Helicobacter pylori: Controversies and an Approach to Management
1990; Elsevier BV; Volume: 65; Issue: 3 Linguagem: Inglês
10.1016/s0025-6196(12)62541-5
ISSN1942-5546
AutoresJ. E. Ormand, Nicholas J. Talley,
Tópico(s)Gastric Cancer Management and Outcomes
ResumoHelicobacter pylori (formerly, Campylobacter pylori) is a gram-negative, spiral-shaped bacterium with a strong affinity for gastric-type epithelium. Convincing evidence indicates that H. pylori plays an etiologic role in the development of chronic, nonspecific gastritis, and it may play an important role in the pathogenesis of duodenal ulcer disease. An etiologic role for this organism in chronic gastric ulceration, nonulcer dyspepsia, and gastric carcinoma is not established. Whereas the diagnosis of H. pylori infection is relatively straightforward, the questions of when and how to treat the infection do not have established answers. A high rate of recrudescence follows most currently used therapeutic interventions. Until the pathogenicity of H, pylori in clinical disease is further supported and additional treatment trials have been completed, a conservative management approach is recommended. Helicobacter pylori (formerly, Campylobacter pylori) is a gram-negative, spiral-shaped bacterium with a strong affinity for gastric-type epithelium. Convincing evidence indicates that H. pylori plays an etiologic role in the development of chronic, nonspecific gastritis, and it may play an important role in the pathogenesis of duodenal ulcer disease. An etiologic role for this organism in chronic gastric ulceration, nonulcer dyspepsia, and gastric carcinoma is not established. Whereas the diagnosis of H. pylori infection is relatively straightforward, the questions of when and how to treat the infection do not have established answers. A high rate of recrudescence follows most currently used therapeutic interventions. Until the pathogenicity of H, pylori in clinical disease is further supported and additional treatment trials have been completed, a conservative management approach is recommended. Helicobacter pylori (formerly, Campylobacter pylori1Goodwin CS Armstrong JA Chilvers T Peters M Collins MD Sly L McConnell W Harper WES Transfer of Campylobacter pylori and Campylobacter mustelae to Helicobacter gen. nov. as Helicobacter pylori comb. nov. and Helicobacter mustelae comb, nov., respectively.Int J System Bacteriol. 1989; 39: 397-405Crossref Scopus (392) Google Scholar) was first isolated in 1983; since then, more than 1,000 articles, letters, and abstracts about this organism have been published in the English literature alone. Despite the intense interest and research time devoted to H. pylori, it remains a controversial entity that has caused considerable confusion. The following questions have been posed: What available evidence supports a pathogenic role for H. pylori in gastritis and ulcer disease? How can a “gastric” infection cause duodenal ulceration? Does the high prevalence rate of H. pylori in asymptomatic “normal” persons refute a pathogenic role for this organism? When (if ever) should studies be done to search for H. pylori? Is efficacious treatment for H. pylori infection available? Should patients who harbor H. pylori be treated? The purpose of this article is to provide a clinically oriented review of H. pylori to highlight the controversies (Table 1) and to address the questions that have been raised. In addition, we propose some general therapeutic recommendations.Table 1Controversial Issues Involving Helicobacter pylori •What is the etiologic role of H. pylori in Duodenal ulceration?Gastric ulceration?Nonulcer dyspepsia?Gastric carcinoma?•What are the appropriate therapeutic approaches?