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1. |
Helicobacter: A New Scientific Journal |
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Helicobacter,
Volume 1,
Issue 1,
1996,
Page 1-3
David Y. Graham,
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ISSN:1083-4389
DOI:10.1111/j.1523-5378.1996.tb00001.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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2. |
Reflections on the First Description of the Presence of Helicobacter Species in the Stomach of Mammals |
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Helicobacter,
Volume 1,
Issue 1,
1996,
Page 4-5
Natale Figura,
Giuseppina Oderda,
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ISSN:1083-4389
DOI:10.1111/j.1523-5378.1996.tb00002.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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3. |
Treatment of Helicobacter pylori Infection: A Review of the World Literature |
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Helicobacter,
Volume 1,
Issue 1,
1996,
Page 6-19
René W.M. Der Hulst,
Josbert J. Keller,
Erik A.J. Rauws,
Guido N.J. Tytgat,
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摘要:
ABSTRACTBackground.None of the currently used anti‐Helicobacter pyloridrug regimens cures the infection 100%, and cure results still vary considerably. The present article reviews the effectiveness of currently used antimicrobial regimens, aimed to cureH. pyloriinfection.Methods.Data collection started from the beginning of the anti‐H. pylori‐therapy era until May 1995. No attempt at formal metanalysis has been made, because many studies have been published only in abstract form. Attempts were made to exclude duplicates of studies by comparison to previously reported ones; the authors of suspected duplicates were contacted. After amalgamation of the number of included patients and the number of successfully treated patients, the mean values of eradication rates and the 95% confidence intervals were calculated.Results.A total of 237 treatment arms were analyzed. Bismuth triple therapy continues to reach high eradication rates worldwide (78–89%). Side effects leading to diminished patient compliance and the marked decline of eradication efficacy in cases of metronidazole resistance are considered to be the major drawbacks of this therapy. Proton pump inhibitor (PPI) dual therapy is better tolerated with fewer side effects than is bismuth triple therapy. The mean eradication rates vary from 55 to 75%, and the extremes lie between 24 and 93%. PPI triple therapies have been shown to be very effective againstH. pylori(eradication rates, 80–89%). Quadruple therapy leads to a mean eradication rate of 96%.Conclusion.Based on efficacy, PPI triple or bismuth triple therapy are recommended as first‐line treatment forH. pyloriinfection. Quadruple therapy could serve as second‐line treatment for eradication of initial failures and in case of metronidazo
ISSN:1083-4389
DOI:10.1111/j.1523-5378.1996.tb00003.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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4. |
Immune Evasion by Helicobacter pylori: Gastric Spiral Bacteria Lack Surface Immunoglobulin Deposition and Reactivity with Homologous Antibodies |
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Helicobacter,
Volume 1,
Issue 1,
1996,
Page 20-27
Peter E. Darwin,
Marcelo B. Sztein,
Qiao‐Xi Zheng,
Stephen P. James,
George T. Fantry,
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摘要:
ABSTRACTBackground.Helicobacter pyloriinfection persists in the presence of potent serum and gastric mucosal anti‐body responses against bacterial antigens. The aim of this article is to report on a study determine whether there is antibody deposition onH. pyloriin vivo in the stomach of infected patients and whether gastric and cultured forms ofH. pyloridiffer in their antibody reactivity.Materials and Methods.Serum, gastric biopsies, and antral brushings were obtained from 10 patients having endoscopy.H. pyloriwas cultured from gastric biopsies. Bacterial samples were stained directly for immunoglobulin deposition and indirectly using rabbit antiurease serum or patient serum. Samples were examined by immunofluorescence microscopy and flow cytometry.Results.Although spiral bacteria could be identified easily by acridine orange staining and antiurease staining of gastric brushings fromH. pyloriinfected patients, gastric bacteria did not have detectable IgG or IgA present, and only one of five samples could be stained for IgG and IgA indirectly using patient serum. In contrast, cultured bacteria could be stained readily with homologous serum for IgG and IgA in the majority of cases. Low pH inhibited immunoglobulin reactivity with culturedH. pylori.Conclusions.GastricH. pylorimay evade humoral defense owing to poor deposition of immunoglobulin in the gastric environment or failure to express surface antigens that are present on cultured forms ofH. pylor
