bluuebunny/crossref_metadata_2025_split huggingface dataset:
Variation in Serum Pepsinogens With Severity and Topography of Helicobacter pylori‐Associated Chronic Gastritis in Dyspeptic Patients Referred for Endoscopy
Authors: Bodger Keith , Wyatt Judy I. , Heatley Richard V. 
Published: March 2003

ABSTRACTBackground.It has long been recognised that specific patterns of gastritis are linked with different gastroduodenal diseases and that serum pepsinogens vary with the histological state of the gastric mucosa. With the discovery of the role of Helicobacter pylori in chronic gastritis and the availability of noninvasive tests for H. pylori infection, individuals with H. pylori gastritis can now be identified without endoscopic biopsy. However, without a knowledge of the pattern and severity of gastritis it is impossible to predict the likelihood of significant associated gastroduodenal pathology.Aims.The aim of this study was to evaluate the diagnostic potential of serum pepsinogens I and II in predicting the topography and severity of gastritis in H. pylori‐infected dyspeptic patients attending for endoscopy.Methods.Fasting serum was obtained from consecutive dyspeptic patients attending for endoscopy, and pairs of gastric biopsies obtained from the mid‐body and antrum. Gastritis was graded according to the Sydney System, and serum pepsinogen levels determined by radio‐immunoassay.Results.Sixty‐nine dyspeptic patients were studied (mean age: 49.6 years) of whom 34 had H. pylori‐associated chronic gastritis (Hp‐gastritis) – antral predominant gastritis (APG) in 41.2%, pangastritis (PAN) in 52.9%, and corpus predominant (CPG) in 5.9%. Serum pepsinogen II levels were significantly higher, and the serum pepsinogen I : II ratio significantly lower, in the H. pylori positive group than in other groups. Within the Hp‐gastritis group, there was a step‐wise decrease in serum pepsinogen I levels with progression from APG through PAN to CPG pattern (a cut‐off value of ≥ 100 ng/ml would have identified APG with a positive predictive value of 77%, though with low sensitivity). Within the Hp‐gastritis group, serum pepsinogen I and II levels were correlated with antral chronic inflammation score and serum pepsinogen II levels also with antral activity score. Serum pepsinogen I and the pepsinogen I : II ratio were lowest in severe gastric corpus atrophy.Conclusion.In dyspeptic patients known to be infected with H. pylori, serum pepsinogen values provide an assessment of the overall topography of gastritis, the severity of antral inflammation and the presence of severe corpus atrophy.
Treatment of Helicobacter pylori in Children With Recurrent Abdominal Pain
Authors: Wewer Vibeke , Andersen Leif P. , Pærregaard Anders , Gernow Anne , Hansen Jens P. H. , Matzen Peter , Krasilnikoff Peter A. 
Published: March 2003

ABSTRACTBackground.The role of Helicobacter pylori remains unclear in children with recurrent abdominal pain (RAP). In this study children with RAP were included in a double blind treatment study to elucidate whether symptoms disappear in children with a H. pylori infection and RAP, if the bacteria are eradicated.Methods.Thirty‐seven H. pylori‐infected children aged 4.9–14.5 years (median 9.8 years) with RAP were included. H. pylori was identified by histology and culture. The children were treated with amoxicillin and metronidazole for 14 days. A re‐endoscopy including biopsies for histology and culture was done at least one month after the end of treatment. Simple questions for symptoms were asked and blood for serology was repeated 3 and 6 months after the end of treatment. During the observation period the results of the re‐endoscopy and the serology 3 and 6 months after the re‐endoscopy were blinded for 23 patients and opened to 14 of the patients according to the choice of the families.Results.The eradication rates were 81% (30/37) in the total group and 74% (17/23) in the blinded group. The IgG antibodies to H. pylori decreased significantly 3 (p = .03) as well as 6 months after end of treatment (p < .001) in children with successful eradication. The number of children with RAP decreased after examination and treatment and the well‐being improved after 6 months in almost 95% of the children. However, no correlation was seen between eradication of H. pylori and disappearance of RAP, neither after 3 nor after 6 months’ observation in the total group of patients (p = .94 and p = .90) or in the blinded group (p = .42 and p = .65).Conclusions.These results do not provide evidence for a causal relationship between RAP and H. pylori.
T Cell‐Mediated Cytotoxicity via Fas/Fas Ligand Signaling in Helicobacter pylori‐Infected Gastric Corpus
Authors: Ishihara Shunji , Fukuda Ryo , Kawashima Kousaku , Moriyama Nobuyuki , Suetsugu Hiroshi , Ishimura Norihisa , Kazumori Hideaki , Kaji Takekazu , Sato Hiroshi , Okuyama Toshihiko , Rumi Karim M. A. , Adachi Kyoichi , Watanabe Makoto , Kinoshita Yoshikazu 
Published: March 2003