•When is therapeutic intervention justified? Open table in a new tab Spiral-shaped organisms overlying human gastric epithelium were probably first appreciated in 1938.2Doenges JL Spirochetes in gastric glands of Macacus rhesus and humans without definite history of related disease.Proc Soc Exp Biol Med. 1938; 38: 536-538Crossref Scopus (90) Google Scholar Earlier, in 1924, “endogenous” gastric urease activity had been described.3Luck JM Seth TN Gastric urease.Biochem J. 1924; 18: 1227-1231Crossref Google Scholar A relationship between these observations and gastritis was established by the identification and isolation of H. pylori by Warren, Marshall, and their associates.4Warren JR Unidentified curved bacilli on gastric epithelium in active chronic gastritis (letter to the editor).Lancet. 1983; 1: 1273PubMed Google Scholar, 5Marshall BJ Unidentified curved bacilli on gastric epithelium in active chronic gastritis (letter to the editor).Lancet. 1983; 1: 1273-1275Google Scholar, 6Marshall BJ Royce H Annear DI Goodwin CS Pearman JW Warren JR Armstrong JA Original isolation of Campylobacter pyloridis from human gastric mucosa.Microbios. 1984; 25: 83-88Google Scholar H. pylori is typically an S-shaped, gram-negative bacterium with four to six unipolar sheathed flagella (Fig. 1).5Marshall BJ Unidentified curved bacilli on gastric epithelium in active chronic gastritis (letter to the editor).Lancet. 1983; 1: 1273-1275Google Scholar These structural features of the organism enable it to move easily in a corkscrew manner through its preferred ecologic niche—the mucous layer.8Hazell SL Lee A Brady L Hennessy W Campylobacter pyloridis and gastritis: association with intercellular spaces and adaptation to an environment of mucus as important factors in colonization of the gastric epithelium.J Infect Dis. 1986; 153: 658-663Crossref PubMed Scopus (348) Google Scholar Because of the known susceptibility of H. pylori to acid environments,8Hazell SL Lee A Brady L Hennessy W Campylobacter pyloridis and gastritis: association with intercellular spaces and adaptation to an environment of mucus as important factors in colonization of the gastric epithelium.J Infect Dis. 1986; 153: 658-663Crossref PubMed Scopus (348) Google Scholar, 9Humphreys H O'Morain C Culture of the organisms and histochemical identification.Scand J Gastroenterol Suppl. 1988; 142: 16-20Crossref Scopus (8) Google Scholar, 10Marshall BJ Barrett L Prakash C McCallum RW Guerrant RL Survival of Campylobacter pyloridis at acid pH (abstract).Gastroenterology. 1987; 92: 1517Google Scholar its detection within or beneath the mucous layer is not surprising. H. pylori organisms have a strong affinity for gastric epithelium11Marshall BJ McGechie DB Rogers PA Glancy RJ Pyloric Campylobacter infection and gastroduodenal disease.Med J Aust. 1985; 142: 439-444Google Scholar, 12Rathbone BJ Wyatt JI Heatley RV Possible pathogenetic pathways of Campylobacter pylori in gastroduodenal disease.Scand J Gastroenterol Suppl. 1988; 142: 40-43Crossref Scopus (15) Google Scholar, 13Steer HW Surface morphology of the gastroduodenal mucosa in duodenal ulceration.Gut. 1984; 25: 1203-1210Crossref PubMed Scopus (121) Google Scholar, 14Talley NJ Cameron AJ Shorter RG Zinsmeister AR Phillips SF Campylobacter pylori and Barrett's esophagus.Mayo Clin Proc. 1988; 63: 1176-1180Abstract Scopus (71) Google Scholar and tend to congregate around epithelial tight junctions, where they presumably have better access to host nutrients.8Hazell SL Lee A Brady L Hennessy W Campylobacter pyloridis and gastritis: association with intercellular spaces and adaptation to an environment of mucus as important factors in colonization of the gastric epithelium.J Infect Dis. 1986; 153: 658-663Crossref PubMed Scopus (348) Google Scholar Ultrastructural studies have shown that these organisms are in intimate contact with surface mucous cells (Fig. 2), and this finding is associated with subcellular changes.7Bode G Malfertheiner P Ditschuneit H Pathogenetic implications of ultrastructural findings in Campylobacter pylori related gastroduodenal disease.Scand J Gastroenterol Suppl. 