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Background & Aims: After a first Helicobacter pylori eradication attempt, approximately 20% of patients will remain infected. The aim of the current study was to assess the effectiveness and safety of second-line empiric treatment in Europe., Methods: This international, multicenter, prospective, non-interventional registry aimed to evaluate the decisions and outcomes of H pylori management by European gastroenterologists. All infected adult cases with a previous eradication treatment attempt were registered with the Spanish Association of Gastroenterology-Research Electronic Data Capture until February 2021. Patients allergic to penicillin and those who received susceptibility-guided therapy were excluded. Data monitoring was performed to ensure data quality., Results: Overall, 5055 patients received empiric second-line treatment. Triple therapy with amoxicillin and levofloxacin was prescribed most commonly (33%). The overall effectiveness was 82% by modified intention-to-treat analysis and 83% in the per-protocol population. After failure of first-line clarithromycin-containing treatment, optimal eradication (>90%) was obtained with moxifloxacin-containing triple therapy or levofloxacin-containing quadruple therapy (with bismuth). In patients receiving triple therapy containing levofloxacin or moxifloxacin, and levofloxacin-bismuth quadruple treatment, cure rates were optimized with 14-day regimens using high doses of proton pump inhibitors. However, 3-in-1 single capsule or levofloxacin-bismuth quadruple therapy produced reliable eradication rates regardless of proton pump inhibitor dose, duration of therapy, or previous first-line treatment. The overall incidence of adverse events was 28%, and most (85%) were mild. Three patients developed serious adverse events (0.3%) requiring hospitalization., Conclusions: Empiric second-line regimens including 14-day quinolone triple therapies, 14-day levofloxacin-bismuth quadruple therapy, 14-day tetracycline-bismuth classic quadruple therapy, and 10-day bismuth quadruple therapy (as a single capsule) provided optimal effectiveness. However, many other second-line treatments evaluated reported low eradication rates. ClincialTrials.gov number: NCT02328131., (Copyright © 2022 AGA Institute. Published by Elsevier Inc. All rights reserved.)

Objective: The best approach for Helicobacter pylori management remains unclear. An audit process is essential to ensure clinical practice is aligned with best standards of care., Design: International multicentre prospective non-interventional registry starting in 2013 aimed to evaluate the decisions and outcomes in H. pylori management by European gastroenterologists. Patients were registered in an e-CRF by AEG-REDCap. Variables included demographics, previous eradication attempts, prescribed treatment, adverse events and outcomes. Data monitoring was performed to ensure data quality. Time-trend and geographical analyses were performed., Results: 30 394 patients from 27 European countries were evaluated and 21 533 (78%) first-line empirical H. pylori treatments were included for analysis. Pretreatment resistance rates were 23% to clarithromycin, 32% to metronidazole and 13% to both. Triple therapy with amoxicillin and clarithromycin was most commonly prescribed (39%), achieving 81.5% modified intention-to-treat eradication rate. Over 90% eradication was obtained only with 10-day bismuth quadruple or 14-day concomitant treatments. Longer treatment duration, higher acid inhibition and compliance were associated with higher eradication rates. Time-trend analysis showed a region-dependent shift in prescriptions including abandoning triple therapies, using higher acid-inhibition and longer treatments, which was associated with an overall effectiveness increase (84%-90%)., Conclusion: Management of H. pylori infection by European gastroenterologists is heterogeneous, suboptimal and discrepant with current recommendations. Only quadruple therapies lasting at least 10 days are able to achieve over 90% eradication rates. European recommendations are being slowly and heterogeneously incorporated into routine clinical practice, which was associated with a corresponding increase in effectiveness., Competing Interests: Competing interests: JPG has served as speaker, consultant and advisory member for or has received research funding from Mayoly, Allergan and Diasorin. OPN has received a research grant from Allergan. JM-I has served as a consultant for Casen Recordati and has received retribution from Allergan for formative actions. MC-F has received retribution from Allergan for formative actions. PB has served as speaker, consultant and advisory member for or has received research funding from Almirall, Allergan and Reckitt Benckiser. APA has received retribution from Allergan and Mylan for formative actions. DSB has served as lecturer for Astellas, AstraZeneca, KRKA and Abbott., (© Author(s) (or their employer(s)) 2021. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: The effect of Helicobacter pylori (H. pylori) infection on gastric acid secretion (GAS) is poorly defined in children., Objective: To determine whether H. pylori infection is associated with abnormal GAS in children., Methods: We studied 30 H. pylori-infected children (identified by a positive urea breath test) and 30 noninfected children of both sexes, aged 2-5 years. Gastric pH and GAS were measured before and 8 weeks after the completion of a 2-week course of anti- H. pylori therapy (omeprazole, clarithromycin, and amoxicillin). Gastric acid output (GAO) was quantified during a 1-h basal period (GAO-B) (mmol/h) and a 1-hour stimulated period (GAO-S) (mmol/hour) following subcutaneous administration of pentagastrin (6 μg/kg)., Results: A significantly greater number of infected children had a high gastric pH (>4.0, p = 0.03) compared with the noninfected group. GAO-B and GAO-S in H. pylori-infected children were significantly lower, around 50%, compared with children without H. pylori infection. H. pylori-eradication therapy resulted in a rise of both the mean GAO-B (paired t-test before vs. after therapy; 0.28 ± 0.40 vs. 0.62 ± 1.0, p = 0.12) and GAO-S (before vs. after therapy; 2.0 ± 1.4 vs. 3.4 ± 2.5, p = 0.001), with values reaching equivalence to those in the H. pylori-negative children (0.71 ± 0.56 for BAO, 3.3 ± 2.0 for SAO, p = NS)., Conclusion: The results suggest that the gastric barrier is compromised in children with H. pylori infection in Bangladesh. Improvement of GAO following anti- H. pylori therapy suggests a causal link between H. pylori infection and depressed GAO in this population., (© 2012 Blackwell Publishing Ltd.)

