Helicobacter pylori Reinfection Rate, in Patients with Cured Duodenal Ulcer

Objective: To determine the reinfection rate of the gastric mucosa in patients previously cured of duodenal ulcers, following the eradication oi Helicobacter pylori . Only those remaining H. pylori-negative beyond 12 months of follow-up were studied, to minimize the potential inclusion of patients with H. pylori recrudescence. Methods: Patients with endoscopically proven duodenal ulcers who had heen treated with triple therapy, resulting in documented eradication of H. pylori and cure of the ulcer for at least 4 years, were recalled and had their H. pylori status determined by the ¹⁴C-urea breath test. Those found positive for H. pylori underwent endoscopic confirmation of the infection. Results: Of the 94 patients restudied, with a follow-up period range of 48–96 months or a total of 549.8 yr, only two (2.2%) were again H. pylori positive. This gives an effective reinfection rate of 0.36% per patient year. In the two H. Pylori -positive patients, one had normal mucosa endoscopically, whereas duodenitis without active ulceration was present in the other. The former was asymptomatic, whereas the latter patient was using ranitidine daily for symptom control. Conclusion: In the Australian setting, following cure of duodenal ulcer disease by eradication of H. pylori , subsequent reinfection is an unusual phenomenon. We conclude that efforts aimed at eradication of H. pylori in duodenal ulcer are justified and are worthwhile.     

Identification and eradication of Helicobacter pylori infection in haemophilic patients

The aim of this study was to identify and eradicate H. pylori infection in patients with haemophilia. Patients were screened for IgG antibodies against H. pylori ; active infection was determined using a ¹³C-urea breath test and infected patients were given combination therapy with antibiotics to eradicate infection. Seventy-eight of 219 (36%) patients with haemophilia were found to have an elevated serum antibody titre against H. pylori ; of 36 antibody-positive patients with confirmatory testing, 14 were found to have active H. pylori infection. H. pylori infection was successfully eradicated in every infectedpatient using acombination of ranitidine plus two antibiotics (usually amoxycillin and metronidazole). It is concluded that eradication of H. pylori infection is likely to be a cost-effective screening strategy in patients with haemophilia, to prevent complications of peptic ulcer disease.     

The Helicobacter pylori breath test: a surrogate marker for peptic ulcer disease in dyspeptic patients.

BACKGROUND: There is interest in noninvasive H pylori testing as a means of predicting diagnosis and determining management in dyspeptic patients. AIMS: To assess the value of the 14C urea breath test as a predictor of peptic ulcer disease in patients presenting with dyspepsia. PATIENTS AND METHODS: 327 consecutive patients referred for investigation of dyspepsia had a 14C urea breath test performed before endoscopy. Patients were not included if they had previously confirmed ulcer disease, previous gastric surgery, or were taking non-steroidal anti-inflammatory drugs. RESULTS: Of the 182 patients with a positive 14C urea breath test, duodenal and/or gastric ulcers were present in 45% and erosive duodenitis in a further 2%. Oesophagitis was present in 12% of the breath test positive patients with two thirds of the oesophagitis patients having co-existent ulcer disease. The prevalence of ulcer disease in the H pylori positive dyspeptic patients was independently related to smoking and previous investigation status. If previously uninvestigated, the prevalence of ulcers was 67% in smokers and 46% in non-smokers. If previous upper gastrointestinal investigations were negative, the prevalence of ulcers was 53% in smokers and 28% in non-smokers. Of the 136 patients with a negative breath test, only 5% had peptic ulcers. The most frequent endoscopic finding in these H pylori negative subjects was oesophagitis, being present in 17%. CONCLUSIONS: This study demonstrates that a positive H pylori test is a powerful predictor of the presence of underlying ulcer disease in dyspeptic patients, especially if smokers, and that a negative H pylori test is a powerful predictor of the absence of ulcer disease. It also indicates that a negative upper gastrointestinal investigation does not preclude subsequent presentation with ulcer disease.     