1988; 142: 25-39Crossref Scopus (117) Google Scholar H. pylori produces several enzymes and toxins of unknown clinical significance.15Goodwin CS Armstrong JA Marshall BJ Campylobacter pyloridis, gastritis, and peptic ulceration.J Clin Pathol. 1986; 39: 353-365Crossref Scopus (496) Google Scholar, 16Figura N Guglielmetti P Rossolini A Barberi A Cusi G Musmanno RA Russi M Quaranta S Cytotoxin production by Campylobacter pylori strains isolated from patients with peptic ulcers and from patients with chronic gastritis only.J Clin Microbiol. 1989; 27: 225-226Crossref Google Scholar, 17Leunk RD Johnson FT David BC Kraft WG Morgan DR Cytotoxic activity in broth-culture filtrates of Campylobacter pylori.J Med Microbiol. 1988; 26: 93-99Crossref Scopus (535) Google Scholar, 18Hupertz V Czinn S Demonstration of a cytotoxin from Campylobacter pylori.Eur J Clin Microbiol Infect Dis. 1988; 7: 576-578Crossref Scopus (24) Google Scholar, 19Kasper GF Natural sources and microbiological characteristics of Campylobacter pylori.Scand J Gastroenterol Suppl. 1988; 142: 14-15Crossref Scopus (6) Google Scholar Two of the enzymes produced may be of particular importance. H. pylori releases large amounts of urea amidohydrolase (urease), an enzyme postulated to alkalinize, and thereby optimize, the environment immediately adjacent to the organism.15Goodwin CS Armstrong JA Marshall BJ Campylobacter pyloridis, gastritis, and peptic ulceration.J Clin Pathol. 1986; 39: 353-365Crossref Scopus (496) Google Scholar, 20Hazell SL Lee A Campylobacter pyloridis, urease, hydrogen ion back diffusion, and gastric ulcers.Lancet. 1986; 2: 15-17Abstract Scopus (172) Google Scholar H. pylori also produces a mucinolytic protease capable of threatening the host's mucus-bicarbonate barrier,21Sarosiek J Slomiany A Slomiany BL Evidence for weakening of gastric mucus integrity by Campylobacter pylori.Scand J Gastroenterol. 1988; 23: 585-590Crossref Scopus (98) Google Scholar, 22Slomiany BL Bilski J Sarosiek J Murty VL Dworkin B VanHorn K Zielenski J Slomiany A Campylobacter pyloridis degrades mucin and undermines gastric mucosal integrity.Biochem Biophys Res Commun. 1987; 144: 307-314Crossref Scopus (148) Google Scholar which theoretically places the underlying mucosa—as well as the organism itself—at risk for further damage from acid and pepsin. These enzymes have been postulated to play a major role in host-organism interactions and, in some instances, in gross pathologic changes.23Ormand JE Talley NJ Campylobacter pylori, mucus, and peptic ulceration: a dynamic interaction.J Clin Gastroenterol. 1989; 11: 492-495Crossref Scopus (17) Google ScholarFig. 2a, Electron micrograph, showing Helicobacter pylori in close approximation to the gastric epithelium (arrows). (×18,000.) b and c, H. pylori forming an adhesion to a surface mucous cell (arrows). (×114,000.)(Part c from Bode and associates.7Bode G Malfertheiner P Ditschuneit H Pathogenetic implications of ultrastructural findings in Campylobacter pylori related gastroduodenal disease.Scand J Gastroenterol Suppl. 1988; 142: 25-39Crossref Scopus (117) Google Scholar By permission of Norwegian University Press.) (Photograph courtesy of Dr. Peter Malfertheiner.)View Large Image Figure ViewerDownload (PPT) Histologic examination is considered one of the standard approaches for establishing the diagnosis of H. pylori infection. The organism is found beneath the mucous layer in close association with the surface epithelium of the gastric crypts and pits7Bode G Malfertheiner P Ditschuneit H Pathogenetic implications of ultrastructural findings in Campylobacter pylori related gastroduodenal disease.Scand J Gastroenterol Suppl. 