ISSN:1083-4389
DOI:10.1111/j.1523-5378.1996.tb00004.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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5. |
Susceptibility of Helicobacter pylori to the Bactericidal Activity of Human Serum |
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Helicobacter,
Volume 1,
Issue 1,
1996,
Page 28-33
Gerardo Gonzalez‐Valencia,
Guillermo I. Perez‐Perez,
Ronald G. Washburn,
Martin J. Blaser,
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摘要:
ABSTRACTBackground.Human serum represents an important barrier to the entry of most mucosal organisms into tissues and to the systemic circulation. If at all present,Helicobacter pyloriwithin gastric tissue is rare, and bacteremia for this organism has been described only once.Methods.To assess the susceptibility ofH. pylorito the bactericidal activity present in normal human serum (NHS), we examined 13H. pyloriisolates. To assess the contributions of the classical and alternative complement pathways to killing, we added either C2‐deficient or factor B‐deficient serum, respectively, to heat‐inactivated NHS. Also we assessed the ability of the strains to bind125I‐C3.Results.After incubation for 60 minutes at 37°C, all 13H. pyloristrains were killed by NHS; heating to 56°C for 30 minutes ablated killing, indicating complement dependence for this phenomenon. In the absence of an antibody source, there was no killing when either an alternative or classical complement pathway source was used. Adding B‐deficient serum to heat‐inactivated normal human serum did not restore killing, but adding C2‐deficient serum permitted partial killing. All of the 13 strains bound125I‐C3. Although the kinetics varied from strain to strain, C3 bound was significantly correlated (r= 0.61,p= 0.03) with serum susceptibility.Conclusions.H. pyloriare susceptible to complement, alternative pathway activation appears critical, and C3 binding is a major loc
ISSN:1083-4389
DOI:10.1111/j.1523-5378.1996.tb00005.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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6. |
Natural and Experimental Helicobacter mustelae Reinfection Following Successful Antimicrobial Eradication in Ferrets |
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Helicobacter,
Volume 1,
Issue 1,
1996,
Page 34-42
Margaret Batchelder,
James G. Fox,
Alison Hayward,
Lili Yan,
Ben Shames,
James C. Murphy,
Lori Palley,
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摘要:
ABSTRACTBackground.Recrudescence or reinfection may occur after eradication ofHelicobacter pyloriin humans.Materials and Methods.We used the ferretHelicobacter mustelaemodel to investigate the effect of prior infection and eradication on reinfection by experimental and natural routes. Two groups of ferrets with naturally acquiredH. mustelaeinfection were treated with an eradication protocol using amoxicillin, metronidazole, and bismuth subsalicylate. The ferrets were monitored for recrudescence by repeated cultures of endoscopic gastric mucosal biopsies. The ferrets were challenged at 17 months (group I) and 6 months (group II) after eradication with a strain ofH. mustelaehaving a distinctive restriction endonuclease analysis pattern. The eradication protocol was repeated to eliminate the infection produced by experimental challenge. The ferrets were then cohoused intermittently with naturally infected ferrets.Results.The originalH. mustelaeinfection was successfully eliminated by the eradication protocol. No recrudescence was observed in group I for 12 months nor for 3 months in group II after eradication. All ferrets became persistently reinfected with the challenge strain. The infection from the challenge strain was eradicated successfully. No ferrets in group I and all ferrets in group II became infected through cohousing.Conclusions.These results suggest that though prior infection withH. mustelaemay confer some protection against reinfection, such protection is not universal in all circumstances; that susceptibility to reinfection by contact with infected animals varies between individuals; and that age may be a factor in this individual variability. These results are applicable to studies of reinfection after eradication ofH. pyloriin humans.