Mini-Dose (1-μCi) 14-Urea Breath Test for the Detection of Helicobacter pylori

Objectives: To develop and evaluate a mini-dose (1-μ Ci ) ¹⁴C-urea breath test (UBT), using a simplified protocol. Methods: Fasting patients (n = 95) were given a drink of 1 μCi (37 kBq) of ¹⁴C-urea. Samples of breath carbon dioxide (2 mmol) were collected at 10, 20, and 30 min later by trapping in hyamine solution; ¹⁴C activity was measured by liquid scintillation counting. Results were expressed as "CO₂ recovery," i.e ., [(% of administered dose recovered/mmol CO₂ trapped) × body weight (kg)]. Reproducibility of the test was assessed by repeat studies on two consecutive days in 11 volunteers. All breath test results were compared with culture for Helicobacter pylori . In 27 patients, results also were compared with ¹³C-urea breath test (European protocol). Results: Using receiver operator characteristic (ROC) analysis, we selected a cut-off value of 0.55 at 20 min to separate those positive and negative for H. pylori . Sensitivity and specificity were 98% and 87%, respectively. Among four patients with negative culture hut positive ¹⁴C-breath tests, three had evidence of infection by serology or ¹³C-UBT. Assuming that these three were genuinely positive, the recalculated specificity improved to 97%, sensitivity remaining at 98%. The reproducibility of the test was good, with only a minor day-to-day variation. Concordance with the ¹³C-UBT was excellent: there was 100% agreement in the diagnostic classification of all 27 patients (19 positive, eight negative). Conclusions: The mini-dose ¹⁴C-urea breath test has a high diagnostic accuracy (sensitivity 98%, specificity 97%) with minimal radiation exposure. It is simple, rapid, and convenient for a busy general hospital.     

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.     

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.     

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).     

Triple Therapy vs. Amoxicillin Plus Omeprazole for Treatment of Helicobacter pylori Infection: A Multicenter, Prospective, Randomized, Controlled Study of Efficacy and Side Effects

Objective : this study compares the efficacy and side effects of the two commonly used treatment regimens for Helicobacter pylori infection. Methods : 118 patients with culture-proven H. pylori infection (61 with duodenal ulcer, 19 with gastric ulcer, three with both duodenal and gastric ulcer, and 35 with non-ulcer dyspepsia) were randomized to receive either triple therapy (tetracycline 250 mg, metronidazole 250 mg, colloidal bismuth subcitrate 120 mg, four times daily) for 14 days or amoxicillin 1000 mg and omeprazole 40 mg both twice daily for 14 days. The isolated H. pylori strain was metronidazole susceptible in 93%. Antral biopsy samples were taken for culture, urease testing, histology and, in most patients, for PCR at least 6 wk after treatment. A separate corpus sample was taken for culture. Eradication was defined as the absence of H. pylori in all specimens. In seven cases, when only histology was doubtfully positive, and all other tests including PCR were negative, a ¹³C-urea breath test was performed, the result of which was considered conclusive. Severity of the side effects was recorded by the patient on a semi-quantitative scale. Results: H. pylori was eradicated by triple therapy in 96.3% and by amoxicillin/omeprazole in 77.2% of the patients ( p = 0.008). Side effects occurred more often with triple therapy (72.7% vs. 50.8 %; p < 0.05) but were mild in most cases. Severe side effects occurred equally in both treatment groups. Conclusions : When the prevalence of metronidazole resistance is low, triple therapy is more effective than amoxicillin/omeprazole. Side effects occur more often in triple therapy but are mild in most cases.     

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 13 C-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).     

Follow up after successful eradication of Helicobacter pylori: Symptoms and reinfection

The important long-term outcomes after Helicobacter pylori eradication are the proportion of patients with continuing symptoms, and the rate of recrudescence of the infection. Patients with proven H. pylori infection prior to treatment and a negative urea breath test at least 4 weeks after completing treatment were invited to return for a further urea breath test and a questionnaire. There were 167 patients and the mean interval since the post-treatment urea breath test was 16 months. The endoscopic diagnoses were duodenal ulcer 72, duodenitis 17, gastric ulcer 26, normal or oesophagitis 52. The ethnic groups were European 86, Maori 25, Pacific Island 28 and other ethnic groups 28. Ten patients (6%) had a positive urea breath test at follow up. The proportion of patients showing recrudescence of H. pylori was related to the delta value (δ) of the post-treatment urea breath test: δ 0–2. five of 146 (3.4%); δ 2–3, two of 18 (11%); and δ 3–4, three of five (60%). A symptom questionnaire was given to 147/157 patients with a persistently negative breath test; 60 had no symptoms, 31 had heartburn, 30 had epigastric pain, 15 had both heartburn and epigastric pain, and 11 had nausea or other symptoms. There were fewer symptoms in patients with gastric ulcer (GU) compared with patients with duodenal ulcer (DU) and non-ulcer patients. Twenty-four patients (16%) were taking H₂-antagonists (including seven DU and five GU), 15 were taking antacids and four were taking omeprazole. There was no difference in medication use between diagnostic groups. Eighteen of the 46 patients (39%) with heartburn stated that this was a new symptom. Heartburn was a common symptom for duodenal ulcer patients after eradication (24/74, 32%). A second urea breath test 6–12 months after eradication is required to definitely prove eradication. Patients with a breath test † value of 2–4 should have a repeat urea breath test.     