abstractBackground. Helicobacter pylori infection induces T helper‐1 immune responses in inflamed mucosa. However, the role of T cell‐mediated cytotoxicity in the induction of epithelial apoptosis is still unclear. The aim of this study was to investigate the involvement of the Fas/Fas ligand (Fas/Fas‐L) system in the H. pylori‐infected gastric corpus.Materials and Methods.Gastric fundic biopsy specimens were taken from patients with and without H. pylori infection. The expression of Fas and Fas‐L was examined by immunohistochemistry and RT‐PCR. Subsets of gastric infiltrating T cells in the biopsy specimens were studied by immunohistochemistry and flow cytometry. In histological sections, apoptosis was detected by the TUNEL method. We studied the in vitro expression of Fas‐L in peripheral T cells after stimulation with H. pylori antigen and interferon‐γ (IFN‐γ). The Fas‐mediated in vitro cytotoxicity of activated T cells was assessed by flow cytometry.Results.The numbers of CD4+ and CD8+ T cells were greater in H. pylori‐infected subjects. Fas expression was abundantly increased on fundic gland epithelium, and Fas‐L was detected on lamina propria mononuclear cells in H. pylori‐infected mucosa. TUNEL‐positive epithelial cells were also increased in H. pylori‐infected subjects. H. pylori antigen and IFN‐γ induced Fas‐L mRNA expression in both CD4+ and CD8+ T cells. In cytotoxic assay, activated T cells induced apoptosis in AGS cells, which could be significantly inhibited by neutralizing Fas‐L antibody.Conclusions.T cell‐mediated cytotoxicity via Fas/Fas‐L signaling may contribute to the induction of apoptosis in gastric epithelial cells during H. pylori infection.
Seroprevalence of Helicobacter pylori Infection in Siberia
Authors: Reshetnikov Oleg V. , Häivä Veli‐Mies , Granberg Christer , Kurilovich Svetlana A. , Babin Vladimir P. 
Published: March 2003

AbstractBackground.Despite many population‐based epidemiological studies of Helicobacter pylori prevalence in different parts of the world, Russia still represents a ‘blank spot’ in this map. The aims of the present study were to evaluate the seroprevalence of H. pylori infection among the population of Siberia and to assess whether there is an association between abdominal symptoms and H. pylori positivity in our population.Methods.Six hundred and forty‐nine adults from five regions of Siberia and the Far East, and 79 children and adolescents from Novosibirsk participated in the study. Antibodies against H. pylori (IgG) were detected in serum using ELISA.Results.The total percentage of infected adults varied from 70% to 92% depending on the region, and was somewhat lower in three populations living to the north of the 60th latitude compared with those under the 60th latitude. A lack of association was found between the presence of H. pylori and the gender, age and abdominal symptoms. Almost maximum prevalence of H. pylori infection occurred by 30 years of age with only a minor increase in older age groups. Half the children were infected with H. pylori by the age of 15.Conclusions. Helicobacter pylori infection is widespread among the Siberian populations with some trend in its prevalence to decrease northward. In Siberia age‐specific prevalence rates of H. pylori infection are similar to those usual for developing countries.
Antibacterial Activities of β‐Lactamase Inhibitors Associated with Morphological Changes of Cell Wall in Helicobacter pylori
Authors: Horii Toshinobu , Mase Kiyomi , Suzuki Yasuhiro , Kimura Taku , Ohta Michio , Maekawa Masato , Kanno Takashi , Kobayashi Miya 
Published: March 2003