Background & Aims: We investigated Helicobacter pylori (H pylori)-infection as a cause of iron deficiency (ID) and iron-deficiency anemia (IDA) or treatment failure of iron supplementation., Methods: We randomized 200 Hp-infected children (positive urea breath test) 2-5 years of age with IDA (hemoglobin level <110 g/L; serum ferritin level <12 microg/L; and soluble transferrin receptor >8.3 mg/L) or ID (serum ferritin level <12 microg/L or soluble transferrin receptor level >8.3 mg/L) to 1 of 4 regimens: 2-week anti-Hp therapy (amoxicillin, clarithromycin, and omeprazole) plus 90-day oral ferrous sulfate (anti-Hp plus iron), 2-week anti-Hp therapy alone, 90-day oral iron alone, or placebo. Sixty noninfected children with IDA received iron treatment as negative control., Results: Hp-infected children receiving iron had significantly less frequent treatment failure compared with those with no iron in correcting IDA (11% [95% confidence interval (CI), 2%-20%] for anti-Hp plus iron, 0% for iron alone vs 33% [95% CI, 26%-46%] for anti-Hp and 45% [95% CI, 31%-59%] for placebo; chi(2) = 127; P < .0001), ID (19% [95% CI, 8%-30%] for anti-Hp plus iron, 7% [95% CI, 0%-14%] for iron alone vs 65% [95% CI, 52%-78%] for anti-Hp alone, and 78% [95% CI, 66%-90%] for placebo; chi(2) = 124; P < .0001), or anemia (34% [95% CI, 20%-40%] for anti-Hp plus iron, 27% [95% CI, 14%-40%] for iron alone vs 65% [95% CI, 52%-78%] for anti-Hp alone and 78% [95% CI, 66%-90%] for placebo; chi(2) = 46; P < .0001). Cure rates of IDA, ID, or anemia with iron were comparable with that of the negative control group. Improvements in iron status also were significantly greater in groups with iron., Conclusions: H pylori is neither a cause of IDA/ID nor a reason for treatment failure of iron supplementation in young Bangladeshi children.