Symptomatic benefit 1-3 years after H. pylori eradication in ulcer patients: impact of gastroesophageal reflux disease

OBJECTIVES: Eradication of Helicobacter pylori (H. pylori) infection markedly reduces the recurrence of duodenal and gastric ulcers. However, there is little information regarding its efficacy in resolving dyspeptic symptoms in ulcer patients. The primary aim of this study was to assess the effect of eradicating H. pylori infection on dyspeptic symptoms in ulcer patients. The secondary aim was to identify predictors of symptomatic response to H. pylori eradication. METHODS: A total of 97 dyspeptic patients with active duodenal and/or gastric ulceration associated with H. pylori infection and unrelated to NSAID use had the severity and character of their dyspeptic symptoms measured before and again 1-3 yr after H. pylori eradication therapy. RESULTS: Pretreatment, the median dyspepsia score was 12 (4-16). Posttreatment, 55% of those eradicated of H. pylori had resolution of dyspepsia (score <2) compared with 18% of those not eradicated of the infection (95% CI for difference, 11-62%). Of the ulcer patients 31% had symptoms and/or endoscopic evidence of coexisting gastroesophageal reflux disease (GERD) at initial presentation and this influenced the symptomatic response to eradication of H. pylori. Of the 22 patients with heartburn or acid reflux as the predominant presenting symptom, but no endoscopic esophagitis, only 27% experienced resolution of dyspepsia after H. pylori eradication, compared with 68% of the 59 without those as predominant symptoms (95% CI for difference, 18-63%). Only one of the five patients with coexisting endoscopic esophagitis at initial presentation experienced resolution of dyspepsia after H. pylori eradication. Symptomatic benefit was unrelated to time lapsed since the infection was eradicated. Only three of 50 subjects developed de novo GERD symptoms after eradication of H. pylori, whereas 21 of 36 subjects experienced resolution of GERD symptoms after eradication of the infection. CONCLUSIONS: A substantial proportion of ulcer patients have symptoms and/or signs of coexisting GERD at initial presentation and this reduces the symptomatic benefit from H. pylori eradication. However, we have found no evidence that eradicating H. pylori induces de novo GERD symptoms in ulcer patients.     

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.     

Five-Day Bismuth-Free Triple Therapy for the Eradication of Helicobacter pylori and Reduction of Duodenal Ulcer Relapse

Previous studies have demonstrated that the eradication of Helicobacter pylori ( H. pytori ) is associated with a significant reduction of the rate of duodenal ulcer (DU) relapse. The aim of this study was to assess the long-term effect of a bismuth-free triple therapy on the eradication of H. pylori and reduction of DU relapse. After informed consent, 61 patients with endoscopically proven DU and H. pylori infection detected on ¹⁴C-urea breath test (BT) were included in the study. All patients received a combination of furazolidone, amoxicillin, and metronidazole, three times a day, for 5 days, in addition to eventual classical antiulcer agents prescribed by their attending physicians. BT was repeated after an interval of at least 60 days to evaluate H. pylori eradication. Endoscopy and another BT were performed again at 6.5 months after therapy to detect possible recurrences. Forty-eight patients completed the trial: 26 (54%) patients were negative for H. pylori at 6.5 months after the end of treatment, and 22 (46%) persisted H. pylori positive. Ninety-two percent of the patients in whom the bacteria were eradicated showed endoscopically healed ulcers and were asymptomatic, and two that were sympatomatic presented only occasional pain not requiring therapy. Among the 22 patients who persisted H. pylori positive, six (27%) showed endoscopically active ulcers ( p = 0.012) and eight (36%) patients continued to be symptomatic ( p < 0.01), and were still using antiulcer drugs ( p < 0.002) 6.5 months after treatment. It is concluded that combined treatment with furazolidone, amoxicillin, and metronidazole for 5 days represents a well-tolerated, inexpensive, and effective therapeutic regime for the eradication of H. pylori and abolition of DU relapse in more than 50% of the patients during a follow-up period of 6.5 months.     

