Revisão Revisado por pares

I. Helicobacter pylori : Its epidemiology and its role in duodenal ulcer disease

1991; Wiley; Volume: 6; Issue: 2 Linguagem: Inglês

10.1111/j.1440-1746.1991.tb01448.x

ISSN

1440-1746

Autores

David Y. Graham,

Tópico(s)

Gastrointestinal disorders and treatments

Resumo

Journal of Gastroenterology and HepatologyVolume 6, Issue 2 p. 105-113 I. Helicobacter pylori: Its epidemiology and its role in duodenal ulcer disease DAVID Y. GRAHAM, Corresponding Author DAVID Y. GRAHAM Departments of Medicine and Molecular Virology, Veterans Affairs Medical Center and Baylor College of Medicine, Houston, Texas, USADavid Y. Graham MD, Digestive Disease Section (111D), VA Medical Center, 2002 Holcombe Blvd, Houston, TX 77030, USA.Search for more papers by this author DAVID Y. GRAHAM, Corresponding Author DAVID Y. GRAHAM Departments of Medicine and Molecular Virology, Veterans Affairs Medical Center and Baylor College of Medicine, Houston, Texas, USADavid Y. Graham MD, Digestive Disease Section (111D), VA Medical Center, 2002 Holcombe Blvd, Houston, TX 77030, USA.Search for more papers by this author First published: April 1991 https://doi.org/10.1111/j.1440-1746.1991.tb01448.xCitations: 255AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL References 1 Massarrat S., Paidlik A., Pittner P., Schmitz-Moorman P. & Wurbs M. The role of certain habits and various diseases in the occurrence of gastritis. Hepato-gastroenterology 1983; 30: 249. 2 Edwards F. & Coghill N. Aetiological factors in chronic atrophic gastritis. BMJ 1966; 2: 1409. 3 Andrews G. R., Haneman B. & Arnold B. J. Atrophic gastritis in the aged. Aust. Ann. Med. 1967; 16: 230. 4 Cheli R., Simon L., Aste H. et al. Atrophic gastritis and intestinal metaplasia in asymptomatic Hungarian and Italian populations. Endoscopy 1980; 12: 105. 5 Siurala M., Isokoski M., Varis K. & Kekki M. Prevalence of gastritis in a rural population. Scand. J. Gastroenterol. 1968; 3: 211. 6 Siurala M. & Varis K. Gastritis. In: W. Sircus, A. N. Smith, eds, Scientific Foundations of Gastroenterology. W. B. Saunders, Philadelphia . 1980; 357– 69. 7 Graham D. Y., Klein P. D., Opekun A. R. et al. Epidemiology of Campylobacter pylori infection: Ethnic considerations. Scand. J. Gastroenterol. 1988; 23 (suppl. 142): 9– 13. 8 Graham D. Y. Campylobacter pylori in human populations: the present and predictions of the future based on the epidemiology of polio. In: H. Menge, M. Gregor, C. A. M. McNulty, B. J. Marshall, G. Tytgat, eds, 2nd International Symposium on Campylobacter pylori. Springer, Berlin . (in press). 9 Klein P. D. The Gastrointestinal Physiology Working Group of Cayetano Herdeia and the Johns Hopkins Universities, Graham D. Y., Opekun A. R. & Sekely S. Helicobacter (Campylobacter) pylori is a waterborne disease in Peruvian children. Gastroenterology 1990; 98: A69. 10 Shahamat M., Vives-Rego J., Paszko-Kolva C., Pearson A. D. & Colwell R. R. Survival of Campylobacter pylori in river water: 3H-thymidine uptake and viability under stimulated environmental conditions. Klin. Wochenschr. 1989; 67 (Suppl. 18): 63. 11 Shahamat M., Paszko-Kolva C., Yamamoto H., Mai U., Pearson A. D. & Colwell R. R. Ecological studies of Campylobacter pylori. Klin. Wochenschr. 1989; 67 (Suppl. 18): 62– 3. 12 Graham D. Y., Alpert L. C., Smith J. L. & Yoshimura H. H. Iatrogenic Campylobacter pylori infection is a cause of epidemic achlorhydria. Amer. J. Gastroenterol. 