bluuebunny/crossref_metadata_2025_split huggingface dataset:
Combined Activity of Azithromycin and Lansoprazole Against Helicobacter pylori
Authors: Trautmann Matthias , Riediger Christine , Möricke Angelika , Vogt Konstanze , Bohr Ulrich , Glasbrenner Bernhard 
Published: March 2003

Background. Due to its unique pharmacokinetic properties, azithromycin may be an attractive combination partner for H. pylori eradication regimens. However, up to 15% of clinical isolates are primarily resistant to azithromycin as well as to other macrolide antibiotics. Combination therapy with lansoprazole, a proton pump inhibitor known to have intrinsic antibacterial activity against H. pylori, may be useful to counteract such resistance. We therefore evaluated the combined effects of azithromycin and lansoprazole in vitro.Materials and Methods. Minimal inhibitory concentrations (MICs) of azithromycin and lansoprazole alone and in combination were determined for 106 clinical H. pylori isolates by means of an agar dilution technique. Killing kinetics of seven isolates were also studied in fluid medium.Results. MIC values for 50 and 90% of the isolates (MIC50, MIC90) were 0.19 and 0.5 mg/l for azithromycin, and 44.5 and 104 mg/l for lansoprazole. Nine strains (8.5%) had an MIC of azithromycin ≥ 16 mg/l and were regarded as resistant. An additive interaction between the two drugs was found in 72 (68%), and indifferent effects in 24 strains (23%). Three of 9 azithromycin‐resistant strains regained sensitivity in the presence of lansoprazole. In fluid culture, synergism between the two drugs occurred in 6 out of 7 strains tested.Conclusion. In the majority of strains, lansoprazole and azithromycin interacted in an additive or synergistic manner depending on the test method employed. Addition of lansoprazole restored in vitro sensitivity to azithromycin in 3 out of 9 azithromycin‐resistant strains. Such effects may enhance the elimination of H. pylori during clinical eradication therapy.
Randomized Placebo‐Controlled Trial of Helicobacter pylori Eradication for Iron‐Deficiency Anemia in Preadolescent Children and Adolescents
Authors: Choe Yon Ho , Kim Soon Ki , Son Byong Kwan , Lee Don Haeng , Hong Yun Chul , Pai Soo Hwan 
Published: March 2003

Background. A few cases relating H. pylori infection to iron‐deficiency anemia have been described recently. We investigated the role of H. pylori infection in iron‐deficiency anemia in preadolescent children and adolescents.Patients and Methods. We conducted a double‐blind, placebo‐controlled therapeutic trial in 43 subjects (mean age, 15.4 years) with iron‐deficiency anemia. Endoscopy was performed, and biopsy specimens were examined by urease test and histological analysis. Twenty‐two of 25 H. pylori–positive patients were assigned randomly to three groups. Group A patients were given oral ferrous sulfate and a 2‐week course of bismuth subcitrate, amoxicillin, and metronidazole. Group B patients were given placebo for iron and a 2‐week course of triple therapy. Group C patients were given oral ferrous sulfate and a 2‐week course of placebo. Iron status was reassessed 4 weeks and 8 weeks after the 2‐week regimen ended.Results. Of the 43 subjects with iron‐deficiency anemia, 25 (58.1%) had H. pylori in the antrum. Group A and B subjects, who received eradication therapy, showed a significant increase in hemoglobin level as compared with group C subjects at 8 weeks after therapy (p = .0086).Conclusions. Treatment of H. pylori infection was associated with more rapid response to oral iron therapy as compared with the use of iron therapy alone. Such treatment also led to enhanced iron absorption even in those subjects who did not receive oral iron therapy.
Prevalence of CagA, VacA Antibodies in Symptomatic and Asymptomatic Children with Helicobacter pylori Infection
Authors: Elitsur Yoram , Neace Cheryl , Werthammer Matthew C. , Triest William E. 
Published: March 2003

