Duodenal Ulcer Recurrence Research Articles

Treatment of Helicobacter pylori in patients with duodenal ulcer hemorrhage— a long-term randomized, controlled study

OBJECTIVE: Eradication of Helicobacter pylori ( H. pylori) in patients with uncomplicated duodenal ulcers prevents long-term recurrence of ulcers. We aimed to study whether treatment of H. pylori prevents the long-term recurrence of duodenal ulcer hemorrhage. METHODS: Patients with duodenal ulcer bleeding and confirmed H. pylori infection were recruited. A total of 120 patients were randomly assigned to triple therapy (DeNoltab 120 mg, amoxycillin 500 mg, and metronidazole 300 mg four times daily) or DeNoltab 120 mg four times daily alone. No maintenance therapy was given during the follow-up period. The endpoints were the cumulative rates of symptomatic and bleeding duodenal ulcer recurrences. RESULTS: Of the patients receiving the triple regimen, 85.1% had H. pylori eradicated as compared to 2.0% of patients receiving DeNoltab ( p < 0.05). More patients in the DeNoltab group than those in the Triple group had recurrence of ulcer bleeding, but this did not reach statistical significance (12/60 vs 6/60, p = 0.20). Logistic regression analysis on clinical, personal, and endoscopic characteristics identified persistent H. pylori infection as the only independent predictor of recurrence of duodenal ulcer bleeding. CONCLUSIONS: Treatment of H. pylori alone with the present bismuth-based triple therapy in patients with duodenal ulcer hemorrhage did not result in significant reduction in further bleeding episodes, although a trend was seen for the group that was given triple therapy. On the other hand, posttreatment H. pylori status was found to be an independent predictor of bleeding recurrence.

Diet and duodenal ulcer.

Despite the fact that the main cause of duodenal ulcer incidence and recurrence is the Helicobacter pylori bacterium, more than 80% of Helicobacter pylori-infected people never develop an ulcer. Diet may be one of the most important environmental factors contributing to duodenal ulcer. To explore the role of diet in causation, treatment and prevention of duodenal ulcer recurrence. All research papers published in English from 1966 to October 1999 present in Medline, involving human subjects, and having duodenal ulcer as outcome, entered the review. Soluble fibre from fruit and vegetables seem to be protective against duodenal ulcer and refined sugars a risk factor. The role of fibre in the treatment and prevention of recurrence of duodenal ulcer is uncertain, as is that of essential fatty acids. However, none of the epidemiological studies on the relationship between diet and duodenal ulcer disease controlled for Helicobacter pylori.

Peptic ulcer

OBJECTIVE: To present a current review about pathogenesis, pathophysiology, diagnosis, and treatment of peptic ulcer disease in children, based on the reviewed publications and the author personal experience. METHODS: We revised the most relevant articles about peptic ulcer in children, published from the last 20 years. RESULTS: The gastroduodenal peptic ulcer is very common in adults, mostly in the developing countries. Although it is less frequent in children, the optical fibroendoscopy has improved the number of diagnosed cases. The peptic ulcer is classified as its etiology in primary and secondary. The secondary peptic ulcer is related to a subjacent disease or use of drugs, while the primary ulcer happens in the absence of underlying systemic diseases The primary duodenal ulcer is the most common presentation, and there are strong evidences of the H. pylori association in the etiology. Clinical presentation changes with age and ulcer type. Secondary ulcers are mostly acute and sometimes dramatic, while the primary ones have a chronic evolution mostly similar to patients with functional recurrent abdominal pain, but the presence of epigastric pain, feeding-related pain, vomiting, bleeding, familiar history for peptic ulcer, nocturnal pain, and male gender are strongly related to peptic ulcer. The acid antisecretory agents have great efficacy on relieving symptoms and solving ulcerate lesion, although the H. pylori eradication itself prevents primary duodenal ulcer recurrence. CONCLUSIONS: The primary peptic ulcer involve many factors in Its etiopathogenesis, being H. pylori the most important of them Although there isn t yet a ideal therapeutic course. The antibiotics play an important role in peptic ulcer and the H. pylori research must be done for na accurate diagnosis and treatment.