Background and Aim: Bangladesh is a developing country with a very high prevalence of Helicobacter pylori infection, which has been ascribed to overcrowding and poor sanitary conditions. It has generally been accepted that the re-infection rate is higher in countries with a high prevalence of H. pylori infection. Short-term follow-up studies support this assumption but no long-term studies are available to confirm or refute this assertion. The present study was aimed to define the long-term H. pylori re-infection rate (6 years after successful eradication) in duodenal ulcer patients., Methods: In a previous study, 90 patients were successfully eradicated for H. pylori and followed-up for 24 months. 17/90 were found to be re-infected (18% re-infection rate per year in the first 12 months) [Gastroenterology 2001;792-798]. The remaining 73 patients were targeted for long-term follow-up. 26/73 were lost to follow-up; 6 symptomatic patients were tested H. pylori positive in the period between 24 and 60 months post-eradication. The remaining 41 patients were evaluated 72 months after successful eradication. The evaluation included clinical history taking, a (13)C-urea breath test (UBT), and endoscopy., Results: Of the 41 H. pylori-eradicated patients analyzed after 72 months, 16 were H. pylori-positive. If the 6 patients, who were tested positive between 24 and 60 months, are added, the total re-infection cases amount to 22 subjects in the period between 24 and 72 months. Therefore, an overall annual re-infection rate 6 years after eradication of 5.02% can be calculated. Six of the 23 symptomatic patients had duodenal ulcer relapse, 5/6 were H. pylori re-infected and one was H. pylori-negative at 72 months post-treatment., Conclusion: The long-term annual H. pylori re-infection rate in Bangladeshi adults is markedly higher than in Western countries but lower than anticipated. In this study, duodenal ulcer relapse is clearly related to H. pylori re-infection., ((c) 2007 S. Karger AG, Basel)

Gastric cancer has been recognized as an important cause of morbidity and mortality all over the world. Helicobacter pylori has been shown to have a causal relationship to gastric cancer. The knowledge into the mechanisms related to this has advanced considerably over the last few years thereby unarguably defining the role of this host-pathogen interaction. Epidemiological studies, research in animal models, molecular pathways involving host and bacterial factors, environmental factors and recent work on stem cells have contributed to understanding the origin and progress of this neoplasia. These form part of the myriad of interplaying factors resulting in the causal relationship. Nevertheless, current evidence is insufficient to accurately identify a definitive population where prevention or treatment strategies have to be targeted. Future trials will have to define the people at risk and shed more light in these areas., (Copyright 2007 S. Karger AG, Basel.)

Aim: To evaluate the prevalence of antibodies against two major markers of virulence of Helicobacter pylori--cytotoxin-associated gene A (cagA) and the vacuolating cytotoxin gene (vacA)--among children in a peri-urban community of Bangladesh, and to evaluate Western blot (WB) assay for detection of H. pylori infection diagnosed by 13C urea breath test (UBT) in such children., Methods: One hundred and eighty-two children aged 18-60 mo, of the peri-urban community of Dhaka, were screened for H. pylori infection using UBT, and the serum samples were analysed for antibody against cagA and vacA by Western blot., Results: The overall prevalence of H. pylori infection by 13C-urea breath test was 80%. The seroprevalence of cagA with or without vacA, vacA with and without cagA, and both cagA and vacA were 82%, 82% and 81%, respectively. Among children with a positive UBT, 95% were seropositive for both cagA and vacA, indicating that the products of these genes are frequently co-expressed in H. pylori infection in this community. The sensitivity, specificity, positive and negative predictive value of the Western blot test for H. pylori infections, compared to UBT, were 94%, 68%, 92% and 76%, respectively., Conclusion: Compared to UBT, Western blot test is reliable for the detection of H. pylori infection. The high seroprevalence of cagA- and vacA-positive virulent H. pylori strains in an asymptomatic paediatric population indicate that such strains are common in this population and may cause characteristic H. pylori infection in Bangladesh.

Helicobacter pylori stool tests are an accurate and noninvasive tool to assess H. pylori status before and after treatment. We are convinced that the current technical shortcomings of H. pylori stool tests, i.e. inter-test variability and reduced specificity after treatment, can be overcome in the near future. The availability of an office-based stool test would offer a considerable advantage since it could be performed in any private practice without further delay. However, it remains to be seen whether the reluctance of patients to collect stool specimens will have an impact on its general use., (Copyright 2003 S. Karger AG, Basel)

Tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) are important for the pathogenesis of Helicobacter pylori-associated gastritis and peptic ulcer disease. Gastric biopsies from H. pylori-positive and -negative patients were used to examine the in situ correlation of TNF-alpha and IFN-gamma with epithelial cell apoptosis, bacterial load, and histological parameters of gastritis. From the same patients, we isolated H. pylori-specific T cell lines and clones and examined their ex vivo release of proinflammatory cytokines. We found a highly significant correlation of TNF-alpha and IFN-gamma production with activity and grade of gastritis (P < 0.01), H. pylori density (P = 0.01), epithelial cell apoptosis (P < 0.001), and Fas/Fas-ligand expression (P < 0.001). T cell lines and clones were all TCR-alphabeta(+) and showed T helper 1 functional phenotype. With the use of serial histological sections, this study showed for the first time the in situ correlation of TNF-alpha and IFN-gamma with epithelial cell apoptosis, bacterial load, and histological severity of disease and emphasizes the role of these cytokines in the pathophysiology of H. pylori-associated disease.

Background & Aims: In developing countries where Helicobacter pylori infection is widespread, posttherapeutic recurrence rates may be high. Many of the limited studies available have methodological problems and show varied recurrence rates. We determined late recrudescence rates, true reinfection, and ulcer recurrence., Methods: One hundred five Bangladeshi patients with H. pylori infection and duodenal ulcer disease were treated with a triple therapy. Follow-up included 13C-urea breath tests, endoscopy, and biopsy-based tests. In reinfected patients, genomic typing compared pretherapeutic and posttherapeutic strains., Results: Recrudescence, associated with nitroimidazole-based treatment, occurred in 15 of 105 patients (14%) within the first 3 months, but only 8 of 105 patients tested positive 4 weeks after therapy ended. True reinfection was diagnosed in 11 of 105 patients between 3 and 18 months after therapy. The annual reinfection rate was 13%, based on a total follow-up of 84.7 patient years. Ulcer relapse occurred in 2 of 15 (13%) recrudescence cases and in 6 of 11 (55%) reinfection cases, but also in 4 of 73 (5%) H. pylori-negative patients., Conclusions: In Bangladesh, late recrudescence of H. pylori after eradication therapy occurs within the first 3 months. The reinfection rate is high and might influence cost-benefit analyses for determining diagnostic and therapeutic procedures.

Objectives: The aim of this study was to assess the still controversial role of treatment of Helicobacter pylori (H. pylori) infection in patients with nonulcer dyspepsia., Methods: We conducted a double-blind, randomized, placebo-controlled, multicenter trial comparing the efficacy of 7 days of eradication treatment (lansoprazole 15 mg b.i.d., amoxicillin I g b.i.d., and clarithromycin 500 mg b.i.d.) with a control treatment (lansoprazole 15 mg b.i.d. and placebo) in H. pylori-infected patients with nonulcer dyspepsia. 13C breath tests were performed at baseline and during follow-up. We assessed patient symptoms, health status (based on the SF-12 questionnaire), patient satisfaction, drug consumption, health care consultation behavior, and absenteeism related to dyspepsia over a 1-yr period., Results: A total of 74 patients randomized to eradication treatment and 70 patients randomized to placebo were compared. The rate of eradication of H. pylori infection was 75% in the active treatment group and 4% in the placebo group (p < 0.005). The symptom score improved to a similar extent in the group receiving active treatment (-4.0; 95% CI = -5.0 to -3.0) and placebo (-3.6; 95% CI = -4.5 to -2.7). Treatment response was not related to the severity or duration of initial symptoms or to the severity of gastritis on histology. Quality of life scores were comparable at 12 months. There was no significant difference in dyspepsia-related absenteeism or satisfaction with management of NUD. Patients receiving active treatment were more likely not to have had to use any dyspepsia treatment over the 12 months (60.8% vs 44.3%; p = 0.047)., Conclusions: This study did not demonstrate any substantial benefit of curing H. pylori infection in patients with nonulcer dyspepsia. The study adds further evidence that H. pylori is not the main pathogenetic or therapeutic target in these patients.