Background. Limited data are available on the prevalence of CagA and VacA Helicobacter pylori antibodies in children. The aim of this study was to investigate the antibody prevalence to the H. pylori virulence factors CagA and VacA in symptomatic and asymptomatic children with H. pylori infection and to correlate these antibodies with the severity of gastric inflammation or density of H. pylori organisms in the gastric mucosa.Materials and Methods. Twenty‐three symptomatic children and 132 asymptomatic children with positive H. pylori serology participated in this study. Anti–H. pylori IgG antibody and CagA or VacA H. pylori antibodies were measured by enzyme immunoassay (HM‐CAP; sensitivity and specificity> 90%) and Western immunoblot (Helicoblot 2.0) methods, respectively. Gastric inflammation and H. pylori density were graded histologically using the revised Sydney criteria.Results. The prevalence of CagA and VacA antibodies were 69% and 35% in symptomatic children and 54% and 52% in asymptomatic children, respectively. Multiple regression analysis showed a correlation between CagA antibody and the severity of gastritis but no correlation with other histological features, including the number of neutrophils or lymphoid follicles. Neither antibody correlated with the degree of bacterial density in the gastric mucosa.Conclusion. CagA and VacA H. pylori antibodies are common in the pediatric population. The combined CagA/VacA antibodies correlated weakly with the degree of mucosal inflammation.
Pretreatment Antimicrobial Susceptibilities of Paired Gastric Helicobacter pylori Isolates: Antrum Versus Corpus
Authors: Ikezawa Kazuto , Kashimura Hiromasa , Kojima Maki , Aikawa Tatsuya , Nakahara Akira , Mutoh Hiroshi , Tanaka Naomi 
Published: March 2003

Background. Antimicrobial susceptibility testing of Helicobacter pylori isolates is the most useful tool for guiding specific therapy, especially when primary resistance is suspected. However, the most informative gastric biopsy site for detection of resistant H. pylori isolates is uncertain. We sought to determine whether susceptibilities to commonly used antimicrobials (amoxicillin, clarithromycin, minocycline, and metronidazole) were related to biopsy site.Methods. H. pylori isolates were obtained from patients who had duodenal ulcer and had not received any therapy directed against H. pylori. Agar‐dilution minimum inhibitory concentrations of each antimicrobial were compared between paired H. pylori isolates from the antrum and the proximal corpus.Results. Differences in minimum inhibitory concentrations exceeding twofold were observed within the pairs of H. pylori isolates in 5 of the 40 patients tested. In three patients with clarithromycin‐resistant isolates and two with metronidazole‐resistant isolates, both antral and corporeal specimens revealed resistance. However, no patient had pairs of isolates categorized as resistant at one site and sensitive at the other.Conclusions. While we found that an individual may have a mixed H. pylori infection with respect to differing antimicrobial susceptibility in different parts of the stomach, a single biopsy specimen from either the antrum or the corpus should provide reliable detection of H. pylori isolates with primary resistance.
Comparative Treatment of Helicobacter pylori–Positive Duodenal Ulcer Using Pantoprazole at Low and High Doses Versus Omeprazole in Triple Therapy
Authors: Catalano Filippo , Branciforte Giuseppe , Catanzaro Roberto , Bentivegna Carmelo , Cipolla Rosanna , Nuciforo Giuseppe , Brogna Alfio 
Published: March 2003