Omeprazole (OME), clarithromycin (CLA) and tinidazole (TIN) for 7 days vs ome, CLA and tin for 7 days plus ome for 21 days in the treatment and recurrence of active duodenal ulcer with H.pylori infection: a double blind placebo controlled trial Leonardo^Marzio

Omeprazole (OME), clarithromycin (CLA) and tinidazole (TIN) for 7 days vs ome, CLA and tin for 7 days plus ome for 21 days in the treatment and recurrence of active duodenal ulcer with H.pylori infection: a double blind placebo controlled trial Leonardo^Marzio

Hypersecretory duodenal ulcer and Helicobacter pylori infection: for-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 mEg/h and 64. 1 mEg/h before treatment vs 16 mEg/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.

The long-term reinfection rate and the course of duodenal ulcer disease after eradication of Helicobacter pylori in a developing country

OBJECTIVE: The aim of this study was to evaluate the effect of Helicobacter pylori ( H. pylori) eradication on the natural history of duodenal ulcer disease and the reinfection rate after treatment in a developing country. METHODS: A total of 111 H. pylori-infected patients with duodenal ulcer were treated with either omeprazole or famotidine plus two antibiotics for 2 wk. Those failed to respond to treatment were retreated with bismuth-based triple therapy. RESULTS: The radication rate was 76% (95% CI: 67–83%). Eventually, H. pylori was eradicated in 96 of the 111 patients (86%), who were followed-up clinically and endoscopically for a mean of 37.2 months. The cumulative reinfection rate after eradication (Kaplan-Meier) was 8% ± 3% in yr 1, 11% ± 4% in yr 2, and 13% ± 4% in yr 3. Nine of the 12 reinfections occurred during yr 1. Recurrence of duodenal ulcer was detected in five patients (5.2%), all of them during yr 1 of follow-up. Histologically, gastritis scores (according to the Sydney system) improved significantly after eradication. CONCLUSIONS: In a high prevalence setting, H. pylori eradication and early reinfection rates after treatment are similar to rates observed in a low prevalence environment, whereas the late reinfection rate seems to be higher. However, up to 3 yr after treatment, most treated patients are free of H. pylori infection and/or ulcer activity. Even longer follow-up studies are necessary to determine whether specific retreatment policies are necessary to maintain long term eradication in developing countries.

The long-term reinfection rate and the course of duodenal ulcer disease after eradication of Helicobacter pylori in a developing country.

The aim of this study was to evaluate the effect of Helicobacter pylori (H. pylori) eradication on the natural history of duodenal ulcer disease and the reinfection rate after treatment in a developing country. A total of 111 H. pylori-infected patients with duodenal ulcer were treated with either omeprazole or famotidine plus two antibiotics for 2 wk. Those failed to respond to treatment were retreated with bismuth-based triple therapy. The radication rate was 76% (95% CI: 67-83%). Eventually, H. pylori was eradicated in 96 of the 111 patients (86%), who were followed-up clinically and endoscopically for a mean of 37.2 months. The cumulative reinfection rate after eradication (Kaplan-Meier) was 8%+/-3% in yr 1, 11%+/-4% in yr 2, and 13%+/-4% in yr 3. Nine of the 12 reinfections occurred during yr 1. Recurrence of duodenal ulcer was detected in five patients (5.2%), all of them during yr 1 of follow-up. Histologically, gastritis scores (according to the Sydney system) improved significantly after eradication. In a high prevalence setting, H. pylori eradication and early reinfection rates after treatment are similar to rates observed in a low prevalence environment, whereas the late reinfection rate seems to be higher. However, up to 3 yr after treatment, most treated patients are free of H. pylori infection and/or ulcer activity. Even longer follow-up studies are necessary to determine whether specific retreatment policies are necessary to maintain long term eradication in developing countries.

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.