ABSTRACTBackground. Recent study has demonstrated that β‐lactamase inhibitors including clavulanate, sulbactam and tazobactam have an vitro antibacterial effect on Helicobacter pylori. Here we describe the relationship between viability and cell profiles of H. pylori exposed to β‐lactamase inhibitors and some antibiotics in a short‐time course.Materials and methods. The antibacterial effects of β‐lactamase inhibitors including clavulanate, sulbactam and tazobactam on the bacterial viability of and morphological changes in H. pylori ATCC43504 were examined.Results. The β‐lactamase inhibitors such as clavulanate and sulbactam alone decreased the viable counts of H. pylori, depending on the antibiotic concentrations. Exposure to these β‐lactamase inhibitors resulted in morphological changes of cell shape, cell‐wall disintegration and cell lysis. Among these β‐lactamase inhibitors, clavulanate was the most active, causing a decrease in viable counts and morphological changes such as short filamentous to sphaeroplast formation and lysis. One × minimum inhibitory concentration (MIC) of amoxicillin plus 1 × MIC of clavulanate decreased viable counts effectively compared with 1 × MIC of amoxicillin or 1 × MIC of clavulanate alone, and induced morphological changes of cell shape and cell wall.Conclusion. Our results suggest that the β‐lactamase inhibitors alone have concentration‐dependent antibacterial activities against H. pylori and affect the morphology of the cell shape and the cell wall in vitro.
Helicobacter pylori does not Mediate the Formation of Carcinogenic N‐Nitrosamines
Authors: Vermeer I. T. M. , Gerrits M. M. , Moonen E. J. C. , Engels L. G. J. B. , Dallinga J. W. , Kleinjans J. C. S. , Van Maanen J. M. S. , Kuipers E. J. , Kusters J. G. 
Published: March 2003

AbstractBackground. Both N‐nitroso compounds and colonization with Helicobacter pylori represent known risk‐factors for the development of gastric cancer. Endogenous formation of N‐nitroso compounds is thought to occur predominantly in acidic environments such as the stomach. At neutral pH, bacteria can catalyze the formation of N‐nitroso compounds. Based on experiments with a noncarcinogenic N‐nitroso compound as end product, and using only a single H. pylori strain, it was recently reported that H. pylori only displays a low nitrosation capacity. As H. pylori is a highly diverse bacterial species, it is reasonable to question the generality of this finding. In this study, several genetically distinct H. pylori strains are tested for their capacity to form carcinogenic N‐nitrosamines.Materials and Methods. Bacteria were grown in the presence of 0–1000 µM morpholine and nitrite (in a 1 : 1 molar ratio), at pH 7, 5 and 3.Results. Incubation of Neisseria cinerea (positive control) with 500 µM morpholine and 500 µM nitrite, resulted in a significant increase in formation of N‐nitrosomorpholine, but there was no significant induction of N‐nitrosomorpholine formation by any of the H. pylori strains, at any of the three pH conditions.Conclusion. H. pylori does not induce formation of the carcinogenic N‐nitrosomorpholine in vitro. The previously reported weak nitrosation capacity of H. pylori is not sufficient to nitrosate the more difficultly nitrosatable morpholine. This probably also holds true for other secondary amines. These results imply that the increased incidence of gastric cancer formation that is associated with gastric colonization by H. pylori is unlikely to result from the direct induced formation of carcinogenic nitrosamines by H. pylori. However, this has to be further confirmed in in vivo studies.
Aberrant Expression of CDX2 in the Gastric Mucosa With and Without Intestinal Metaplasia: Effect of Eradication of Helicobacter pylori
Authors: Satoh Kiichi , Mutoh Hiroyuki , Eda Akashi , Yanaka Ichiro , Osawa Hiroyuki , Honda Sayaka , Kawata Hiroshi , Kihira Ken , Sugano Kentaro 
Published: March 2003