Background. Helicobacter pylori eradication has become the standard treatment for peptic ulcer disease. H. pylori–eradicating triple therapy with omeprazole plus two antibiotics has been used until recently; however, the efficacy of pantoprazole and antibiotics for H. pylori eradication has not been researched thoroughly until now. The aim of this randomized clinical trial was to verify the efficacy of triple oral therapy comparing the effects of pantoprazole using two different doses versus omeprazole twice daily in H. pylori eradication, in ulcer healing and relapses, and in gastritis improvement.Materials and Methods. We enrolled 243 patients with H. pylori–positive duodenal ulcer and randomized them into three treatment groups: 84 patients (group Ome40) were assigned to receive omeprazole, 20 mg twice daily, plus amoxicillin, 1 gm twice daily, and clarithromycin, 500 mg twice daily for 10 days; 79 patients (group Pan40) were treated with pantoprazole, 40 mg daily, plus amoxicillin and clarithromycin at the same doses as those of group Ome40; and 80 patients (group Pan80) were treated with pantoprazole, 40 mg twice daily, plus amoxicillin and clarithromycin at the same doses as those of group Ome40.Results. Ulcer healing was observed in 81 of 84 patients (96.4%) in group Ome40; in 66 of 79 patients (83.5%) in group Pan40; and in 77 of 80 patients (96.2%) in group Pan80. H. pylori was eradicated in 79 of 84 patients (94%) in group Ome40; in 63 of 79 patients (79.7%) in group Pan40; and in 75 of 80 patients (93.7%) in group Pan80.Conclusions. We found that 10‐day triple therapy with amoxicillin, clarithromycin, and either pantoprazole, 80 mg daily, or omeprazole, 40 mg daily, is highly effective in ulcer healing and is very well tolerated, achieving the 90% cure recommended for an ideal first‐line anti–H. pylori positive duodenal ulcer treatment regimen.
13C‐Urea Breath Test and Gastric Mucosal Colonization by Helicobacter pylori in Children: Quantitative Relation and Usefulness for Diagnosis of Infection
Authors: Vincent Pascal , Michaud Laurent , De Lasalle Elisabeth Martin , Benon Benoît , Turck Dominique , Gottrand Frédéric 
Published: March 2003

Objective. Because in children Helicobacter pylori colonization could differ as compared to that in adults, gastric metabolism of urea and the reliability of the breath test must be evaluated. The aim of this study was to quantify the relationship between breath test and colonization.Methodology. We studied data from 50 endoscopies performed in 39 children and adolescents (20 girls, 19 boys, aged 3–18 years); 28 were infected with H. pylori. Biopsies were analyzed for histological and microbiological diagnosis of infection and for quantitative antral culture of H. pylori. A 13C urea breath test was performed on the same day as that of endoscopy (
n = 33) or delayed between 2 and 90 days (
n = 17).Results. Using a cut‐off value of 3 δ‰, sensitivity was 96.5%, and specificity was 91.5%. The three children showing discrepancies between breath test and biopsy results had a δ‰ value close to the cut‐off. For the 26 cases with a positive culture, we noted a significant correlation (r = 0.63; p < .001) that was not affected by the delay between breath test and gastroscopy.Conclusion. This quantitative relation between bacterial density and δ‰ permits increasing the reliability of the test by interpreting carefully those results that approach the cut‐off value.
Factors Affecting the Validity of the 13C‐Urea Breath Test for In Vivo Determination of Helicobacter pylori Infection Status in a Mouse Model
Authors: Hammond Paul D. , Stutzenberger Fred J. , Butler Ross N. , Read Leanna C. , Davidson Geoffrey P. 
Published: March 2003

Background. The mouse model using a human isolate of Helicobacter pylori is being widely accepted as an economical means of studying gastric infection. A noninvasive monitoring method would be useful for repeated testing to establish the time course of infection and the efficacy of treatments. In this study, we describe factors that affect interpretation of 13C urea breath test results for the assessment of H. pylori infection status in this model.Materials and Methods. Female C57Bl/6 mice that underwent gavage with H. pylori or saline were breath‐tested using 50 μg of 13C urea at intervals up to 2 months after inoculation. The generation of 13CO2 (excess δ13CO2) by infected mice was compared to that of uninfected controls. The effects of diet, fasting, and coprophagy on the reliability of the 13C urea breath test were quantitated.Results. Both commercial and synthetic mouse diets exhibited marked in vitro urease activity. A minimum fasting time of 13 hours prior to breath testing significantly reduced this dietary contribution to excess δ13CO2 values. The coprophagic tendency of the mice caused spuriously high excess δ13CO2 counts in the breath of both control and H. pylori–infected mice.Conclusions. Although the dietary contribution to spuriously high values of excess δ13CO2 in mice breath‐tested for H. pylori infection was reduced by fasting, the high nonspecific urease activity generated by coprophagy severely limited the reliability of the urea breath test in the assessment of H. pylori infection status.
Duodenal Ulcer Relapse Is Not Always Associated with Recurrence of H. pylori Infection: A Prospective Three‐Year Follow‐Up Study
Authors: Martino Gina , Paoletti Marco , Marcheggiano Adriana , D'ambra Giancarlo , Fave Gianfranco Delle , Annibale Bruno 
Published: March 2003