Background: Clarithromycin and nitroimidazoles such as metronidazole and ornidazole are among the most frequently used antibiotics for curing Helicobacter pylori infection. However, controversial data exist on whether their in vitro resistance has a negative impact on treatment outcome., Methods: Patients with H. pylori positive active peptic ulcer disease were randomly assigned to receive lansoprazole 30 mg o.d., amoxycillin 1 g b.d. and ornidazole 500 mg b.d. (LAO) or lansoprazole 30 mg o.d., amoxycillin 1 g b.d. and clarithromycin 500 mg b.d. (LAC) for 2 weeks. Pre-treatment resistance to ornidazole and clarithromycin was assessed by Epsilometer (E-) test. Four weeks after completion of treatment, patients underwent a 13C urea breath test to assess H. pylori status., Results: Data from 80 patients with active peptic ulcer disease and positive H. pylori status were analysed. The prevalence of primary drug resistance was 25% for metronidazole and 7.5% for clarithromycin. In patients treated with LAO, effective treatment was achieved in 87% of metronidazole-susceptible, but only 30% of metronidazole-resistant strains (P < 0.01). In the LAC group, therapy was successful in 81% of clarithromycin-susceptible strains, whereas treatment failed in all patients with primary clarithromycin resistance (n = 3)., Conclusion: Resistance against nitroimidazoles significantly affects treatment outcome in H. pylori eradication therapy.

H. pylori is the cause of one of the most common infectious diseases worldwide. Infection with H. pylori leads to exaggerated synthesis of several inflammatory cytokines. Only a minority of infected patients develops peptic ulcer disease. H. pylori strains associated with peptic ulcer disease induce strong mucosal infiltration with inflammatory cells and increased expression of several cytokines. Cytokines may contribute to ulcer development by different mechanisms, including stimulation of gastrin and pepsinogen release, suppression of somatostatin synthesis and activation of inflammatory cells.

Background/aims: Helicobacter pylori is considered to be the primary cause of most forms of gastritis, but its role as a causative agent in gastric erosions is unclear. The aim of this study was to estimate the prevalence of gastric erosions and H. pylori infection in asymptomatic volunteers., Methods: 175 asymptomatic subjects underwent upper gastrointestinal endoscopy. Antral biopsies were taken for bacterial cultures, histology and quick urease (CLO) test. A (13)C-urea breath test was performed after endoscopy. NSAID intake, alcohol consumption and smoking habits were also recorded in each subject., Results: 33 (19%) of 175 asymptomatic volunteers had macroscopic lesions on upper gastrointestinal endoscopy, 7 were H. pylori positive, 26 were H. pylori negative. Gastric erosions occurred in 8% (14 subjects) of all volunteers. 10 subjects were H. pylori negative and 4 H. pylori positive. In 11 volunteers, gastric erosions were restricted to the prepyloric antrum. Only 1 of 14 subjects had a history of NSAID intake and 6 subjects were alcohol abstainers., Conclusion: We conclude that gastric erosions occur in a considerable amount of asymptomatic volunteers. They are predominantly localized in the prepyloric antrum and are most likely not associated with H. pylori infection, NSAID intake, smoking or alcohol consumption., (Copyright 2000 S. Karger AG, Basel.)

Helicobacter pylori is an important cause of chronic gastritis and plays important roles in the etiology of peptic ulcer disease, gastric cancer and non-ulcer dyspepsia. While H. pylori infections occur worldwide, the great majority of information is from the developed countries, and little is known about the epidemiology of H. pylori in the developing countries, particularly in children.

A cohort of 151 infants and young children aged 1-23 months from a poor peri-urban community of Bangladesh was studied to determine the relationship between Helicobacter pylori colonization and morbidity due to diarrhoea. A 13C urea breath test was performed to detect the presence of H. pylori. Children were followed up at home every alternate day for 6 months and diarrhoeal morbidity data were collected. Diarrhoeal morbidity was compared between H. pylori-positive and H. pylori-negative children. Sixty-eight (45 per cent) children were H. pylori positive and 83 (55 per cent) were H. pylori negative. During the first 1-month period following the breath test, three (4.4 per cent) H. pylori-positive and four (4.8 per cent) H. pylori-negative children had diarrhoea. Thirty-two (47 per cent) of the children in the positive group and 43 (52 per cent) in the negative group had one or more episodes of diarrhoea during the 6-month follow-up period. Median number of diarrhoeal episodes was 1.0 (range 1.0-4.0) in the H. pylori-positive children and 2.0 (range 1.0-5.0) in the H. pylori-negative children (p = 0.19). No significant difference was observed in the cumulative days with diarrhoea. The results of this study suggest that H. pylori colonization is not associated with diarrhoeal morbidity in infants and young children.