1988; 142: 25-39Crossref Scopus (117) Google Scholar, 8Hazell SL Lee A Brady L Hennessy W Campylobacter pyloridis and gastritis: association with intercellular spaces and adaptation to an environment of mucus as important factors in colonization of the gastric epithelium.J Infect Dis. 1986; 153: 658-663Crossref PubMed Scopus (348) Google Scholar (Fig. 3). Various stains, including hematoxylin and eosin, are capable of demonstrating the organism in endoscopic biopsy specimens, but Warthin-Starry silver stain and Giemsa preparations are preferred because of their enhanced sensitivity in detecting H. pylori.4Warren JR Unidentified curved bacilli on gastric epithelium in active chronic gastritis (letter to the editor).Lancet. 1983; 1: 1273PubMed Google Scholar, 24Aymard B Labouyrie E de Korwin JD Ferry R Duprez A Histological staining methods for detection of gastric Campylobacter like organisms (GCLOs): a comparative study (abstract).Gastroenterology. 1988; 94: A16Google Scholar A minimum of two gastric specimens, at least one of which should be antral, is indicated because H. pylori infection is patchy in nature.25Hazell SL Hennessy WB Borody TJ Carrick J Ralston M Brady L Lee A Campylobacter pyloridis gastritis II: distribution of bacteria and associated inflammation in the gastroduodenal environment.Am J Gastroenterol. 1987; 82: 297-301Google Scholar, 26Goodwin CS Blincow ED Warren JR Waters TE Sanderson CR Easton L Evaluation of cultural techniques for isolating Campylobacter pyloridis from endoscopic biopsies of gastric mucosa.J Clin Pathol. 1985; 38: 1127-1131Crossref Scopus (189) Google Scholar Both the sensitivity and the specificity of the histologic diagnosis of H. pylori infection range from 85 to 100%.27Marshall BJ Guerrant RL Plankey MW Dye KR Barrett L Frierson HF Hoffman SR McCallum RW Comparison of 14C-urea breath test, microbiology and histology for the diagnosis of Campylobacter pylori (abstract).Gastroenterology. 1988; 94: A284Google Scholar, 28Schnell GA Schubert TT Barnes WG Rupani MK Comparison of urease, H&E, and culture tests for Campylobacter pylori (abstract).Gastroenterology. 1988; 94: A410Google Scholar, 29Faisal MA Santogade PJ Bokkenheuser V Scholes JV Holt PR Kotler DP Sensitivity and specificity of the serologic diagnosis of Campylobacter pylori infection (abstract).Gastroenterology. 1988; 94: A121Google Scholar, 30Westblom TU Madan E Kemp J Subik MA Evaluation of a rapid urease test to detect Campylobacter pylori infection.J Clin Microbiol. 1988; 26: 1393-1394PubMed Google Scholar The gross appearance of the mucosa at endoscopy is of no value in detecting H. pylori infection.11Marshall BJ McGechie DB Rogers PA Glancy RJ Pyloric Campylobacter infection and gastroduodenal disease.Med J Aust. 1985; 142: 439-444Google Scholar The macroscopic appearance in infected persons ranges from completely normal to gross ulceration. Culture is the definitive “gold standard” for establishing the diagnosis of H. pylori infection. H. pylori bacteria are fastidious organisms that require a warm (37°C), humid, microaerobic environment in order to propagate.6Marshall BJ Royce H Annear DI Goodwin CS Pearman JW Warren JR Armstrong JA Original isolation of Campylobacter pyloridis from human gastric mucosa.Microbios. 1984; 25: 83-88Google Scholar Gastric biopsy specimens must be promptly placed in 2 to 3 ml of “sterile” isotonic saline or 20% glucose and transported to the microbiology laboratory within a few hours if organisms are to be recovered. Once in the laboratory, crushed or minced biopsy specimens are plated on supplemented media such as chocolate agar or Skirrow's selective medium and allowed to incubate for 5 to 7 days.5Marshall BJ Unidentified curved bacilli on gastric epithelium in active chronic gastritis (letter to the editor).Lancet. 