ISSN:1083-4389
DOI:10.1111/j.1523-5378.1996.tb00006.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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7. |
Characterization and Therapy for Experimental Infection by Helicobacter mustelae in Ferrets |
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Helicobacter,
Volume 1,
Issue 1,
1996,
Page 43-51
Steven J. Czinn,
John C. Bierman,
Richard W. Diters,
Thomas G. Blanchard,
Robert D. Leunk,
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摘要:
ABSTRACTBackground.Numerous clinical trials evaluating the efficacy of various antimicrobial compounds againstHelicobacter pyloriinfection have been performed in humans. A convenient animal model forHelicobacterinfection would facilitate the evaluation of novel therapies. These experiments were performed to evaluate the use of ferrets as a model ofHelicobacterinfection.Materials and Methods.Ferrets were infected experimentally withHelicobacter mustelaeand subsequently treated with bismuth subsalicylate (BSS) triple therapy (BSS, metronidazole, and amoxicillin), or left untreated. The status of infection and serology was assessed during treatment and for 8 weeks posttreatment. Seven ferrets successfully treated with triple therapy were challenged withH. mustelaeand monitored for infection for an additional 5 weeks.Results.Infection of ferrets byH. mustelaewas accompanied by gastritis and a specific antibody response. Treatment ofH. mustelae‐infected ferrets with BSS suppressed bacterial growth in four of nine animals but did not eradicate infection. Triple therapy eradicated infection in all nine ferrets with a reduction in gastric inflammation. No relapse of infection occurred up to 8 weeks posttherapy. Challenge withH. mustelaeof ferrets successfully treated with triple therapy resulted in a 100% rate of reinfection.Conclusions.H. mustelaeinfection can be eliminated by triple therapy, but this does not result in protective immunity against reinfection byH. mustelae.This model, using a strain ofHelicobacterindigenous to the host, may be useful for assessing therapeutic efficacy of novel therapies for the treatment of human infection byH. pylor
ISSN:1083-4389
DOI:10.1111/j.1523-5378.1996.tb00007.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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8. |
Atrophic Changes of Gastric Mucosa Are Caused by Helicobacter pylori Infection Rather Than Aging: Studies in Asymptomatic Japanese Adults |
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Helicobacter,
Volume 1,
Issue 1,
1996,
Page 52-56
Masahiro Asaka,
Mototsugu Kato,
Mineo Kudo,
Masao Katagiri,
Keiko Nishikawa,
Hiromi Koshiyama,
Hiroshi Takeda,
Jun‐Ichi Yoshida,
David Y. Graham,
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摘要:
ABSTRACTBackground.The current study was designed to evaluate the effect of aging andHelicobacter pyloriinfection on the gastric mucosa in asymptomatic Japanese adults.Materials and Methods.Eighty‐five asymptomatic healthy adults were recruited from a health‐screening center in Sapporo. All subjects underwent endoscopy and gastric biopsy, and serum was obtained for IgG antibodies toH. pylori, serum gastrin, and pepsinogen levels.Results.The prevalence of atrophic change of the gastric mucosa assessed by pathological findings increased with age (49% in the 30‐ to 39‐year‐old group compared to 89% in those 60 years and older,p<.001). The frequency of intestinal metaplasia also increased with age (38% in the 30‐ to 39‐year‐old group compared to 82% in those 60 years and older,p<.001). In contrast, the frequency of atrophic gastritis and intestinal metaplasia was extremely low in theH. pyloriseronegative group regardless of age. Mean serum gastrin level inH. pylori‐positive adults was significantly greater than in those who wereH. pylori‐negative (114.3 ± 11.2 compared to 65.8 ± 6.5 pg/ml,p<.03). The serum pepsinogen I‐II ratio was significantly lower in those withH. pyloriinfection than in those without (3.1 compared to 6.6,p<.0001).Conclusions.These results suggest that the chronological changes in the gastric mucosa in Japanese individuals are either entirely related toH. pyloriinfection or the process is greatly accelerat
ISSN:1083-4389
DOI:10.1111/j.1523-5378.1996.tb00008.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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9. |