Nondispersive infrared spectrometry (NDIRS) was used to detect Helicobacter pylori infection with the 13C-urea breath test. The results were compared with those of standard isotope ratio mass spectrometry (IRMS). Both methods accurately distinguished between H. pylori-positive and H. pylori-negative individuals. The results demonstrate that NDIRS technology is accurate and therefore of equal value to standard IRMS for detection of H. pylori infection. It can be recommended for routine clinical application. As NDIRS technology is much cheaper than current IRMS machines, we consider the new method extremely useful for clinical applications.

The aim of this study was to determine the age-specific prevalence of Helicobacter pylori infection in infants and children aged 1-99 months from a poor periurban community in Bangladesh. We also examined the frequency of infection among infants and their 53 immediate family members and evaluated the relationship between infection and fasting serum group II pepsinogen (pepsinogen II) concentration in 76 children. Sixty-one percent of 1-3 month-old infants tested positive for H. pylori; this rate declined steadily to 33% in children aged 10-15 months and then increased to 84% in children aged 5-8 years. The H. pylori infection rate was 2.5 times higher in children with illiterate mothers. No difference in infection rate was detected among the family contacts of infected vs. noninfected infants. H. pylori-infected children had significantly higher serum pepsinogen II concentrations than did noninfected children (P < .001). We conclude that infection with H. pylori is highly prevalent and occurs at an early age. An environmental factor or factors, rather than or in addition to intrafamilial spread of this infection, are important in poor communities of Bangladesh. The higher levels of serum pepsinogen II in H. pylori-positive children might indicate the presence of gastritis in such asymptomatic children.

Background: The gastric acid barrier, an important host defence against small bowel infection, may be compromised by infection with Helicobacter pylori. In developing countries, H. pylori infection occurs early in life and prevalence of hypochlorhydria is high particularly in the malnourished, which may predispose a child to repeated gastrointestinal infection and diarrhoea. Diarrhoea being a leading cause of childhood mortality and morbidity in developing countries, we investigated the prevalence of H. pylori infection in children in a poor Bangladeshi community and explored its association with socioeconomic and nutritional status., Methods: The study was conducted in a poor periurban community among 469 children aged 1-99 months. Parents were interviewed using a questionnaire. To detect active infection with H. pylori a 13C-urea breath test was performed and weight was recorded on a beam balance with a sensitivity of 20 g., Results: In all, 61% of 36 infants aged 1-3 months were positive for H. pylori; this rate dropped steadily with increasing age and was 33% in 10-15 month old children and then rose to 84% in 6-9 year olds. Overall H. pylori infection had no association with nutritional state of the child, or family income but the infection rate was 2.5 times higher in children of mothers with no schooling., Conclusions: The H. pylori infection rate is very high in early infancy in a poor periurban community of Bangladesh. The reason for a drop in the infection rate in late infancy is unclear but could be due to initial clearance of the infection by the body's defence mechanisms but with possible alteration of the gastric mucosa which sustains infection. Maternal education may be protective and may operate through some unidentified proximate behavioural determinants. The rate of H. pylori infection in infants and young children may predispose them to repeated gastrointestinal infection and diarrhoea.

In this pilot study we investigated the value of a fourteen-day regimen with amoxicillin (1 g bid), ranitidine (300 mg/d) and ursodeoxycholic acid (300 mg tid) in eradicating Helicobacter pylori. 15 patients with non-ulcer dyspepsia (reactive CLO test, positive histology or 13C urea breath test) were enrolled. Helicobacter pylori was eradicated in 6 of 13 patients (13C urea breath test 4 weeks after the end of treatment). 2 patients were not followed up because of too short treatment (< 1 week). Only 5/15 patients had no side effects (33%). These results strongly suggest that ursodeoxycholic acid in this application regimen is not of use in eradicating Helicobacter pylori.

Although H. pylori is well established as an etiological agent of type B gastritis and a predisposing factor for peptic ulcer, knowledge about its transmission is unclear. In this study we examined the prevalence of H. pylori infection in the family members of index infants infected with this organism as indicated by positive [13C]-urea breath test (UBT). We performed UBT among family members of 15 predominantly breastfed infants, eight with and seven without H. pylori infection. Infection rates were 82% and 91% in family contacts of the infected and noninfected infants respectively, the average infection rate being 85%, which is rated to be high. There was no difference in infection rates among the parents of the infected and noninfected infants. Fifty percent and 70% families belonging to infected and noninfected infants, respectively, were found to have all members infected with H. pylori. No evidence of sex predilection of infection was found. We conclude that in communities with high prevalence of H. pylori infection, there is almost an equal infection rate among the family contacts of infected and noninfected infants, suggesting that environmental factors may be more important than intrafamilial transmission.

