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Notes: The purpose of the study was to evaluate the serological prevalence of Helicobacter pylori (H. pylori) infection during infancy and childhood in Germany.〈section xml:id="abs1-2"〉〈title type="main"〉Patients and Methods.We quantified specific IgG antibody titers against H. pylori by enzyme-linked immunosorbent assay (ELISA) technique (BIO-RAD G.A.P. IgG-test) from healthy children under 18 years (n = 216) admitted to hospital for minor surgical procedures. All patients were age 0–18 years and lived in the southern part of Germany (Bavaria and Baden-Wuerttemberg). For each age group, 12 different sera were obtained and were determined in duplicate. We analyzed the 216 sera within 6 age groups of equal size. Mean titers〉 19 U/ml were considered positive for H. pylori infection.〈section xml:id="abs1-3"〉〈title type="main"〉Results.None of the sera of 48 children less than 4 years old were positive for anti-H. pylori specific IgG antibodies. Titers above 19 U/ml were found in 8.3% (3/36 sera each, CI 95% 1–21.7%) in the children age three to five and nine to 11 years. Six- to eight-year-old children showed a 19.4% seroprevalence (7/36 sera, CI 95% 8.2-48%) and children 12–14 years old showed a seropositivity of 16.7% (6/36 sera, CI 95% 6.6–  46.1%). In contrast, 47.2% (17/36 sera, CI 26.5–70.3%) of the adolescents older than 14 years had positive H. pylori antibody titers (p 〈 .01, compared to the age-group 12–14 years). The test for linear trend (seropositivity and age) was significant with p 〈 .001. The overall incidence increase with age in prevalence of H. pylori infection was found to be 0.9% per year within this population.〈section xml:id="abs1-4"〉〈title type="main"〉Conclusions.In contrast to published data from other European and non-European countries, we could not detect H. pylori infection in German infants less than four years old by measurement of IgG antibodies. In the older subjects, seropositivity increased significantly and linearly with age.

Notes: Helicobacter pylori plays a role in the pathogenesis of both duodenal and gastric ulcers. The aim of this study was to evaluate the effect of the proton pump inhibitor (PPI), lansoprazole, commonly used in eradication regimens, on growth, bactericidal activity and morphology of H. pylori in vitro in comparison with other PPIs.〈section xml:id="abs1-2"〉〈title type="main"〉Materials and Methods.Growth inhibitory activity of each of the PPIs was evaluated by determining minimum inhibitory concentrations using an agar dilution method. Bactericidal activity was determined by analysis of the viable cells in culture at various time points after incubation with different concentrations of the PPIs. Bacterial morphology was examined using scanning electron microscopy of fixed cells after exposure to the test substances. Urease activity in cell extracts of H. pylori that had been incubated with increasing concentrations of the PPIs was determined by colorimetry.〈section xml:id="abs1-3"〉〈title type="main"〉Results.The growth inhibitory activity of lansoprazole was significantly more potent than that of omeprazole or pantoprazole (MIC90 6.25 vs. 25 and 100~μg/ml, respectively). Exposure of H. pylori to lansoprazole produced loss of viability and an aberrant bacterial morphology, which was more extensive than seen with omeprazole or pantoprazole. Lansoprazole dose dependently inhibited urease activity; its effectiveness was comparable with omeprazole but more potent than pantoprazole.〈section xml:id="abs1-4"〉〈title type="main"〉Conclusions.The mechanism of action that leads to loss of viability of H. pylori cells appears to differ between the three PPIs investigated; lansoprazole was the most potent of the three agents in terms of growth inhibition and disruption of bacterial morphology.

Notes: Serological rapid whole-blood tests for the detection of H. pylori are presently being promoted for use in primary care. We conducted a multi-center study to investigate the diagnostic accuracy of the Boehringer Mannheim Helicobacter pylori® test (BM test), which is identical with the Cortecs Helisal® test.〈section xml:id="abs1-2"〉〈title type="main"〉Patients and Methods.A previous diagnosis of H. pylori, a history of peptic ulcer diseases, or proton-pump inhibitor, bismuth or antibiotic use during the preceding month were exclusion criteria. The BM test was performed prior to endoscopy by 7 primary care physicians, 5 practicing gastroenterologists, or a single physician in the university hospital outpatient service. During endoscopy, antral and corpus biopsies were obtained for histology and rapid urease testing (RUT). H. pylori positivity was defined by histology and/or RUT as reference methods. H. pylori IgG-ELISA was performed additionally.〈section xml:id="abs1-3"〉〈title type="main"〉Results.Of the 203 patients included, 151 were H. pylori-positive by reference methods (74.4%). The overall accuracy of the BM test was 77.3%. Eight BM tests were indeterminate, and in the other 195 patients the test performed as follows: sensitivity 80.3%, specificity 81.3%, positive predictive value 92.9%, negative predictive value 57.4%. Using IgG-ELISA as reference, the BM test performance was similar. It also did not differ substantially among the three groups of physicians involved.〈section xml:id="abs1-4"〉〈title type="main"〉Conclusions.We found the performance of the BM test to be insufficiently accurate, as both over- and underdiagnosis of H. pylori infection were not infrequent. This test needs to be improved before its use in primary care can be recommended.