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

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. 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. 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. 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.

Duodenal ulcer relapse is not always associated with recurrence of H. pylori infection: a prospective three-year follow-up study.

Long-term data concerning the reappearance of Helicobacter pylori infection and duodenal ulcer (DU) recurrence after successful eradication are still few and conflicting. Inadequate histological assessment or use of indirect tests for the determination of H. pylori and bias in the selection of patients to be controlled can influence reported results. The aim of this study was to determine the rate of recurrence of H. pylori infection and ulcer relapse in a population of cured DU patients followed up for 3 years irrespective of their symptomatology. Between 1992 and 1994, 126 patients with DU disease were treated with double or triple therapy. Patients using nonsteroidal antiinflammatory drugs or aspirin or receiving maintenance antisecretory therapy were excluded. H. pylori infection was assessed by three bioptic tests from both the antrum and the body (culture, urease, histopathological examination). After 2 months from cessation of treatment, DU had healed and H. pylori infection was cured in 102 of 126 patients (81%). These patients were endoscopically followed up after 1 and 3 years, respectively, and were advised to contact us at symptom recurrence. At 1 and 3 years, we studied 95 (93.2%) and 79 (77.4%) patients, respectively, of the 102 who were cured. The other patients were untraceable or refused endoscopy because they were asymptomatic. After 1 year, no patient had H. pylori recurrence, whereas three patients had a relapse of DU without evidence of infection. After 3 years, recurrence of H. pylori occurred in six patients (annual rate, 2.5%), DU relapsed in five H. pylori-positive patients (6.3%) and in two H. pylori-negative patients (annual rate, 1.9%). Fasting gastrin and acid secretion values studied in all relapsed patients were within the normal range except for one H. pylori-positive patient. Recurrence of H. pylori infection is very low where treatment is effective, but a DU relapse, not related to acid hypersecretion, can occur in a small percentage of cured patients.

Is Helicobacter pylori the primary cause of duodenal ulceration?

Helicobacter pylori infection may not be the primary cause of duodenal ulceration in cases not associated with non-steroidal anti-inflammatory drugs, but may be a secondary complication. In developing countries with a uniformly high prevalence of H. pylori infection there are marked regional differences in the prevalence of duodenal ulcer (DU). In some countries, especially those with a low prevalence of H. pylori, 30-40% or more patients with DU may be H. pylori negative. The absence of H. pylori infection in early cases of DU is also reported. In DU patients with antral H. pylori infection, duodenal colonization by H. pylori may often be absent. After complete H. pylori eradication, recurrence of DU within 6 months in some reports is as high as 20%. The evidence suggests that high acidity and reduced duodenal mucosal resistance remain the primary causes of DU and that H. pylori infection, when present, results in chronicity. Reduced mucosal resistance results in duodenal gastric metaplasia which permits colonization of the duodenum with H. pylori from the antrum. Therefore, whatever causes reduced mucosal resistance may be the primary factor and evidence suggests that this cause may be diet related. This would explain the enigma of regional variations in DU prevalence unrelated to H. pylori prevalence.

Stable and unstable amoxicillin resistance in Helicobacter pylori: should antibiotic resistance testing be performed prior to eradication therapy?