AbstractBackground. The intestine‐specific transcription factor CDX2 plays an important role in differentiation and maintenance of intestinal epithelial cells. Development and progression of intestinal metaplasia (IM) in the stomach is closely associated with Helicobacter pylori‐gastritis. We investigated expression of CDX2 protein in the gastric mucosa with and without IM before and after eradication of H. pylori.Materials and Methods. The subjects comprised five normal controls and 29 H. pylori‐positive patients (15 with antral IM and 14 without IM), who were followed for 12 months after eradication of H. pylori. Biopsies were taken from the greater curvatures of the antrum and middle body. Expression of CDX2 was evaluated immunohistochemically using anti‐CDX2 antibody.Results. CDX2 expression was not found in controls. Strong nuclear staining was observed extensively in IM, but rarely in the gastric epithelium, except for the focal area in only four antral biopsies (three with and one without IM). Fine granular cytoplasmic staining was also observed in the perinuclear regions of IM and the gastric epithelial cells in half of the patients. In 13 of the 15 patients with IM, IM did not regress after eradication of H. pylori, and the extent of nuclear staining in IM did not change. The extent of cytoplasmic staining did not change either.Conclusions. Our results indicate that CDX2 expression in the gastric mucosa is found in patients with chronic gastritis and is closely associated with IM. CDX2 expression in IM or the gastric epithelial cells did not disappear after eradication of H. pylori.
Seroreactivity to 19.5‐kDa Antigen in Combination with Absence of Seroreactivity to 35‐kDa Antigen is Associated with an Increased Risk of Gastric Adenocarcinoma
Authors: Chua Tju Siang , Fock Kwong Ming , Chan Yiong Huak , Dhamodaran Subbiah , Sim Chee Seng , Ng Tay Meng , Teo Eng Kiong 
Published: March 2003

AbstractBackground. Only a minority of those infected with Helicobacter pylori will develop gastric cancer. Stratification of H. pylori strains based on carcinogenic potential will provide a basis for selective surveillance and eradication therapy. We studied the anti‐H. pylori antibody profile in Asian patients with gastric adenocarcinoma to identify any H. pylori antigen that may be associated with an increased or decreased risk of gastric carcinoma.Patients and Methods. A case‐control study comparing the seroprevalence of antibodies with various H. pylori antigens in Singaporeans with gastric adenocarcinoma and the normal Singaporean population was carried out using both conventional immunoglobulin (Ig) G enzyme‐linked immunosorbent assay (ELISA) and Western blot immunoassay.Results. The seroprevalence among 44 gastric adenocarcinoma cases (70.5% males, mean age 66.7 ± 13.5 years) and 261 controls (49.8% males, mean age 61.5 ± 4.1 years) was 90.9% vs. 50.2% by IgG ELISA. In the H. pylori‐positive male population, those suffering from gastric adenocarcinoma had significantly lower seroreactivity to the 35‐kDa antigen compared with asymptomatic controls (p = .0198, OR = 3.79, 95% CI 1.24–11.61). Seropositivity to the 19.5 kDa antigen was also found to be associated with the presence of gastric adenocarcinoma in Singaporean males (p = .022, OR = 4.17, 95% CI 1.22–14.28). A ‘high‐risk’ phenotype consisting of absence of a band at 35‐kDa in combination with the presence of a band at 19.5‐kDa was significantly associated with the presence of gastric adenocarcinoma (p = .002, OR = 3.7, 95% CI 1.6–8.6).Conclusions. Stratification of H. pylori strains based on their potential for carcinogenesis, such as those strains that are seropositive for the 19.5 kDa antigen and seronegative for the 35‐kDa antigen, may provide a basis for selective eradication of H. pylori infection and future vaccine development.
Relationship Between Gastric Ulcer and Helicobacter pylori VacA Detected in Gastric Juice Using Bead‐ELISA Method
Authors: Shirasaka Daisuke , Aoyama Nobuo , Sakashita Masanori , Kuroda Kohei , Maekawa Shuji , Wambura Casmir Marwa , Miyamoto Masaki , Tamura Takao , Yahiro Kinnosuke , Wada Akihiro , Kurazono Hisao , Hirayama Toshiya , Kasuga Masato 
Published: March 2003