1983; 1: 1273-1275Google Scholar, 6Marshall BJ Royce H Annear DI Goodwin CS Pearman JW Warren JR Armstrong JA Original isolation of Campylobacter pyloridis from human gastric mucosa.Microbios. 1984; 25: 83-88Google Scholar, 31Dent JC McNulty CAM Evaluation of a new selective medium for Campylobacter pylori.Eur J Clin Microbiol Infect Dis. 1988; 7: 555-558Crossref Scopus (111) Google Scholar Culture has a reported sensitivity of 50 to 95% but is 100% specific.27Marshall BJ Guerrant RL Plankey MW Dye KR Barrett L Frierson HF Hoffman SR McCallum RW Comparison of 14C-urea breath test, microbiology and histology for the diagnosis of Campylobacter pylori (abstract).Gastroenterology. 1988; 94: A284Google Scholar, 28Schnell GA Schubert TT Barnes WG Rupani MK Comparison of urease, H&E, and culture tests for Campylobacter pylori (abstract).Gastroenterology. 1988; 94: A410Google Scholar, 29Faisal MA Santogade PJ Bokkenheuser V Scholes JV Holt PR Kotler DP Sensitivity and specificity of the serologic diagnosis of Campylobacter pylori infection (abstract).Gastroenterology. 1988; 94: A121Google Scholar, 30Westblom TU Madan E Kemp J Subik MA Evaluation of a rapid urease test to detect Campylobacter pylori infection.J Clin Microbiol. 1988; 26: 1393-1394PubMed Google Scholar, 32Graham DY Klein PD Evans Jr, DJ Evans DG Alpert LC Opekun AR Boutton TW Campylobacter pylori detected noninvasively by the 13C-urea breath test.Lancet. 1987; 1: 1174-1177Abstract PubMed Scopus (668) Google Scholar, 33Vaira D Holton J Soosay G Polydorou A Cairns SR Dowsett JF D'Anastasio C Salmon PR Giemsa, Gram, and haematoxylin & eosin (HE) gastric brushing stains vs histology, culture and CP-test for detecting Campylobacter pylori (CP) (abstract).Gastroenterology. 1988; 94: A474Google Scholar In vitro antibiotic sensitivity studies show H. pylori to be susceptible to a wide array of antimicrobial agents.34Kasper G Dickgiesser N Antibiotic sensitivity of “Campylobacter pylori” (letter to the editor).Eur J Clin Microbiol. 1984; 3: 444Crossref Scopus (22) Google Scholar, 35McNulty CAM Dent J Wise R Susceptibility of clinical isolates of Campylobacter pyloridis to 11 antimicrobial agents.Antimicrob Agents Chemother. 1985; 28: 837-838Crossref Scopus (136) Google Scholar, 36Goodwin CS Blake P Blincow E The minimum inhibitory and bactericidal concentrations of antibiotics and anti-ulcer agents against Campylobacter pyloridis.J Antimicrob Chemother. 1986; 17: 309-314Crossref Scopus (140) Google Scholar, 37Lambert T Mégraud F Gerbaud G Courvalin P Susceptibility of Campylobacter pyloridis to 20 antimicrobial agents.Antimicrob Agents Chemother. 1986; 30: 510-511Crossref Scopus (84) Google Scholar, 38Andreasen JJ Andersen LP In vitro susceptibility of Campylobacter pyloridis to cimetidine, sucralfate, bismuth and sixteen antibiotics.Acta Pathol Microbiol Immunol Scand [B]. 1987; 95: 147-149Google Scholar It is uniformly resistant only to trimethoprim-sulfamethoxazole, vancomycin, and nalidixic acid. Unfortunately, the in vitro data do not translate well to the in vivo situation, in which antibiotics, when used alone, have thus far proved incapable of eradicating the bacteria.39Glupczynski Y Burette A Labbe M Deprez C De Reuck M Deltenre M Campylobacter pylori-associated gastritis: a double-blind placebo-controlled trial with amoxicillin.Am J Gastroenterol. 1988; 83: 365-372Google Scholar, 40McNulty CAM Gearty JC Crump B Davis M Donovan IA Melikian V Lister DM Wise R Campylobacter pyloridis and associated gastritis: investigator blind, placebo controlled trial of bismuth salicylate and erythromycin ethylsuccinate.Br Med J. 1986; 293: 645-649Crossref Scopus (277) Google Scholar, 41Weil J Bell GD Jones PH Gant P Trowell JE Harrison G “Eradication” of Campylobacter pylori: are we being misled? (letter to the editor).Lancet. 