Amoxicillin is often implemented in Helicobacter pylori treatment protocols. To date, amoxicillin-resistant H. pylori strains have rarely been detected, and only a total of 14 have been reported in the literature (1). Conspicuously, complete loss of the resistant phenotype was observed after these strains were stored at −80°C. Only one amoxicillin-resistant H. pylori strain has been isolated, in The Netherlands, in which in contrast, the amoxicillin resistance remained stable after repeated cycles of freezing and culture (5). The MIC for this strain was 8 μg/ml, which is relatively low. Since 1996, we have isolated seven H. pylori strains exhibiting high-level amoxicillin resistance (MIC > 256 μg/ml) (Table ​(Table1).1). Four of these exhibited a stable resistance phenotype (strains ACR3, -4, -5, and -7). Strains ACR1, -2, and -4 were isolated from two 11-year-old girls and one 15-year-old girl with recurrent abdominal pain. They received triple therapy in accordance with the results of antibiotic susceptibility testing, and symptoms subsided. The H. pylori strains ACR3 (stable amoxicillin resistance) and ACR6 (unstable resistance) were isolated from an 8-year-old boy and an 11-year-old girl, respectively. Eradication therapy with amoxicillin, clarithromycin, and omeprazole was empirically initiated but remained without effect. Similarly, H. pylori strains ACR5 and ACR7 (stable amoxicillin resistance) were isolated from a 17-year-old girl and a 40-year-old woman with recurrent duodenal ulcers who had been unsuccessfully treated with triple combinations containing amoxicillin. Following treatment failure, the patients were examined by gastrointestinal endoscopy and H. pylori was isolated from both antral and corpus biopsy specimens. Identification was confirmed by 16S rRNA gene sequence analysis, and antibiotic resistance determinations revealed both strains to be highly resistant to amoxicillin. TABLE 1 MICs of antibiotics for seven H. pylori strains with stable and unstable amoxicillin resistance After storage at −70°C and reculture, strains ACR1, -2, and -6 lost their amoxicillin resistance, whereas strains ACR3, -4, -5, and -7 remained stable despite repetitive subculture or freeze-thaw cycles (Table ​(Table1).1). Although β-lactamase activity could not be detected by the nitrocefin assay, amoxicillin resistance was overcome by clavulanic acid in three strains (ACR4, -5, and -6). In contrast, strains ACR3 and -7 were also resistant to amoxicillin-clavulanic acid. All four strains with stable amoxicillin resistance were also resistant to cefuroxime. The antibiotic resistance phenotypes suggest the existence of multiple resistance mechanisms in H. pylori. Antibiotic resistance testing of these bacteria may become increasingly necessary in patients experiencing treatment failures. In four of our cases, amoxicillin resistance correlated with treatment failure. There are general causes for concern. (i) The amoxicillin-resistant phenotype is transferable in vitro to amoxicillin-susceptible strains (5), presumably due to DNA exchange by transformation or a conjugation-like mechanism (2). Colonization of the stomach with other β-lactam-resistant bacteria may also lead to transfer of amoxicillin resistance to H. pylori. (ii) Amoxicillin MICs have been observed to increase upon repeated exposure of H. pylori to the antibiotic (3, 4). To date, MICs for stable amoxicillin-resistant bacteria have been in the range of 8 μg/ml. However, we report the emergence of high-level amoxicillin resistance, the MICs for our strains being >256 μg/ml, which may represent a major threat regarding an effective H. pylori eradication therapy. In conclusion, it may be prudent to perform antibiotic susceptibility testing of H. pylori at an early stage whenever a treatment failure becomes apparent.

Helicobacter pylori status and endoscopy follow-up of patients having a history of perforated duodenal ulcer

Background: The aim of this study was to determine whether the recurrence of symptoms or ulcer disease in patients with a history of perforated duodenal ulcer is related to Helicobacter pylori infection. Methods: One hundred sixty-three consecutive patients with history of perforated duodenal ulcer unrelated to nonsteroidal anti-inflammatory drugs underwent upper endoscopy. Any recurrent symptoms or complications were documented. Regardless of the endoscopic findings, three antral biopsy specimens were taken for histologic examination and a rapid urease test. Results: There was a preponderance of men (male/female = 5.3:1). The mean age was 55.9 years. Sixty-seven (41.1%) patients gave a history of recurrent epigastric pain, seven of whom also had a history of bleeding ulcer. Upper endoscopy was performed at a mean of 74.5 ± 7.1 months after operation. Positive endoscopic findings were noted in 68 (41.7%) patients; H pylori was found in the biopsy specimens from 77 (47.2%) patients. Recurrent duodenal ulcer was found in 29 (17.8%) patients and was significantly related to male gender, recurrent epigastric pain, bleeding ulcer, longer interval from previous operation, and positive H pylori status. Positive H pylori status and male gender were independent factors associated with recurrent duodenal ulcer. Conclusions: Recurrent ulcer disease in patients with a history of perforated duodenal ulcer is related to H pylori infection. (Gastrointest Endosc 1999;50:58-62.)