Gastroduodenal ulcers are strongly associated with Helicobacter pylori (HP) infection. Successful eradication drastically diminishes ulcer recurrence. Most of the eradication schemes include metronidazole (Flagyl). The present study was designed to establish the metronidazole resistance rate in Switzerland. Antral biopsies were taken in 153 patients with suspected ulcers (115 men, 38 women, mean age 46 +/- 16 [SD] years) during upper endoscopy for bacteriological testing. Metronidazole resistance (> 8 micrograms/ml) was found in 47/153 (31%) of the isolates. Resistance was found in no case to amoxicillin (Clamoxyl) (0/104 = 0%) and only in 3% (2/66) to clarithromycin (Klazid). Metronidazole resistance of HP in a third of the isolates studied is comparable to numbers found in other European countries. These findings raise the question whether eradication schemes including metronidazole without prior sensitivity testing are justified. Amoxicillin and clarithromycin appear to be valid alternatives.

The pathogenesis of peptic ulcer disease is complex. It is associated with a spiral organism, Helicobacter pylori, which induces chronic gastritis. The evidence for a causal association between H. pylori and peptic ulcer disease stems primarily from the observation that eradication therapy with bismuth and various antibiotics may produce normalization of gastritis and possible cure of ulcer disease. The prevalence of H. pylori infection and potential implications for therapy are discussed. Who should undergo eradication therapy, and how? The problem remains that--despite the fact that a cure is possible--no simple therapy is available.

The relation between Helicobacter pylori (H pylori) infection and fasting gastrin and pepsinogen-I and -II concentrations was evaluated in 278 volunteers without symptoms and the results were compared with the values obtained in 35 patients with duodenal ulcers. H pylori infection was determined with the 13C-urea breath test in subjects without symptoms and with endoscopy, biopsy (histology and culture), and quick urease test (CLO-test) in patients with duodenal ulcers. Gastrin and pepsinogen-I and -II concentrations were assayed with specific radioimmunoassay systems. The results clearly indicate that fasting gastrin and pepsinogen-I and -II concentrations were significantly higher in H pylori positive compared with H pylori negative subjects. Neither age nor sex affected basal gastrin and pepsinogen concentrations in H pylori negative subjects. Fasting gastrin, pepsinogen-I and -II concentrations in serum samples were similar in H pylori positive persons with no symptoms and those with duodenal ulcers suggesting that similar mechanisms are involved in increasing plasma concentrations of these variables in both populations. Hypergastrinaemia and hyperpepsinogenaemia are therefore probably secondary to active H pylori infection.

A simplified 13C-urea breath test (UBT) for detection of Helicobacter pylori (Hp) infection was evaluated in 50 patients. Following upper gastrointestinal endoscopy the patients received 100 ml of a liquid test meal with 100 mg 13C-urea. Breath samples were obtained at baseline and 30 minutes respectively. The UBT was positive (difference of 13CO2 enrichment exceeding 5%) in 33/35 patients with culture-proven Hp infection and negative in 14/15 patients in whom microbiological culture, histology and a urease test (CLO-test) were negative. We conclude that in view of its high sensitivity (94%) and specificity (93%) the UBT is useful for rapid, non-invasive diagnosis of Hp infection.

1. Helicobacter pylori has been associated with chronic type-B gastritis, which in turn is always present in duodenal ulcer patients; therefore, it is likely that Helicobacter pylori is an important cofactor in the pathogenesis of peptic ulcer disease. An eradication of Helicobacter pylori is associated with the reduced ulcer relapse rate, but an effective therapy for eradication is not yet available and should be restricted to experimental protocols. 2. Omeprazole is an antagonist of the proton pump of the acid-producing cell of the human stomach. With once-daily omeprazole treatment it is possible to almost abolish 24-hour intragastric acidity in the majority of duodenal ulcer patients; therefore, omeprazole allows alternative treatment of different causes of peptic disease.