1988; 2: 1245Abstract Scopus (27) Google Scholar, 42Gastrointestinal Physiology Working Group of Cayetano Heredia and the Johns Hopkins Universities Morgan D Kraft W Bender M Pearson A Nitrofurans in the treatment of gastritis associated with Campylobacter pylori.Gastroenterology. 1988; 95: 1178-1184Google Scholar, 43Stone JW Wise R Donovan IA Gearty J Failure of ciprofloxacin to eradicate Campylobacter pylori from the stomach (letter to the editor).J Antimicrob Chemother. 1988; 22: 92-93Crossref Scopus (34) Google Scholar, 44Börsch G Mai U Müller K-M Monotherapy or polychemotherapy in the treatment of Campylobacter pylori-related gastroduodenal disease.Scand J Gastroenterol Suppl. 1988; 142: 101-106Crossref Scopus (35) Google Scholar The ability of H. pylori to produce large amounts of urease has been exploited in two different manners to aid in diagnosis. The first of these applications is the biopsy urease test, in which a gastric biopsy specimen is placed in a yellow urea-containing gel pellet or broth and allowed to incubate. If H. pylori is present, the urease it produces will metabolize the urea and create ammonium. The resulting increase in pH will cause a pH indicator in the milieu to change from yellow to pink. Usually, this reaction occurs quickly, within 30 minutes after incubation.45Morris A McIntyre D Rose T Nicholson G Rapid diagnosis of Campylobacter pyloridis infection (letter to the editor).Lancet. 1986; 1: 149Abstract Scopus (69) Google Scholar, 46McNulty CAM Wise R Rapid diagnosis of Campylobacter pyloridis gastritis (letter to the editor).Lancet. 1986; 1: 387Abstract Scopus (21) Google Scholar This rapid reaction is an advantage but is somewhat offset by the lower sensitivity and specificity of the test (ranging from 65 to 95% and 60 to 100%, respectively).27Marshall BJ Guerrant RL Plankey MW Dye KR Barrett L Frierson HF Hoffman SR McCallum RW Comparison of 14C-urea breath test, microbiology and histology for the diagnosis of Campylobacter pylori (abstract).Gastroenterology. 1988; 94: A284Google Scholar, 28Schnell GA Schubert TT Barnes WG Rupani MK Comparison of urease, H&E, and culture tests for Campylobacter pylori (abstract).Gastroenterology. 1988; 94: A410Google Scholar, 33Vaira D Holton J Soosay G Polydorou A Cairns SR Dowsett JF D'Anastasio C Salmon PR Giemsa, Gram, and haematoxylin & eosin (HE) gastric brushing stains vs histology, culture and CP-test for detecting Campylobacter pylori (CP) (abstract).Gastroenterology. 1988; 94: A474Google Scholar, 46McNulty CAM Wise R Rapid diagnosis of Campylobacter pyloridis gastritis (letter to the editor).Lancet. 1986; 1: 387Abstract Scopus (21) Google Scholar, 47Tobin A Gilligan D Ward R McKenna D Casey E Hutchinson L Keane C Sweeney E O'Morain C A comparative study of tests used in the diagnosis of Campylobacter pylori (abstract).Gastroenterology. 1988; 94: A462Google Scholar, 48Engstrand L Gustavsson S Påhlson C Schwan A Rapid identification of Campylobacter pyloridis with monoclonal antibodies (abstract).Gastroenterology. 1987; 92: 1383Google Scholar The 13C- and 14C-urea breath tests also depend on the production of urease by H. pylori. The subject is given a small dose of radiolabeled urea to drink. If H. pylori is present in the stomach, its urease will split a labeled carbon from the urea molecule, and this carbon will be absorbed and incorporated into bicarbonate in the blood-stream. This carbon will then be transformed into carbon dioxide at the respiratory interface and expired in the subject's breath. This radiolabeled carbon can then be captured in a solution of hydroxide of hyamine and counted, and the resultant excretion curve over time can be constructed.32Graham DY Klein PD Evans Jr, DJ Evans DG Alpert LC Opekun AR Boutton TW Campylobacter pylori detected noninvasively by the 13C-urea breath test.Lancet. 