Background. 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.Methods. 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.Results. 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.Conclusions. 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.
Colonization and Tissue Tropism of Helicobacter pylori and a Novel Urease‐Negative Helicobacter Species in ICR Mice Are Independent of Route of Exposure
Authors: McCathey Sonya N. , Shomer Nirah H. , Schrenzel Mark D. , Whary Mark T. , Taylor Nancy S. , Fox James G. 
Published: March 2003

Background. In humans, Helicobacter pylori is known to colonize the stomach and to induce persistent gastritis; selected reports also suggest it causes extragastric disease, including hepatitis. H. pylori and a novel urease‐negative Helicobacter sp. induce gastritis and typhlocolitis, respectively, when inoculated orally into mice. Experimental typhlocolitis and hepatitis have been caused by intraperitoneal (IP) injection of H. hepaticus, H. bilis, and the novel Helicobacter spp. However, the route by which IP‐inoculated organisms localize to specific areas of the gastrointestinal system is unknown.Materials and Methods. To determine whether Helicobacter spp. can be isolated from blood, can preferentially colonize specific tissues, and can cause pathological changes, we inoculated 6‐week‐old outbred mice orally or intraperitoneally with H. pylori or a novel Helicobacter sp.Results. When these mice were inoculated by the IP route, H. pylori was cultured from lungs, spleen, liver, cecum, and stomach on day 1 after inoculation, from liver and stomach mucosa on day 3 after inoculation, and from the stomach on day 30 after inoculation, suggesting preferential colonization of the stomach. After inoculation by the IP route, the novel intestinal Helicobacter sp. was cultured from the blood, lungs, spleen, liver, kidneys, cecum, and feces but not from stomach mucosa on day 1 after inoculation. By day 30 after inoculation, the novel Helicobacter sp. was cultured from cecum and feces only, suggesting that it had preferentially colonized the lower bowel. By the IP route, the novel Helicobacter sp. induced hepatitis that persisted for 30 days after inoculation. Though mice inoculated intraperitoneally with H. pylori developed an acute hepatitis, the liver lesion began to resolve 30 days after inoculation. Mice inoculated orally with either H. pylori or the novel Helicobacter sp. did not have hepatitis on day 30 after inoculation but developed 100% colonization of stomach and cecum, respectively.Conclusion. The isolation of H. pylori and the novel Helicobacter sp. from multiple tissues infers that a transient helicobacter bacteremia occurs when Helicobacter spp. are injected intraperitoneally, but organisms are cleared rapidly from nontarget tissues and preferentially colonize specific regions of the gastrointestinal tract.
Eradication ofH. pyloriwith Pantoprazole, Clarithromycin, and Metronidazole in Duodenal Ulcer Patients: A Head‐to‐Head Comparison Between Two Regimens of Different Duration
Authors: Dammann Hans‐Gerd , Fölsch Ulrich R. , Hahn Eckhart G. , Von Kleist Detlef‐Hasso , Klör Hans‐Ulrich , Kirchner Thomas , Strobel Sonja , Kist Manfred 
Published: March 2003

Background.The study was conducted to compare the efficacy and tolerability of two pantoprazole‐based triple therapies of different length in the eradication ofH. pylori.Methods.In this double‐blind, multicenter parallel group comparison,H. pylori‐positive patients were randomly assigned to either the PCM‐7 group (7 days of pantoprazole 40 mg bid, clarithromycin 500 mg bid, metronidazole 500 mg bid) or the PCM‐14 m group (modified 14 day therapy of the same regimen with metronidazole only given for 10 days due to labeling reasons).H. pyloristatus was determined by urease test, histology, culture, and13C‐urea breath test. Treatment outcome was assessed 6 weeks after intake of the last study medication.Results.The following eradication rates were achieved: for PCM‐7 in the MITT population 83% (89/107), in the PP population 84% (81/97); for PCM‐14 m in MITT 87% (92/106), in PP 88% (91/104). Ulcer healing rates were: for PCM‐7 in MITT population 99% (106/107), in the PP population 99% (96/97); for PCM‐14 m in MITT 99% (105/106), in PP 99% (103/104). Gastrointestinal symptoms and gastritis scores decreased in both treatment groups. Equivalence of treatment regimens could be proven for all populations. In total, 64 patients reported adverse events. Five serious adverse events occurred, all unrelated to the study medication.Conclusion.The two pantoprazole‐based triple therapies tested in this study are equally effective inH. pylorieradication, ulcer healing and relief from ulcer pain. It is concluded that 7 days of triple therapy are generally sufficient.
Analysis of iceA1 transcription in Helicobacter pylori
Authors: Donahue John P. , Peek Richard M. , Van Doorn Leen‐Jan , Thompson Stuart A. , Xu Qing , Blaser Martin J. , Miller Geraldine G. 
Published: March 2003