1988; 83: 974– 80. 13 Langenberg W., Rauws E. A., Oudbier J. H. & Tytgat G. N. J. Patient-to-patient transmission of Campylobacter pylori infection by fiberoptic gastroduodenoscopy and biopsy. J. Infect. Dis. 1990; 161: 507– 11. 14 Mitchell H. M., Lee A. & Carrick J. Increased incidence of Campylobacter pylori infection in gastroenterologists: further evidence to support person-to-person transmission of C. pylori. Scand. J. Gastroenterol. 1989; 24: 396– 400. 15 Krajden S., Fuksa M., Anderson J. et al. Examination of human stomach biopsies, saliva and dental plaque for Campylobacter pylori. J. Clin. Microbiol. 1989; 27: 1397– 8. 16 Gear M. W. L. & Barnes R. J. Endoscopic studies of dyspepsia in general practice. BMJ 1980; 280: 1136– 7. 17 Perez-Perez G. I., Dworkin B. M., Chodos J. E. & Blaser M. J. Campylobacter pylori antibodies in humans. Ann. Intern. Med. 1988; 109: 11– 7. 18 Morris A., Nicholson G., Lloyd G., Haines D., Rogers A. & Taylor D. Seroepidemiology of Campylobacter pylori-dis. N.Z. Med. J. 1986; 99: 657– 9. 19 Czunn S. J., Dahms B. B., Jacobs G. H., Kaplan B. & Rothstein F. H. Campylobacter-like organisms in association with symptomatic gastritis in children. J. Pediat. 1986; 109: 80– 3. 20 Gnarpe H., Unge P., Blomqvist C. & Makitalo S. Campylobacter pylori in Swedish patients referred for gastroscopy. APMIS 1988; 96: 128– 32. 21 Weir R. D. & Backett E. M. Studies of the epidemiology of peptic ulcer in a rural community: prevalence and natural history of dyspepsia and peptic ulcer. Gut 1968; 9: 75– 83. 22 Dwyer B., Nanxiong S., Kaldor J., Tee W., Lambert J., Luppino M. & Flannery G. Antibody response to Campylobacter pylori in an ethnic group lacking peptic ulceration. Scand. J. Infect. Dis. 1988; 20: 63– 8. 23 Graham D. Y., Malaty H. M., Evans D. G., Evans D. J. Jr, Klein P. D. & Adam E. Epidemiology of Helicobacter pylori in an asymptomatic population in the United States: effect of age, race and socioeconomic status. Gastroenterology (in press). 24 Fiedorek S. C., Malaty H. M., Evans D. G. et al. Factors influencing the epidemiology of Helicobacter pylori infection in children. Pediatrics (in press). 25 Al-Moagel M. A., Evans D. G., Abdulghani M. E. et al. Prevalence of Helicobacter (formerly Campylobacter) pylori infection in Saudi Arabia: comparison of those with and without upper gastrointestinal symptoms. Amer. J. Gastroenterol. 1990; 85: 944– 8. 26 Jones D. M., Eldridge J. & Whorwell P. J. Antibodies to Campylobacter pyloridis in household contacts of infected patients. BMJ 1987; 294: 615. 27 Mitchell H. M., Bohane T. D., Berkowicz J., Hazell S. L. & Lee A. Antibody to Campylobacter pylori in families of index children with gastrointestinal illness due to C. pylori. Lancet 1987; ii: 681– 2. 28 Drumm B., Perez-Perez G. I., Blaser M. J. & Sherman P. M. Intrafamilial clustering of Helicobacter pylori infection. N. Engl. J. Med. 1990; 322: 359– 63. 29 Paul J. R. Epidemics in Sweden. Medin and his clinical contributions. In: A History of Poliomyelitis. Yale University Press, New Haven : 1971; 71– 8. 30 Paul J. R. Historical and geographical aspects of the epidemiology of poliomyelitis. Yale J. Biol. Med. 1954; 27: 101– 13. 31 Paul J. R. Serological surveys and antibody patterns. Endemicity versus epidemicity. In: A History of Poliomyelitis. Yale University Press, New Haven . 1971; 357– 68. 