GRUPOS SANGUINEOS ABO, LEWIS, STATUS SECRETOR E INFECÇAO PELO HELICOBACTER PYLORI

(especial para SIIC © Derechos reservados)
Os grupos sangüíneos ABO, Lewis e o status secretor têm sido avaliados, isoladamente ou em conjunto, como marcadores de suscetibilidade à infecção pelo Helicobacter pylori e algumas doenças a ele relacionadas
demattos9.jpg Autor:
De mattos, luiz carlos
Columnista Experto de SIIC

Institución:
Biotechnology Research Centre Auckland University of Technology Scott Laboratory Building Auckland, New Zealand


Artículos publicados por De mattos, luiz carlos
Recepción del artículo
3 de Mayo, 2004
Aprobación
15 de Septiembre, 2004
Primera edición
4 de Noviembre, 2004
Segunda edición, ampliada y corregida
7 de Junio, 2021

Resumen
Os grupos sangüíneos ABO, Lewis e o status secretor têm sido avaliados, isoladamente ou em conjunto, como marcadores de suscetibilidade à infecção pelo Helicobacter pylori e algumas doenças a ele relacionadas. Os resultados das análises envolvendo indivíduos normais e pacientes com diferentes doenças gastroduodenais, bem como os dados experimentais, são discordantes. Se por um lado há demonstrações que reforçam a importância dos antígenos ABH-Lewis na aderência do H. pylori à mucosa gástrica dos indivíduos do grupo O, por outro, nem todos os estudos epidemiológicos suportam estas proposições e portanto, persistem as divergências entre os dados clínicos e os laboratoriais. Como os antígenos ABH-Lewis do trato gastrointestinal apresentam um perfil polimórfico que pode ser diferenciado daquele observado nos eritrócitos, parece oportuno que outros aspectos relacionados à expressão destes glicoconjugados devem ser avaliados para dar maior suporte à interpretação dos resultados observados na presença ou ausência de infecção e nas doenças relacionadas ao H. pylori. Isso poderá contribuir para a compreensão da importância biológica e evolutiva desses marcadores genéticos nas doenças infecciosas.

Palabras clave
Grupos sangüíneos; sistema ABO; sistema Lewis


Artículo completo

(castellano)
Extensión:  +/-4.71 páginas impresas en papel A4
Exclusivo para suscriptores/assinantes

Abstract
The ABO and Lewis blood groups and the secretor status have been available, either in isolation or jointly, as markers for Helicobacter pylori infection susceptibility or infection by some related diseases. Results from analysis involving apparently normal individuals and patients suffering from varying gastroduodenal diseases, as well as experimental data, are contradictory. If on one hand there are demonstrations that reinforce the importance of ABH-Lewis antigens in the adherence of H. pylori to the gastric mucous membrane of O blood group individuals, on the other hand, not all epidemiological studies support these premises and thus, divergences between clinical and laboratory data remain. As the ABH-Lewis antigens of the gastroduodenal tract present a polymorphic profile which can be discriminated from those observed in red blood cells, it seems sensible that other aspects related to the expression of these glycoconjugates should be assessed. This will give greater support to the interpretation of the results in the presence or absence of infection and in diseases associated to H. pylori and may contribute to the understanding of the biological and evolutionary importance of these genetic markers in infectious diseases.

Key words
Blood groups, ABO, Lewis, secretor phenotypes, secretor status, Helicobacter pylori


Clasificación en siicsalud
Artículos originales > Expertos de Iberoamérica >
página   www.siicsalud.com/des/expertocompleto.php/

Especialidades
Principal: Genética Humana, Inmunología
Relacionadas: Epidemiología, Gastroenterología, Hematología, Infectología