Lack of Reinfection after Helicobacter Pylori Eradication in Duodenal Ulcer Disease: A Prospective Study from Turin, Italy

Theobjective of our study was to assess the incidence ofreinfection and new ulceration events after demonstratedHelicobacter pylori eradication, in a cohort of patientswith recurrent duodenal ulcers.Materials and MethodsWe followed up the natural history of duodenal ulcerdisease in 115 patients (83 males, mean age 54.8 years).All of them had a previous diagnosis of recurrent duodenalulcer documented by endoscopy, and associated H. pyloriinfection as shown by histology and serology.The starting point of the study was considered theconfirmed eradication of the bacterium and DU absence atthree months after the end of antibiotic treatment. Eachpatient underwent the monitoring scheme at 6, 12 and 24months after the starting point.The presence of Helicobacter pylori infection wasjudged: 1) by histology (Giemsa staining) on biopsiesobtained during endoscopy from the antrum and thefundus; and 2) by measuring specific IgG antibodiesagainst H. pylori by a commercial enzyme-linkedimmunosorbent assay (ELISA).

Which therapy for reducing the recurrence of duodenal ulcers?

Which therapy for reducing the recurrence of duodenal ulcers?

Helicobacter pylori reinfection rate and duodenal ulcer recurrence in Korea.

In the short term, the eradication of Helicobacter pylori in patients with duodenal ulcer (DU) is deemed to be clearly effective; the long-term effectiveness apparently depends on the H. pylori reinfection rate. We conducted the present study to investigate the rates of H. pylori reinfection and DU recurrence in 45 patients previously cured of DU in whom H. pylori had been eradicated. These patients underwent gastroscopy and tests for H. pylori at least 1 year after eradication. In a control group comprising 31 patients with DU who were not treated with H. pylori eradication regimen, the DU recurrence rate was checked annually for 4 years. Twenty of 45 patients (44.4%) in whom the mean follow-up period was 3.5 years were again found to be H. pylori positive, and the reinfection rate was 12.8% per year. DU recurred in 8 of these 20 (40%) but not in any nonreinfected patients. In the control group, the DU recurrence rate was 61% within 1 year, 81% within 2 years, 84% within 3 years, and 90% within 4 years. The respective recurrence rates in the 45 patients in whom the bacteria had been eradicated were 0%, 4%, 13%, and 18%. The H. pylori reinfection rate was as high as 12.8% per year in Korea, but in that the DU recurrence rate is significantly lower (p < 0.01; odds ratio, 129.5) in the H. pylori-eradicated group than in the control group, the eradication of H. pylori in DU patients is effective over the long term (at least 4 years).

Helicobacter pylori eradication as a surrogate marker for the reduction of duodenal ulcer recurrence.