32 Walton M. & Melnick J. L. Poliomyelitis antibodies in two differing socioeconomic groups within the same city. Yale J. Biol. Med. 1955; 27: 350– 70. 33 Mitchell H. M., Lee A., Berkowicz J. & Barody T. The use of serology to diagnose active Campylobacter pylori infection. Med. J. Aust. 1988; 149: 604– 9. 34 von Wulffen H. & Grote H. J. Enzyme-linked immunosorbent assay for detection of immunoglobulin A and G antibodies to Campylobacter pylori. Eur. J. Clin. Microbiol. Infect. Dis. 1988; 7: 559– 65. 35 Jones D. M., Lessells A. M., Eldridge J. Campylobacter-like organisms on the gastric mucosa: culture, histological and serological studies. J. Clin. Pathol. 1984; 37: 1002– 6. 36 Jones D. M., Eldridge J., Fox A. J., Sethi A. J. & Whorwell P. J. Antibody to the gastric campylobacter-like organism ('Campylobacter pyloridis'): clinical correlations and distribution in the normal population. J. Med. Microbiol. 1986; 22: 57– 62. 37 Dwyer B., Nanxiong S., Kaldor J. et al. Antibody response to Campylobacter pylori in an ethnic group lacking peptic ulceration. Scand. J. Infect. Dis. 1988; 20: 63– 8. 38 Megraud F., Brassens-Rebbe M-P., Denis F., Belbouri A. & Hoa D. Q. Seroepidemiology of C. pylori infection in various populations. J. Clin. Microbiol. 1989; 27: 1870– 3. 39 Alpert L. C., Graham D. Y., Evans D. J. Jr et al. Diagnostic possibilities for Campylobacter pylori infection. Eur. J. Gastroenterol. Hepatol. 1989; 1: 17– 26. 40 Evans D. J. Jr., Evans D. G., Graham D. Y. & Klein P. D. A sensitive and specific serologic test for detection of Campylobacter pylori infection. Gastroenterology 1989; 96: 1004– 8. 41 Evans D. J., Jr., Evans D. G., Smith K. E. & Graham D. Y. Serum antibody responses to the N-acetylneuraminyllactose-binding hemagglutinin of Campylobacter pylori. Infect. Immun. 1989; 57: 644– 7. 42 von Wulffen M., Grote H. J., Gatermann S., Loning T., Berger B. & Buhl C. Immunoblot analysis of immune response to Campylobacter pylori and its clinical associations. J. Clin. Pathol. 1988; 41: 653– 9. 43 Vira D., D'Anastasio C. D., Holton J. et al. Campylobacter pylori in abattoir workers: is it a zoonosis. Lancet 1988; 2: 725– 6. 44 Siurala M., Sipponen P. & Kekki M. Chronic gastritis: dynamic and clinical aspects. Scand. J. Gastroenterol. 1985; 20 (suppl. 109): 69– 76. 45 Correa P., Cuello C., Duque E. et al. Gastric cancer in Colombia. III. Natural history of precursor lesions. J. Natl Cancer. Inst. 1976; 57: 1027– 33. 46 Graham D. Y., Adam E., Klein P. D. et al. Epidemiology of Campylobacter pylori. Gastroenterol. Clin. Biol. 1989; 13: 84B– 88B. 47 Correa P., Fontham E., Pickle L. W., Chen V., Lin Y. & Haenszel W. Dietary determinants of gastric cancer in south Louisiana inhabitants. J. Natl Cancer Inst. 1985; 75: 1985. 48 Fox J. G., Correa P., Taylor N. S. et al. Campylobacter pylori-associated gastritis and immune response in a population at increased risk of gastric carcinoma. Amer. J. Gastroenterol. 1989; 84: 775– 81. 49 Fontham E., Zavala D., Correa P. et al Diet and chronic atrophic gastritis: a case-control study. J. Natl Cancer Inst. 1986; 76: 621– 7. 50 Magnus H. A. Gastritis. In: F. Avery Jones, ed., Modern Trends in Gastroenterology. Butterworth & Co., London . 1952; 323– 51. 51 Borsch G. Campylobacter pylori: New and renewed insights into gastritis-associated ulcer disease (GAUD). Hepatogastroenterology. 1987; 34: 191– 3. 52 Graham D. Y. Campylobacter pylori and peptic ulcer disease. Gastroenterology 1989; 96 (suppl.): 615– 25. 