion, at the time of the survey, the use of anti-H pylori therapy had been accepted by a majority of specialist UK gastroenterologists in the management of upper gastrointestinal disease. There was, however, a substantial degree of uncertainty and divergence about which patients should be treated.     

Antibody response to Helicobacter pylori CagA and heat-shock proteins in determining the risk of gastric cancer development

OBJECTIVE: To investigate whether the systemic antibody response to Helicobacter pylori heat shock protein B can be considered, in addition to anti cytotoxin-associated protein [CagA) antibody determination, a further serological marker of increased risk of gastric cancer development. METHODS: A total of 98 Giemsa positive Helicobacter pylori patients (28 with gastric cancer, 30 with duodenal ulcer and 40 with nonulcer dyspepsia) were studied. Serum samples obtained from all patients were tested for IgG antibodies to CagA (116 kDa), VacA [89kDa) and heat skock protein B (54 kDa) antigens of Helicobacter pylori by the Western blot technique. RESULTS: 26/28 patients [(92.9% with gastric carcinoma, 29/30 patients [96.7%) with duodenal ulcer and 30/40 patients (75.0%) with non-ulcer dyspepsia were seropositive for CagA protein. The prevalence of serum IgG antibody to CagA in the cancer patients was not significantly higher than in duodenal ulcer and non-ulcer dyspepsia patients. The prevalence of antibodies to VacA was not significantly different between gastric carcinoma and non-ulcer dyspepsia patients. In contrast the prevalence of systemic antibodies to heat skock protein B was significantly higher in gastric cancer patients (78.6%) than in duodenal ulcer (36.7%, p=0.002) or nonulcer dyspepsia patients (52.5%, p=0.029). CONCLUSIONS: The detection of antibodies to heat shock protein B is proposed as an additional test which, in association with the determination of serum antibodies to CagA, could help in determining the risk of developing severe gastroduodenal disease, and gastric cancer, in particular.     

Helicobacter pylori and risk of ulcer bleeding among users of nonsteroidal anti-inflammatory drugs: a case-control study.

BACKGROUND & AIMS: Peptic ulcer complications related to use of nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most common serious adverse drug reactions. Whether Helicobacter pylori infection potentiates this gastrointestinal toxicity of NSAIDs is still unresolved. In this study, we investigated the role of H. pylori as a cause of bleeding peptic ulcer among NSAID users. METHODS: A case-control study of current users (n = 132) of NSAIDs (including acetylsalicylic acid), admitted because of bleeding peptic ulcer, was performed. Controls were 136 NSAID users without gastrointestinal complications. H. pylori was diagnosed by either increased levels of serum immunoglobulin G or by 13C-urea breath test. RESULTS: Fifty-eight (44%) case subjects had a bleeding gastric ulcer, 54 (41%) had a bleeding duodenal ulcer, 12 (9%) had both gastric and duodenal ulcers, and 8 (6%) had hemorrhagic gastritis. H. pylori was present in 75 (57%) cases compared with 59 (43%) controls. The adjusted odds ratio of bleeding peptic ulcer among NSAID users associated with H. pylori infection was 1.81 (95% confidence interval, 1.02-3.21). H. pylori accounted for approximately 24% of bleeding peptic ulcers among elderly NSAID users. CONCLUSIONS: NSAID users infected with H. pylori have an almost twofold increased risk of bleeding peptic ulcer compared with NSAID users without H. pylori.     

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.     

Longitudinal study of influence of Helicobacter pylori on current risk of duodenal ulcer relapse. The Hvidovre Ulcer Project Group.

Seventy-four patients with duodenal ulcer were followed up longitudinally for 2 years after initial ulcer healing. Endoscopy including biopsy of the antral mucosa was performed every 3rd month and whenever clinical symptoms of relapse occurred. The presence of Helicobacter pylori in the biopsy specimens was scored as 0 (none), 1 (sporadic occurrence), 2 (clusters), and 3 (numerous bacteria found diffusely in the mucus layer). The incidence rates of ulcer relapse per patient-month, grouped in accordance with these scores, were (with 95% confidence intervals) 0.073 (0.048-0.111), 0.083 (0.052-0.133), 0.123 (0.096-0.157), and 0.069 (0.041-0.116), respectively. No significant differences in incidence rates across H. pylori scores were observed when taking into account the observation period after healing of the first ulcer, number of ulcer recurrence (1st, 2nd, 3rd), sex, age, smoking habits, peak acid output, time of healing of the preceding ulcer, treatment of the present ulcer (cimetidine, antacids, or no treatment), or type and degree of gastritis. Thus, although H. pylori is prevalent in patients with duodenal ulcer disease, the present study indicates that H. pylori does not have a substantial note in the precipitation of active duodenal ulcer.