Notes: Background. Enterohepatic Helicobacter species are emerging pathogens, which are increasingly isolated from humans with enteric diseases. Nevertheless, current methods to detect Helicobacteraceae in the human gut have significant limitations.Methods. Based on 16S-rRNA gene alignments and computer aided primer analysis a set of group-specific PCR primers was designed. The evaluation of the PCR assay was performed using 36 ATCC reference strains and intestinal biopsies from 10 patients with defined gastric Helicobacter pylori status. The amplification products derived from clinical samples were cloned and subsequently analyzed by DNA sequencing. Sensitivity of the PCR-assay was determined by spiking previously negative tested samples with decreasing amounts of Helicobacter DNA.Results. The analysis of the ATCC reference strains revealed amplification products in all 14 Helicobacter strains and Wolinella succinogenes, 21 other microorganisms representing negative controls did not produce PCR fragments. Four out of the 10 patient-derived samples were positive. Three of them represented H. pylori-derived DNA confirming the gastric H. pylori infection in these patients. In the fourth patient, who was suffering from Crohn's disease, H. pullorum was identified. The sensitivity of the PCR assay was 0.1 pg of Helicobacter-derived DNA representing about 40 bacteria.Conclusion. The novel PCR assay described here is an important new tool in rapid and sensitive assessment for the presence of Helicobacteraceae in human gut.

Notes: This paper reviews new literature data from March 2004 to April 2005 about the association between Helicobacter pylori and non-malignant disease of the upper gastrointestinal tract. Eradication of H. pylori is indicated for all patients with non-malignant diseases associated with this pathogen. However, its effect is variable, ranging from the highest benefit in the cure of peptic ulcer disease to a small benefit in patients with non-ulcer dyspepsia. Test and treat strategy is still cost-effective for management of patients with uninvestigated dyspepsia. The only limitations of the strategy are the patient's age and the cost benefit ratio in case of low prevalence of the infection. H. pylori eradication is of value in chronic NSAID users, but is insufficient to prevent NSAID-related ulcer disease. In developed countries H. pylori eradication does not cause gastro-esophageal reflux disease (GORD), however, a negative association between H. pylori and GORD does exist, especially in Asia, but the nature of this relationship should be further clarified.

Notes: Since the bacterium H. pylori was identified in 1982, overwhelming evidence has implicated it as the causal factor in the occurrence and relapse of peptic ulcer disease. The major objective of this study was to examine the extent to which physicians recognize H. pylori as a causal agent in peptic ulcer disease or as potential cofactor in other gastrointestinal diseases, and the extent to which this knowledge has influenced diagnostic and therapeutic practices.〈section xml:id="abs1-2"〉〈title type="main"〉Materials and Methods.Using a national mail survey in Germany in September 1995, 1197 family practitioners and 1197 gastroenterologists were selected for the study.〈section xml:id="abs1-3"〉〈title type="main"〉Results.Of the surveyed physicians, 756 (32%) responded. Family practitioners treated almost 50% of their patients with initial presentation of suspected ulcer disease without ordering further diagnostic tests. More than 25% of the family practitioners and 14% of the gastroenterologists reported that they do not treat diagnosed H. pylori infection in the first presentation of duodenal ulcer. At the time we conducted the study, 22% of responding family practitioners and 5% of responding gastroenterologists treated the first presentation of H. pylori-positive ulcer disease with regimens determined to be ineffective according to the available literature.〈section xml:id="abs1-4"〉〈title type="main"〉Conclusions.Gastroenterologists preferred to treat H. pylori infection when the associated disease was one for which a causal relationship had been more clearly established, while family practitioners showed less discrimination. In order to provide optimal therapy aimed at minimizing the course and consequences of H. pylori-related diseases, researchers in the field must ensure continuous dissemination of current knowledge.