53 Wyatt J. I., Rathbone B. J., Dixon M. F. & Heatley R. V. Campylobacter pyloridis and acid-induced gastric metaplasia in the pathogenesis of duodenitis. J. Clin. Pathol. 1987; 40: 841– 8. 54 Steer H. W. The gastro-duodenal epithelium in peptic ulceration. J. Pathol. 1985; 146: 355– 62. 55 Shousha S., Parkins R. A. & Bull T. B. Chronic duodenitis with gastric metaplasia: electron microscopic study including comparison with normal. Histopathology 1983; 7: 873– 85. 56 Jenkins D., Goodall A., Gillet F. R. & Scott B. B. Defining duodenitis: quantitative histological study of mucosal responses and their correlations. J. Clin. Pathol. 1985; 38: 1119– 26. 57 Johnston B. J., Reed P. I. & Ali M. H. Campylobacter-like organisms in duodenal and antral endoscopic biopsies: relationship to inflammation. Gut 1986; 27: 1132– 7. 58 Whitehead R., Roca M., Meikle D. D., Skinner J. & Truelove S. C. The histological classification of duodenitis in fibreoptic biopsy specimens. Digestion 1975; 13: 129– 36. 59 James A. H. Gastric epithelium in the duodenum. Gut 1964; 5: 285– 94. 60 Meikle D. D., Taylor K. B., Truelove S. C. & White-head R. Gastritis, duodenitis, and circulating level of gastrin in duodenal ulcer before and after vagotomy. Gut 1976; 17: 719– 28. 61 Isenberg J. K., Selling J. A., Hogan D. L. & Koss M. A. Impaired proximal duodenal mucosal bicarbonate secretion in patients with duodenal ulcer. N. Engl. J. Med. 1987; 361: 374. 62 Carrick J., Lee A., Hazell S., Ralston M. & Daskalopoulos G. Campylobacter pylori, duodenal ulcer, and gastric metaplasia: possible role of functional heterotopic tissue in ulcerogenesis. Gut 1989; 30: 790– 7. 63 Card W. I. & Marks I. N. The relationship between the acid output of the stomach following 'maximal' histamine stimulation and the parietal cell mass. Clin. Sci. 1960; 19: 147– 63. 64 Lanzon-Miller S., Pounder R. E., Hamilton M. R. et al. Twenty-four hour intragastric acidity and plasma gastrin concentration in healthy subjects and patients with duodenal or gastric ulcer or pernicious anemia. Aliment. Pharmacol. Therap. 1987; 1: 225– 37. 65 McGuigan J. E. & Trudeau W. L. Difference in rates of gastrin release in normal persons and patients with duodenal ulcer disease. N. Engl. J. Med. 1973; 288: 64– 6. 66 Walsh J. H., Richardson C. T. & Fordtran J. S. pH dependence of acid secretion and gastrin release in normal and ulcer patients. J. Clin. Invest. 1975; 55: 462– 9. 67 Hirschowitz B. I. Controls of gastric secretion. A roadmap to the choice of treatment for duodenal ulcer. Amer J. Gastroenterol. 1982: 77: 281– 93. 68 Walsh J. & Grossman M. Medical progress: gastrin. N. Engl. J. Med. 1975; 292: 1324– 32. 69 Walsh J. H. Gastrointestinal Hormones. In: L. R. Johnson, ed., Physiology of the Gastrointestinal Tract, 2nd edn. Raven Press, New York . 1987; 182– 95. 70 Fordtran J. S. & Walsh J. H. Gastric acid secretion rate and buffer content of the stomach after eating. J. Clin. Invest. 1973; 52: 645– 57. 71 Johnson L. R. The trophic action of gastrointestinal hormones. Gastroenterology 1976; 70: 278– 88. 72 Fiddian-Green R. G., Bank S., Marks I. N. & Louw J. H. Maximum acid output and position of peptic ulcer. Lancet 1976; ii: 1370– 3. 73 Hobsley M., Whitfield P. F., Faber R. G., Parkin J. V. Hypersecretion and length of history in duodenal ulceration. Lancet 1975; ii: 101– 4. 