1987; 1: 1174-1177Abstract PubMed Scopus (668) Google Scholar, 49Marshall BJ Surveyor I Carbon-14 urea breath test for the diagnosis of Campylobacter pylori associated gastritis.J Nucl Med. 1988; 29: 11-16Google Scholar This test has the advantages of being noninvasive and relatively inexpensive, and a positive test result is indicative of an active infection. In addition, it seems to be both sensitive (90 to 100%) and specific (95 to 100%) in diagnosing H. pylori infection, although further validation studies are needed.27Marshall BJ Guerrant RL Plankey MW Dye KR Barrett L Frierson HF Hoffman SR McCallum RW Comparison of 14C-urea breath test, microbiology and histology for the diagnosis of Campylobacter pylori (abstract).Gastroenterology. 1988; 94: A284Google Scholar, 32Graham DY Klein PD Evans Jr, DJ Evans DG Alpert LC Opekun AR Boutton TW Campylobacter pylori detected noninvasively by the 13C-urea breath test.Lancet. 1987; 1: 1174-1177Abstract PubMed Scopus (668) Google Scholar, 49Marshall BJ Surveyor I Carbon-14 urea breath test for the diagnosis of Campylobacter pylori associated gastritis.J Nucl Med. 1988; 29: 11-16Google Scholar, 50Bell GD Weil J Harrison G Morden A Jones PH Gant PW Trowell JE Yoong AK Daneshmend TK Logan RFA 14C-urea breath analysis, a non-invasive test for Campylobacter pylori in the stomach (letter to the editor).Lancet. 1987; 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109: 11-17Crossref Scopus (389) Google Scholar, 60Evans Jr, DJ Evans DG Graham DY Klein PD A sensitive and specific serologic test for detection of Campylobacter pylori infection.Gastroenterology. 1989; 96: 1004-1008Google Scholar Apparently, specificity may be lost when whole extracts of H. pylori are used as antigen for the enzyme-linked immunosorbent assay because of cross-reactivity with other bacteria, including C. jejuni.61Perez-Perez GI Blaser MJ Conservation and diversity of Campylobacter pyloridis major antigens.Infect Immun. 1987; 55: 1256-1263Google Scholar Thus, serologic studies done with use of whole organism extracts54Jones DM Eldridge J Fox AJ Sethi P Whorwell PJ Antibody to the gastric Campylobacter-like organism (“Campylobacter pyloridis”)—clinical correlations and distribution in the normal population.J Med Microbiol. 1986; 22: 57-62Crossref Scopus (214) Google Scholar, 55Morris A Nicholson G Lloyd G Haines D Rogers A Taylor D Seroepidemiology of Campylobacter pyloridis.N Z Med J. 1986; 99: 657-659Google Scholar, 56Rathbone BJ Wyatt JI Worsley BW Shires SE Trejdosiewicz LK Heatley RV Losowsky MS Systemic and local antibody responses to gastric Campylobacter pyloridis in non-ulcer dyspepsia.Gut. 1986; 27: 642-647Crossref Scopus (229) Google Scholar, 58Perez-Perez GI Dworkin BM Chodos JE Blaser MJ Campylobacter pylori antibodies in humans.Ann Intern Med. 1988; 109: 11-17Crossref Scopus (389) Google Scholar, 59Booth L Holdstock G MacBride H Hawtin P Gibson JR Ireland A Bamforth J DuBoulay CE Lloyd RS Pearson AD Clinical importance of Campylobacter pyloridis and associated serum IgG and IgA antibody responses in patients undergoing upper gastrointestinal endoscopy.J Clin Pathol. 1986; 39: 215-219Crossref Scopus (96) Google Scholar, 62Mégraud F Brassens-Rabbé M-P Denis F Belbouri A Hoa DQ Seroepidemiology of Campylobacter pylori infection in various populations.J Clin Microbiol. 1989; 27: 1870-1873PubMed Google Scholar may need to be interpreted with caution. To date, the best results have been obtained by using high-molecular-weight cell-associated proteins from H. pylori as the antigen (sensitivity 99%, specificity 100%).60Evans Jr, DJ Evans DG Graham DY Klein PD A sensitive and specific serologic test for detection of Campylobacter pylori infection.Gastroenterology. 1989; 96: 1004-
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