An Increase in Helicobacter pylori Strains Resistant to Metronidazole: A Five‐Year Study |
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Helicobacter,
Volume 1,
Issue 1,
1996,
Page 57-61
Thomas K.W. Ling,
Augustine F.B. Cheng,
Joseph J.Y. Sung,
Phyllis Y.L. Yiu,
Sydney S.C. Chung,
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摘要:
ABSTRACTBackground.Metronidazole is one of the most commonly used antimicrobial agents for the treatment ofHelicobacter pyloriinfection. Resistance to metronidazole has been reported worldwide but with a wide range of prevalence. We started using the classical triple therapy (bismuth, tetracycline, and metronidazole) forH. pyloriinfection in 1991 but recently have experienced a decline in its efficacy in curing the infection. Thus our aim was to investigate in a single center the prevalence of metronidazole‐resistantH. pyloriover a period of 5 years.Materials and Methods.A total of 1,015 differentH. pyloristrains collected over a period of 5 years were tested for sensitivity against metronidazole, ampicillin, tetracycline, and imipenem. Antibiotic sensitivity was tested by the disk diffusion and agar dilution methods. To elucidate further the possible relationship between these metronidazole‐resistant strains, genomic DNA digestion by theHaeIII endonuclease and ribotyping were undertaken in a selected group of isolates.Results.In 1991, 29 of 132 (22.0%) tested strains ofH. pyloriwere found to be resistant to metronidazole. Since our initiation at that time of a triple therapy of bismuth, metronidazole, and tetracycline, the prevalence of metronidazole‐resistant strains rose rapidly to 73.2% in 1995. AllH. pyloriisolates were sensitive to ampicillin, tetracycline, and imipenem. A high degree of genomic heterogeneity was found among these isolates. Thus it is unlikely that the resistant strains ofH. pyloriwere originated from a single clone.Conclusions.This study shows a rapid increase in metronidazole‐resistantH. pyloriwith the use of an anti‐Helicobacterregimen that contains metronidazole. We anticipate that the efficacy of metronidazole‐containing anti‐Helicobacterregimens will decline with the rapid rise in resistant strain
ISSN:1083-4389
DOI:10.1111/j.1523-5378.1996.tb00009.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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10. |
Culture of Helicobacter pylori: Effect of Preimmersion of Biopsy Forceps in Formalin |
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Helicobacter,
Volume 1,
Issue 1,
1996,
Page 62-64
Mahmoud M. Yousfi,
Rita Reddy,
Michael S. Osato,
David Y. Graham,
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摘要:
ABSTRACTBackground.Treatment of antibiotic‐resistantHelicobacter pylorishould be based on bacterial sensitivity testing that requires the ability to isolate the bacterium from gastric mucosal biopsies. The aim of this study was to determine whether the yield for detectingH. pyloriinfection by culture is reduced by immersion of biopsy forceps in formalin prior to obtaining the specimen.Materials and Methods.Gastric antral mucosal biopsies (100 specimens) from 50 patients were obtained for culture ofH. pylori.An antral biopsy was taken for culture, and with the same forceps a biopsy was taken for histological examination. The biopsy specimen was removed by shaking, whereas the forceps was immersed in 10% buffered formalin for the histological investigation. The forceps was then used without rinsing to obtain a second specimen for culture from an area adjacent to the first site.H. pyloristatus was determined by histological assessment with the Genta stain and a rapid urease test.Results.Fifty patients withH. pyloriinfection documented by histological inquiry and positive rapid urease testing entered the study; 29 had duodenal ulcers, 5 had gastric ulcers, 1 had mucosal associated lymphoid tissue (MALT) lymphoma, and 15 were without ulcer disease. The results of culture both before and after immersion in formalin were identical. One patient had both cultures negative; the sensitivity of culture for detection ofH. pyloriinfection was 98% (95% confidence interval =93%‐100%).Conclusion.Preimmersion of biopsy forceps in formalin does not adversely affect the ability to cultureH. pyl
ISSN:1083-4389
DOI:10.1111/j.1523-5378.1996.tb00010.x
出版商:Blackwell Publishing Ltd
年代:1996
数据来源: WILEY
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