74 Fiddian-Green R. G. Is peptic ulceration a hormonal disease? Lancet 1977; i: 74– 6. 75 Graham D. Y., Opekun A. R., Lew G. M., Evans D. J. Jr., Klein P. D. & Evans D. G. Ablation of exaggerated meal-stimulated gastrin release in duodenal ulcer patients after clearance of Helicobacter (Campylobacter) pylori infection. Amer. J. Gastroenterol. 1990; 85: 394– 8. 76 McColl K. E. L., Fullarton G. M., El Nujumi A. M., Macdonald A. M., Brown I. L. & Hilditch T. E. Lowered gastrin and gastric acidity after eradication of Campylobacter pylori in duodenal ulcer (Letter). Lancet 1989; ii: 499– 500. 77 Graham D. Y., Opekun A. R., Lew G. M., Klein P. D. & Walsh J. H. Helicobacter pylori infection and gastrin release in duodenal ulcer patients. Gastroenterology 1990; 98: A53. 78 Levi S., Beardshall K., Haddad G., Playford R., Ghosh P. & Calam J. Campylobacter pylori and duodenal ulcers: the gastrin link. Lancet 1989; i: 1167– 8. 79 Tasman-Jones L. T., Morris A., Wiggins P., Lee S. & Forlong C. Ammonia produced by Campylobacter pylori neutralizes H+ moving through gastric mucus. Scand. J. Gastroenterol. 1989; 24: 761– 8. 80 Graham D. Y., Opekun A. R., Klein P. D. & Walsh J. H. Is an increase in antral amine concentration related to the postprandial increase in serum gastrin in man? Gastroenterology 1987; 92: 1412. 81 Lichtenberger L. M., Nelson A. A. & Graziani L. A. Amine trapping: physical explanation for the inhibitory effect of gastric acidity on the postprandial release of gastrin. Gastroenterology 1986; 90: 1223– 31. 82 Alpert L. C., Lew G. M., Michaletz P. A., David L. & Graham D. Y. Comparison of the extent and severity of C. pylori infection between duodenal ulcer patients and age-matched asymptomatic C. pylori-infected subjects. Gastroenterology 1989; 96: A10. 83 Tarpila S., Kekki M., Samloff I. M., Sipponen P. & Siurala M. Morphology and dynamics of the gastric mucosa in duodenal ulcer patients and their first-degree relatives. Hepato-gastroenterology 1983; 30: 198– 201. 84 Sankey E. A., Helliwell P. A. & Dhillon A. P. Immunostaining of antral gastrin cells is quantitatively increased in Helicobacter pylori gastritis. Histopathology 1990; 16: 151– 5. 85 Smith J. T. L., Pounder R. E., Evans D. J., Evans D. G. & Graham D. Y. Inappropriate 24 hour hypergastrinaemia in asymptomatic C. pylori infection. Gastroenterology 1989; 96: A479. 86 Smith J. T. L., Pounder R. E., Nwokolo C. U. et al. Inappropriate hypergastrinaemia in asymptomatic healthy subjects infected with Helicobacter pylori Gut 1990; 31. 87 Villako K., Kekki M., Tamm A. & Savisaar E. Development and progression of chronic gastritis in the antrum and body nucosa: results of long-term follow-up examinations. Ann. Clin. Res. 1986; 18: 121– 3. 88 Kimura K. & Takemoto T. An endoscopic recognition of the atrophic border and its significance in chronic gastritis. Endoscopy 1969; 3: 87– 97. 89 Fiddian-Green R. G., Bank S., Marks I. N. & Louw J. H. Maximum acid output and risk of peptic ulcer. Lancet 1976; ii: 1367– 9. 90 Hsu H. Y., Chang M. H., Chen D. S., Lee C. Y. & Sung J. L. Changing seroepidemiology of hepatitis A virus infection in Taiwan. J. Med. Virol. 1985; 17: 297– 301. 91 Frosner G., Wilers H., Muller R., Schenzle D., Deinhardt F. & Hopken W. Decrease in incidence of hepatitis A infections in Germany. Infection 1978; 6: 259– 60. Citing Literature Volume6, Issue2April 1991Pages 105-113 ReferencesRelatedInformation

Referência(s)