Comprar este artículo
Extensión: 4.71 páginas impresas en papel A4

file05.gif (1491 bytes) Artículos seleccionados para su compra



Enviar correspondencia a:
de Mattos, Luiz Carlos
Patrocinio y reconocimiento:
Agradecimentos: O autor agradece o apoio recebido da Faculdade de Medicina de São José do Rio Preto (FAMERP) e da Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES - BEX 1542-03-6).
Bibliografía del artículo
  1. Mourant AE, Kopec AC; Domaniewska-Sobczak K. Blood groups and diseases. A study of associations of diseases with blood groups and others polymorphisms. London: Oxford University Press, 1978. 328p.
  2. Henry SM, Samuelsson BE. ABO polymorphisms and their putative biological relationships with disease. In: King MJ, E. Human blood cells: consequences of genetic polymorphisms and variations. London: Imperial College Press, 2000. p15-103.
  3. Oriol R. ABO, Hh, Lewis and Secretion: serology, genetics and tissue distribution. In: Cartron JP, Rouger P. Blood Cell Biochemistry: molecular basis of human blood group antigens. New York: Plenum, 1995. p37-73.
  4. Clarke CA, Edwards JW, Haddock DRW et al. ABO blood groups and secretor character in duodenal ulcer. Brit Med J, 1956;2:725:731.
  5. Clark CA; Evand DAP; McConnell RB et al. Secretion of blood groups antigens and peptic ulcer. Brit Med J. 1959;1:603-607.
  6. Mourant AE; Kopec AC; Domaniewska-Sobczak K. The distribution of the human blood groups and others polymorphisms. London: Oxford University Press, 1976. 140p.
  7. Yip SP. Sequence variation at the human ABO locus. Ann Hum Genet. 2002;66:1-27.
  8. Svensson L; Petersson A; Henry SM. Secretor genotyping for A385T, G428A, C571T, C628T, 685delTGG, G849A, and other mutations from single PCR. Transfusion. 2000;40:856-860.
  9. Grahn A; Elmgren LA; Svensson L et al. Determination of Lewis FUT3 gene mutations by PCR using sequence-specific primers enables efficient genotyping of clinical samples. Hum Mutat. 2000;18(4):359-359.
  10. Warren JR. Unidentified curved bacilli on gastric epithelium in active chronic gastritis. Lancet. 1983;4:1273-1275.
  11. NIH Consensus Conference. Helicobacter pylori in peptic ulcer. JAMA. 1994;272(1):65-69.
  12. Pounder RE; Ng D. The prevalence of Helicobacter pylori infection in different countries. Alimentary Pharmacology & Therapeutics. 1995;9:33-40.
  13. Feldman RA. Epidemiologic observations and open questions about disease and infection caused by Helicobacter pylori. In: Achtman M, Sauerbaum S. Helicobacter pylori: molecular and cell biology. Wymondham, UK: Horizon Scientific Press, 2001.p29-51.
  14. Sauerbaum S; Michetti P. Helicobacter pylori infection. N Engl J Med. 2002;347(15):1175-1186.
  15. Borén T, Falk P, Roth KA, et al. Attachment of Helicobacter pylori to human gastric epithelium mediated by blood group antigens. Science, 1993;262:1892-5.
  16. Ilver D, Arnqvist A, Ögren J, et al. Helicobacter pylori adhesion binding fucosulated histo-blood group antigens revealed by retagging. Science, 1998;279(5349):373-7.
  17. Alkout AM; Blackwell CC; Weir DM et al. Isolation of cell surface component of Helicobacter pylori that binds H type 2, Lewis a and Lewis B antigens. Gastroenterology. 1997;112:1179-1187.
  18. Hook-Nikanne J; Sistonen P; Kosunen TU. Effect of ABO blood group and secretor status on the frequency of Helicobacter pylori antibodies. Scan J Gastroenterol. 1990;25:815-818.
  19. Loffeld RJF; Stobberingh E. Helicobacter pylori and ABO blood groups. J Clin Pathol. 1991;44:516-517.
  20. Robertson MS; Cade JF; Savoia HF et al. Helicobacter pylori infection in the Australian community: current prevalence and lack of association with ABO blood groups. Intern Med J. 2003;33(4):163-167.
  21. Dickey W; Collins JSA; Watson RGP et al. Secretor status and Helicobacter pylori infection are independent risk factors for gastroduodenal disease. Gut. 1993;34:351-353.
  22. Niv Y; Fraser G; Delpre G et al. Helicobacter pylori infection and blood groups. Am J Gastroenterol. 1996;91(1):101-104.
  23. Keller R; Dinkel KC; Christl SU et al. Interrelation between ABH blood group O, Lewis (B) blood group antigen, Helicobacter pylori infection, and occurrence of peptic ulcer. Z Gastroenterol. 2002;40(5):273-276.
  24. Wu TC; Chen LK; Hwang SJ. Seroprevalence of Helicobacter pylori om school-aged Chinese Taipei City and relationship between ABO blood groups. World J Gastroenterol. 2003;9(8):1752-1755.
  25. Henriksson K; Uribe A; Sandstedt B et al. Helicobacter pylori infection, ABO blood group, and effect of misoprostol on gastroduodenal mucosa in NSAID treated patients with rheumatoid arthritis. Dig Dis Sci. 1993;38:1688-1696.
  26. Carneiro F; Amado M; Lago P et al. Helicobacter pylori infection and blood groups. Am J Gastroenterol. 1996;91(12):2646-2647.
  27. Lin CW; Chang YS; Wu SC et al. Helicobacter pylori in gastric biopsies of taiwanese patients with gastroduodenal diseases. Jpn J Med Sci Biol. 1998;51(1):13-23.
  28. Heneghan MA; Moran AP; Feeley KM et al. Effect of host Lewis and ABO blood antigen expression on Helicobacter pylori colonization density and consequent inflammatory response. FEMS Immunol Med Microbiol. 1998;20(4):257- 266.
  29. Alkout AM; Blackwell CC; Weir DM. Increased inflammatory responses of persons of blood group O to Helicobacter pylori. J Inf Dis. 2000;181:1364-1369.
  30. Mattos LC; Cintra JR; Sanchez FE et al. ABO, Lewis, secretor and non-secretor phenotypes in patients infect or uninfected by the Helicobacter pylori bacillus. Sao Paulo Med J. 2002;120(2):55-58.
  31. Cintra JR; Caetano A; Silva RCMA et al. Grupos sangüíneos ABO e gene CagA do Helicobacter pylori em pacientes submetidos a endoscopia digestiva alta. HB Cientifica. 2003;(Suplemento Especial - IX ECIF):26.
  32. Henry SM. Molecular diversity in the biosynthesis of GI tract glycoconjugates. A blood group related chart microorganism receptors. Transf Clin Biol. 2001;8:226-230.
  33. Henry SM. Review: phenotyping for Lewis and secretor histo-blood group antigens. Immunohematology. 1999;12(2):51-61.

 
 
 
 
 
 
 
 
 
 
 
 
Está expresamente prohibida la redistribución y la redifusión de todo o parte de los contenidos de la Sociedad Iberoamericana de Información Científica (SIIC) S.A. sin previo y expreso consentimiento de SIIC.
ua31618
Inicio/Home

Copyright siicsalud © 1997-2024 ISSN siicsalud: 1667-9008