AbstractBackground. VacA is an important pathogenetic factor produced by Helicobacter pylori. VacA has often been detected in supernatants of liquid cultures or lysates of whole bacterial cells. However, no studies have ever tried to assay VacA produced in the human stomach. We applied a very sensitive and simple method, bead‐ELISA, to detect VacA in gastric juice.Materials and Methods. Forty‐eight H. pylori‐positive patients (16 nonulcer dyspepsia, 16 gastric ulcer, and 16 duodenal ulcer) and four H. pylori‐negative nonulcer dyspepsia patients had endoscopy performed and gastric juice were aspirated. Polystyrene beads coated with the antibody to VacA, were used in this bead‐ELISA method. The nucleotide sequences of vacA in the signal and middle regions were investigated.Results. Of the 48 samples that were positive for H. pylori, 21 [43.8%] were found to be VacA positive in gastric juice. The average and maximum concentrations of detected VacA in gastric juice were 143.2 ± 216.5 and 840 pg/ml, respectively. The average density of VacA from gastric ulcer patients (227.5 ± 276.7 pg/ml) was higher than that found in nonulcer dyspepsia (51.8 ± 39.8 pg/ml) and duodenal ulcer (49.2 ± 21.5 pg/ml) patients. There was no relationship between VacA in gastric juice and vacA genotype.Conclusions. VacA in gastric juice could be directly detected by bead‐ELISA. In this study, the diversity of disease outcome was associated with not the quality but the quantity of VacA. Therefore, not only the quality but also the quantity of VacA is important etiological factors in the pathogenesis of mucosal damage.
Intrafamilial Spread of Helicobacter pylori: A Genetic Analysis
Authors: Roma‐Giannikou Eleftheria , Karameris Andreas , Balatsos Basilios , Panayiotou Joanna , Manika Zisoula , Van‐Vliet Catherina , Rokkas Theodore , Skandalis Nikolaos , Kattamis Christos 
Published: March 2003

ABSTRACTBackground. A high incidence of Helicobacter pylori among family members of children with H. pylori gastritis has previously been documented on biopsy material. The main objective of this study was the genetic clarification of H. pylori strains involved in intrafamilial dispersion.Materials and Methods. Formalin‐fixed, paraffin‐embedded material of antral mucosa from 32 members of 11 families was studied for the presence of genetic homogeneity. To achieve this goal, the entire genome of H. pylori was studied by the polymerase chain reaction (PCR)‐based random amplified polymorphic DNA (RAPD) fingerprinting method. Furthermore, the Urease A gene was analyzed using a multiplex PCR‐assay and an alternative mutation detection method based on the Hydrolink™ analysis.Results. RAPD fingerprinting confirmed that closely related H. pylori strains were involved in the intrafamilial dispersion. Mutations and small deletions in Urease A gene were found in 22 out of 32 individuals.Conclusions. The homology of the H. pylori genome in members of the same family strongly supports the hypothesis of transmission of H. pylori from person‐to‐person or from a common source.
Extragastric Helicobacter species
Authors: On Stephen L.W. , Hynes Sean , Wadström Torkel 
Published: March 2003

AbstractThe genus Helicobacter has expanded at a rapid pace and no fewer than 31 species have been named since the proposal of the genus in 1989. Of these 31 species, 22 are principally associated with extragastric niches and there is increasing interest in the role of these taxa in diseases of humans and animals. Substantial evidence attests to certain species playing a role in the pathogenesis of enteric, hepatic and biliary disorders and some taxa demonstrate zoonotic potential. The importance of extragastric Helicobacters is likely to be an important topic for research in the near future. Here, important papers published in the field this last year are reviewed.
Improving the Pain Management Standard of Care in a Community Hospital
Authors: Bell Anita , Wheeler Richard 
Published: March 2003

purpose: The purpose of this article is to outline the development, implementation, and progress of one community hospital in improving the pain management standards of care and to describe why collaboration within the community and with a nationally recognized research facility, such as the City of Hope in California, is beneficial for the educational needs of a community‐based hospital and for a framework‐improvement model of pain management.overview: Most patients with cancer receive care in community facilities. It is essential that optimal pain relief be provided to these patients. A model used by Mercy Health Center in Oklahoma demonstrates how community facilities can tap into national resources. The adaptation of research and educational information that was made available by the City of Hope National Medical Center has allowed multiple strategies to be implemented to target pain management education and clinical practice effectively to meet the American Pain Society quality improvement standards. Ongoing data collection and monitoring of pain management outcomes can provide direction and support for improved pain management patient satisfaction and other pain management outcomes. With continuous quality improvement monitoring, education, and administrative support, a pain management patient “safety net” can been developed to improve the standard of care for all patients within the organization.clinical implications: Effective pain management according to accepted national clinical standards can be implemented and improved on by adapting national resources to guide multidisciplinary strategic planning.