Helicobacter pylori infection in dyspeptic cirrhotic patients

BACKGROUND/AIMS: To date, few studies have focused on the role of Helicobacter pylori (H. pylori) in cirrhotic patients with gastroduodenal disease and reported results are conflicting. The aim of this study was to assess the H. pylori infection rate in dyspeptic cirrhotic patients with or without gastroduodenal lesions at endoscopy. METHODOLOGY: In a prospective study, 226 consecutive dyspeptic cirrhotic patients were enrolled in the study upon assessment of H. pylori infection. Two-hundred dyspeptic non-cirrhotic patients were also included as controls. The presence of H. pylori was detected by rapid urease test and histology (Giemsa staining) in 3 biopsy specimens from the antrum and 3 from the gastric body. RESULTS: H. pylori infection was found in 135 (59.7%) cirrhotics and in 121 (60.5%) controls (p = NS). The prevalence of gastric ulcer was higher in cirrhotics than in controls (16% vs. 2.5%, p = 0.0001), while the prevalence of duodenal ulcer was similar (11% vs. 12%, respectively). The H. pylori infection rate was similar between cirrhotics and controls, both with gastric (83% vs. 80%) and with duodenal (88% vs. 96%) ulcers. Moreover, in our study, a H. pylori-related peptic lesion was the cause of previous gastroduodenal bleeding in 6 of 50 (12%) cirrhotic patients. CONCLUSIONS: Our results indicated that H. pylori infection is implicated in the pathogenesis of peptic ulcer in cirrhotic patients, similar to findings in non-cirrhotic patients.     

Microdose 14C-Urea Breath Test Offers Diagnosis of Helicobacter pylori in 10 Minutes

Objectives: The urea breath test diagnoses Helicobacter pylori infection of the stomach by identifying the urease enzyme activity of the bacterium. In this "micro-dose" version of the test, 1 μCi ¹⁴C-urea is given orally in a capsule. Our objectives were: 1) to evaluate a microdose ¹⁴C-urea breath test capsule in a gastroenterology outpatient setting, 2) to determine the diagnostic ranges of the ¹⁴C-urea breath test for HP-positive and HP-negative patients, 3) to define the sensitivity and specificity of the test, and 4) to see whether breath sample results changed when they were mailed to a remote site for analysis. Methods: In a prospective blinded study, we breath-tested 200 fasted patients before elective outpatient endoscopy. At endoscopy, two gastric biopsy samples were taken and were examined for curved organisms; a third biopsy specimen was evaluated with a rapid urease test (CLOtest). Breath samples were mailed in aluminized balloons to a testing laboratory. Results: Using a single breath sample collected at 10 min, with ≥ 200 dpm as positive, the breath test correctly classified 63 of 65 HP-positive patients (sensitivity 97%, CI 89–99%), and 128 of 135 HP-negative patients (specificity 95%, CI 90–98%). Radiation exposure from the test equated to natural background received in 1 day. No adverse events were caused by the breath test. Conclusions: The ¹⁴C-urea capsule breath test (PYtest) is a convenient noninvasive test for the detection of gastric H. pylori infection. Accuracy is equivalent to invasive methods such as histology. Results can be obtained within 15 min if a counting instrument is nearby, or breath samples can be mailed to a testing laboratory for analysis.     

Influence of the level of renal insufficiency on endoscopic changes in the upper gastrointestinal tract

AIM: Lesions of the gastrointestinal tract are frequent finding in uremic patients but their actual nature is not completely clear. The aim of this study was to detect any correlation between endoscopic lesions of patients with different levels of renal insufficiency. METHODS: This prospective study involved 244 cases, with dyspeptic difficulties including 124 patients in different stages of renal insufficiency, and a control group of 120 patients with normal renal function. Upper esophagogastroscopy was performed in all patients because of the appearance of dyspeptic difficulties. Helicobacter pylori infection was detected by the urease test. RESULTS: H. pylori infection (P=0.009), gastric erosions (P=0.019), gastric ulcer (P=0.002), and duodenal ulcer (P<0.001) were more common in the control group of patients. Significant negative correlations were found between the level of renal insufficiency and H. pylori infection (Kendall's tau=-0.346; P=0.003), stomach erosions (Kendall's tau=-0.272; P=0.019), stomach ulcer (Kendall's tau=-0.347; P=0.003), and duodenal ulcer (Kendall's tau=-0.531; P<0.001). CONCLUSIONS: In patients with end stage renal disease, endoscopic lesions of the gastrointestinal tract are detected less frequently in relation to patients without kidney disease.     