Background. Transcription of the Helicobacter pylori iceA1 gene is induced following adherence of the bacterium to gastric epithelial cells in vitro, suggesting that this gene might be involved in H. pylori pathogenesis. Consequently, the current studies were undertaken to characterize iceA1 transcription and to define the structure of iceA1‐containing transcripts to evaluate the potential of this gene to encode functional proteins.Materials and Methods. Northern blots and primer extension of RNA isolated from broth‐grown cultures of various H. pylori strains was done to analyze iceA1‐specific gene transcription. Reverse transcriptase (RT)‐PCR was used to determine the levels of iceA1 transcripts derived from readthrough transcription that was initiated upstream of iceA1 within the 5′‐flanking cysE gene.Results. Three major transcripts were detected and each was initiated from a common promoter, designated PI. Two of these transcripts were comprised of iceA1 sequence, while a third transcript was dicistronic and included the downstream gene, hpyIM. In addition, 10‐fold lower levels of iceA1 transcripts were initiated upstream of PI, either within or immediately downstream of cysE.Conclusions. The present analysis suggests that iceA1 does not encode a functional protein in the majority of H. pylori strains. However, transcription of hpyIM, which encodes a highly conserved DNA adenine methyltransferase, is linked to iceA1 transcription. Therefore, iceA1 may affect H. pylori virulence in vivo through transcriptional regulation of hpyIM expression levels, which may result in specific variations in DNA methylation patterns leading to alteration in the expression of genes involved in virulence or pathogenesis.
The Pathological Examinations of Gastric Mucosa in Patients with Helicobacter pylori–Positive and –Negative Pernicious Anemia
Authors: Sari Ramazan , Ozen Suleyman , Aydogdu Ismet , Yildirim Bulent , Sevinc Alper 
Published: March 2003

Background. The basic histopathological finding in gastric mucosa is chronic atrophic gastritis in patients with pernicious anemia.Materials and Methods. We evaluated the frequency of Helicobacter pylori and pathological examinations of gastric mucosa in pernicious anemia (n = 30) by endoscopical findings and biopsy. The results were compared with gastric mucosa specimens of patients with H. pylori–positive nonulcer dyspepsia (n = 36) and H. pylori–negative nonulcer dyspepsia (n = 21).Results. H. pylori was diagnosed in 12 patients (40%) with pernicious anemia. Fundal biopsy examinations showed atrophic gastritis in 30 patients (100%), intestinal metaplasia in 13 patients (43.3%), lymphoid follicle in 15 patients (50%), and dysplasia in 6 patients (20%). Antral biopsy examinations showed atrophic gastritis in 8 patients (26.6%), intestinal metaplasia in 8 patients (26.6%), lymphoid follicle in 8 patients (26.6%), and dysplasia in 3 patients (10%). The frequency of fundal inflammation, atrophy, intestinal metaplasia, lymphoid follicle, and dysplasia and antral intestinal metaplasia and mild antral dysplasia were found to be higher in those in the pernicious anemia group than in the nonulcer dyspeptic patients. Antral inflammation, atrophy, and moderate and severe antral dysplasia were found to be higher in those in the nonulcer dyspeptic group.Conclusions. Particularly, fundal precancerous lesions were found to be more frequent in patients with pernicious anemia independent of H. pylori.