An abundance of data exists documenting the association of H. pylori eradication with the reduction in duodenal ulcer recurrence. To evaluate the validity of using H. pylori eradication as a surrogate marker for the reduction in duodenal ulcer recurrence using rigorously controlled studies. Three controlled clinical trials were conducted in patients with uncomplicated, active duodenal ulcers. Patients were treated with various combinations of omeprazole and amoxycillin. Ulcer healing and H. pylori eradication were assessed. For patients whose duodenal ulcer healed, duodenal ulcer recurrence was determined over a 6-month period in patients with H. pylori eradication and those remaining positive for H. pylori at least 4 weeks after treatment. To support the data obtained from these clinical trials, a search of the medical literature was conducted to identify additional human clinical trials in which duodenal ulcer recurrence rates were measured and categorized by H. pylori status at least 1 month post-treatment. In 11 controlled trials, the overall 6-18-month duodenal ulcer recurrence rate was 54% among patients remaining positive for H. pylori at least 4 weeks after treatment compared to 6% among patients with H. pylori eradication following treatment. This finding was corroborated by the uncontrolled trials, in which the duodenal ulcer recurrence rate was 64% among patients found to be H. pylori-positive and 6% for patients found to be H. pylori-negative at least 4 weeks after treatment. A time course of duodenal ulcer recurrence rates using pooled data from both controlled and uncontrolled studies demonstrated that duodenal ulcer recurrence rates for H. pylori-negative patients persisted for up to 4 years following treatment. Duodenal ulcer recurrence rates for H. pylori-positive patients increased for the first year, then levelled off. A comparison of the duodenal ulcer recurrence rates for different treatment regimens revealed that eradication regimens based on omeprazole plus antibiotics and bismuth plus antibiotics exhibited similar duodenal ulcer recurrence rates for H. pylori-positive and -negative patients. Regardless of treatment regimens, H. pylori eradication produced a consistent and significant reduction in duodenal ulcer recurrence. Therefore H. pylori eradication, 4 weeks post-therapy, can be used as a surrogate marker for reduced duodenal ulcer recurrence in investigational clinical trials.

Helicobacter pylori and peptic ulcer disease therapies: a survey of gastroenterologists in Israel.

Eradication of Helicobacter pylori has become a therapeutic option in the treatment of patients with peptic ulcer disease. The aim of this study was to evaluate the current management strategies of Israeli gastroenterologists in the diagnosis and treatment of H. pylori-related peptic ulcer disease, 14 years after the discovery of H. pylori. A questionnaire was mailed to all specialists in gastroenterology, members of the Israel Gastroenterological Association (IGA). Replies were received from 60% of Israel Board-certified gastroenterology specialists. Over 89% of the gastroenterologists (89.1%) noted that they recommend anti-H. pylori treatment. 94.5% said that they treat duodenal ulcer in the first presentation with anti-H. pylori medication and 75% said that they do so in cases of recurrent duodenal ulcer. According to the replies received, there is a strong consensus towards triple treatment as the favored anti-H. pylori treatment; no one noted the use of dual treatment. Seven-day triple treatment was prescribed by 83.6% of the gastroenterologists who responded. Of these, the great majority, 89.1%, stated that they use proton pump inhibitors (PPI) in combination with any two of the following antibiotics: metronidazole (47.3%), tinidazole (29.1%), clarithromycin (61.8%), and amoxicillin (40%). At the time of the survey, most Israel Board-certified gastroenterology specialists prescribed triple anti-H. pylori treatment of one-week's duration.

Prevention of duodenal ulcer recurrence following eradication of Helicobacter pylori: A prospective 6 years study

Prevention of duodenal ulcer recurrence following eradication of Helicobacter pylori: A prospective 6 years study

What Is the Role of Helicobacter pylori in Complicated Ulcer Disease?

The role of Helicobacter pylori in the pathogenesis of duodenal and gastric ulcer and ulcer recurrence is widely known. Bleeding, perforation, and obstruction represent the most serious, potentially life-threatening manifestations of ulcer disease (hemorrhage in 15%-20%). The lifetime prevalence of perforation and obstruction is much lower (approximately 5% and 2%, respectively). Despite improved diagnostic and therapeutic options, bleeding-related mortality rates remain at 6%-7% in the United States and between 4% and 14% in Europe. H. pylori and nonsteroidal anti-inflammatory drugs are now recognized as the two primary causes of ulcer disease. Eradication of H. pylori in patients with uncomplicated ulcers results in recurrence rates of < 10%, suggesting that eradication of H. pylori in patients with bleeding ulcers may virtually prevent recurrence of both the disease and its complications. Although the prevalence of H. pylori infection is almost 100% in duodenal and 80%-90% in gastric ulcer patients not using nonsteroidal anti-inflammatory drugs, the prevalence of the organism in bleeding duodenal and gastric ulcers does not reach 70% and 60%, respectively, which may be due to false-negative test results.