Notes: It was our goal to evaluate the efficacy and safety and patient compliance with omeprazole-based dual and triple therapy for eradication of Helicobacter pylori in peptic ulcer disease.〈section xml:id="abs1-2"〉〈title type="main"〉Materials and Methods.One hundred seventy-five consecutive patients with H. pylori infection and associated active peptic ulcer were included. H. pylori infection was assessed by rapid urease test and histological analysis. Patients were randomized among three treatments: group 1 (56 patients): omeprazole, 20 mg bid, and amoxicillin, 1 gm bid, for 2 weeks; group 2 (61 patients): omeprazole, 20 mg bid, plus amoxicillin, 1 gm bid, and metronidazole, 500 mg bid, for 1 week; and group 3 (58 patients): omeprazole, 20 mg bid, plus amoxicillin, 1 gm bid, and clarithromycin, 500 mg bid, for 1 week. Ulcer healing and cure of infection were evaluated at 4 to 6 weeks after cessation of therapy. Eradication rate was calculated per-protocol and by an intention-to-treat analysis.〈section xml:id="abs1-3"〉〈title type="main"〉Results.At posttreatment endoscopy, duodenal ulcer was healed in 98.3% of patients. Eleven patients (6%) were lost to follow-up. H. pylori infection was treated successfully in 55% (95% confidence interval [CI] = 41%–69%) of patients of group 1; 86% (95% CI = 77%–95%) of group 2 (p 〈 .001 vs. group 1); and 93% (95% CI = 85%–100%) of group 3 (p 〈 .001 vs. group 1). On intention-to-treat analysis, eradication was 52%, 80%, and 86% in groups 1, 2, and 3, respectively. A good compliance was observed in more than 90% of patients of all groups. Side effects were reported by 7% of patients in group 1, 9% in group 2, and 11% in group 3. None of the patients stopped therapy because of side effects.〈section xml:id="abs1-4"〉〈title type="main"〉Conclusions.Dual-therapy omeprazole-amoxicillin for 2 weeks is associated with significantly lower eradication rate than is 1-week omeprazole-based triple therapies. Triple therapy is well-tolerated and produces side effects similar to those of dual therapy. The highest cure rate of H. pylori infection was achieved with triple therapy of omeprazole, amoxicillin, and clarithromycin for 1 week.

Notes: Helicobacter pylori eradication has become the recognized standard and widely adopted therapy to cure peptic ulcer disease. Other H. pylori associated conditions with potential benefit from eradication therapy are still subject to clinical investigations. The current state of evidence for these indications is summarized in this article.For NSAID associated peptic ulcer disease the current evidence needs to be grouped in three subsets of clinical conditions: a) H. pylori eradication for prevention of ulcers before starting NSAIDs therapy is advisable; b) eradication during PPI treatment for NSAID associated active ulcer shows no advantage on healing; and c) eradication alone is not sufficient for secondary prevention of ulcer complications induced by NSAID, however it appears to protect from further episodes of aspirin induced bleeding.In nonulcer dyspepsia the latest Cochrane collaboration review supports a small benefit in favour of H. pylori eradication.New insight in the relationship of H. pylori with GERD is provided from clinical trials which show that H. pylori eradication does not influence the clinical course of patients with reflux esophagitis.Finally important new data are presented regarding the management of dyspepsia at the primary care level with the confirmation that the H. pylori‘test and treat’ strategy in the appropriate setting is more cost-effective than endoscopy.

Notes: This paper reviews the new literature from the past year on the association between colonization with Helicobacter pylori and non-malignant disease of the upper gastrointestinal tract. This issue has, in the past year, remained a topic of wide research interest yielding many important new data. These data show that H. pylori eradication is the most effective therapy for peptic ulcer disease, but that a considerable proportion of ulcer patients remain to have dyspeptic symptoms. The discussion on the interaction between H. pylori and NSAID use in the etiology of ulcer disease has not yet been settled. Several studies, both from Asia and Europe, now reported that H. pylori eradication has a minimal effect on the primary prevention of ulcer disease in NSAID users, but eradication appears of relevance for the secondary prevention of ulcer disease in addition to proton pump inhibitor maintenance therapy. Various studies brought further support for the hypothesis that H. pylori eradication is of some benefit for patients with non-ulcer dyspepsia, although the effects are limited. The prevalence of H. pylori is lower among GERD patients than among controls, but H. pylori eradication has not been consistently shown to increase the risk for the newly development of GERD in an individual subject undergoing H. pylori eradication. The discussion on H. pylori and GERD should not preclude us from treating H. pylori-infected patients for accepted clinical indications. In patients using proton pump inhibitors for GERD, H. pylori eradication leads to a resolution of their corpus-predominant pangastritis, without impairing the efficacy of PPI therapy.

Notes: Eradication of Helicobacter pylori has lead to a significant decrease in the prevalence of peptic ulcer disease world-wide. Despite the fact that H. pylori eradication is the only way to cure peptic ulcer disease, a substantial number of patients still need antisecretory agents to be symptoms-free after eradication. During the past year several randomized controlled trials on H. pylori eradication in patients taking NSAIDs have been published but contradictory results have been obtained. In certain parts of the world, NSAIDs are becoming the main cause of peptic ulcer disease complications such as bleeding or perforation. Some patients with nonulcer dyspepsia do benefit from eradication of H. pylori as was shown in several studies. Long-term trials with cost/efficacy analysis are still needed to demonstrate the benefit of H. pylori eradication over acid inhibition in this group of patients. H. pylori prevalence is lower in patients with gastro-esophageal reflux disease, but according to recent systematic reviews it varies geographically. There are more data now to show that eradication of H. pylori in duodenal ulcer patients does not increase the incidence of GERD. The ‘test and treat’ strategy for patients with uninvestigated dyspepsia was strongly supported by both meta-analysis and the results of recent randomized controlled trials. Even in developed countries where the prevalence of H. pylori decreases, this strategy allows resolution of symptoms in a larger number of patients with dyspepsia compared to empirical treatment with proton pump inhibitors and reduces the endoscopic workload.