Gastric metaplasia and Helicobacter pylori infection.

Duodenal and antral mucosal biopsy specimens were obtained from 139 patients with dyspeptic complaints to study the prevalence and extent of gastric metaplasia in the duodenal bulb in relation to Helicobacter pylori (H pylori) infection and duodenal ulcer disease. On logistic regression, the presence and extent of gastric metaplasia was not significantly associated with H pylori infection. The prevalence of gastric metaplasia, however, was found to be higher in patients with current or past evidence of duodenal ulcer disease in comparison with subjects with functional dyspepsia (p = 0.01). A follow up study on 22 patients before and at least one year after eradication of H pylori showed that the mean extent of gastric metaplasia did not change significantly after eradication and did not differ when compared with 21 patients with persisting infection. It is concluded that the unchanged gastric acid output after eradication of H pylori is a more important factor in the development of gastric metaplasia than the H pylori related inflammatory process.     

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.     

Cure of Helicobacter pylori Infection: Role of Duration of Treatment with Omeprazole and Amoxicillin

Objectives : To date, some studies have suggested that short-term therapy may be a promising therapeutic concept for the eradication of Helicobacter pylori . The primary objective of the present study was to elucidate the role of the duration of treatment in the cure of H. pylori infection. Methods : Forty consecutive patients with H. pylori -positive peptic ulcer disease were randomly allocated to four study groups. The groups were treated with a 14-day course of 20 mg omeprazole b.i.d. orally combined with 2 g amoxicillin t.i.d. intravenously for 1 day (n = 10; six women, age range 40–84 yr), for 3 days (n = 10; three women, age range 29–74 yr), for 5 days (n = 10; five women, age range 21–82 yr), and for 7 days (n = 10; five women, age range 42-82 yr), respectively. Initially, a standardized clinical evaluation of symptoms and an upper GI tract endoscopy were performed for assessment of H. pylori infection of the gastric mucosa (biopsy urease test, specific culture, and histology). At least 4 wk after cessation of omeprazole medication, H. pylori eradication was evaluated either as described or with the help of the ³¹C-urea breath test. Results: H. pylori eradication, defined as negative bacterial findings in urease test, culture, and histology or ³¹C-urea breath test at least 4 wk after discontinuation of omeprazole therapy, was achieved in one of 10 patients (10%) in the one-day group, none of 10 patients (0%) in the 3- and 5-day groups and six of 10 patients (60%) in the 7-day group. Conclusions : We conclude that short-term therapies with the proton pump inhibitor omeprazole and the antibiotic amoxicillin must be considered completely ineffective if performed as a short-term therapy for up to 5 days. A therapy duration of 7 days seems to mark a turning point in antibiotic effectiveness, with a rapid increase in eradication rates.     

Eradication of helicobacter pylori reduces the rate of duodenal ulcer rebleeding: a long-term follow-up study

Objectives: The long-term efficacy of Helicobacter pylori eradication to reduce the rate of recurrence of peptic ulcer bleeding is still uncertain. We evaluated the rate of duodenal ulcer rebleeding for 48 months after H. pylori eradication.
Methods: Thirty-two male patients with H. pylori infection and duodenal ulcer bleeding were treated with omeprazole (40 mg/day for 4 wk), colloidal bismuth (480 mg/day for 2 wk), amoxicillin (2 g/day for 1 wk), and metronidazole (750 mg/day for 1 wk), and followed up for 48 months. Endoscopy and tests for H. pylori infection were repeated every year.
Results: Ulcer healed in all patients, but H. pylori infection persisted or recurred in 11 patients. Within 48 months, rebleeding occurred in nine (81.8%) of these patients, whereas the 21 patients who were persistently negative for H. pylori infection remained asymptomatic without rebleeding (0/21 = 0%,   p < 0.002  ) during the whole follow-up.
Conclusions: Eradication of H. pylori can reduce the rate of duodenal ulcer rebleeding for at least 4 yr, thus potentially modifying the natural history of the disease.