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ABO blood group, secretor status and detection of Helicobacter pylori among patients with gastric or duodenal ulcers

Published online by Cambridge University Press:  15 May 2009

A. Mentis ,
C. C. Blackwell ,
D. M. Weir ,
C. Spiliadis ,
A. Dailianas  and
N. Skandalis
A. Mentis
Affiliation:
Hellenic Institute Pasteur, Athens
C. C. Blackwell*
Affiliation:
Department of Medical Microbiology, The Medical School, University of Edinburgh, Edinburgh
D. M. Weir
Affiliation:
Department of Medical Microbiology, The Medical School, University of Edinburgh, Edinburgh
C. Spiliadis
Affiliation:
Department of Gastroenterology, General Hospital of Athens, Athens
A. Dailianas
Affiliation:
Department of Gastroenterology, General Hospital of Athens, Athens
N. Skandalis
Affiliation:
Department of Gastroenterology, General Hospital of Athens, Athens
*
* Corresponding author.
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Patients (454) referred for gastroscopy to the General Hospital of Athens were examined to determine (1) if non-secretors were over-represented among patients with ulcers and (2) is there was an association with ABO blood group or secretor status and carriage of Helicobacter pylori.

Compared with the local population, among patients with either gastric ulcer (51) or duodenal ulcer (96) there was a significant increase in the proportion of those who were blood group O (P < 0·025); however, there were no significant differences in the proportions of non-secretors. H. pylori was identified in 62 % of the 454 patients: 59·5 % of those without evidence of ulcers; 62·5 % of those with gastric ulcer; 88% of those with duodenal ulcer (P < 0·0005). These bacteria were cultured more often and in higher numbers from patients with duodenal ulcer (P < 0·025). There was no association between ABO blood group and prevalence of H. pylori. The prevalence of H. pylori among non-secretors with gastric ulcer (12·5%) was significantly lower than that for non-secretors with duodenal ulcer (100%) (P < 0·0005). This was not observed for secretors.

Type
Special Article
Information
Epidemiology & Infection , Volume 106 , Issue 2 , April 1991 , pp. 221 - 229
Copyright
Copyright © Cambridge University Press 1991

References

REFERENCES

1.Mourant, AE, Kopec, AC, Domaniewska-Sobezak, K. Blood groups and diseases. Oxford: Oxford University Press, 1978.Google Scholar
2.Blackwell, CC. The role of ABO blood groups and secretor status in host defences. FEMS Microbiol Immunol 1989; 47: 341–50.CrossRefGoogle Scholar
3.Blackwell, CC. Genetic susceptibility to infectious agents. Proc Roy Coll Physic (Edinburgh) 1989; 19: 129–38.Google Scholar
4.Haverkorn, MJ, Goslings, WRO. Streptococci, ABO blood groups and secretor status. Am J Hum Genet 1969; 21: 360–75.Google ScholarPubMed
5.Blackwell, CC, Weir, DM, James, VS et al. , Secretor status, smoking and carriage of Neisseria meningitidis. Epidemiol Infect 1990; 104: 203–9.CrossRefGoogle ScholarPubMed
6.Burford-Mason, AP, Welsby, JCP, Willoughby, JMT. Oral carriage of Candida albicans, ABO blood group and secretor status in healthy individuals. J Med Vet Mycol 1988; 26: 49–56.CrossRefGoogle Scholar
7.Blackwell, CC, Aly, FZM, James, VS et al. , Blood group, secretor status and oral carriage of Candida and other fungal species among patients with diabetes mellitus. Diabet Res 1989; 12: 101–4.Google Scholar
8.Andersen, J, Lauritzen, E. Blood groups and diabetes mellitus. Diabetes 1960; 9: 20–4.CrossRefGoogle ScholarPubMed
9.Blackwell, CC, James, VS, Weir, DM et al. , Secretor status of patients with insulin dependent or non-insulin dependent diabetes mellitus. Br Med J 1987; 295: 1024–5.CrossRefGoogle ScholarPubMed
10.Collier, A, Patrick, AW, Toft, AD, Blackwell, CC, James, VS, Weir, DM. Increased prevalence of non-secretors in patients with Graves' disease – evidence for an infective aetiology. Br Med J 1988; 296: 1162.CrossRefGoogle ScholarPubMed
11.Shinebaum, R, Blackwell, CC, Forster, PJG, Hurst, NP, Weir, DM, Nuki, G. Non-secretion of ABO blood group antigens as a host susceptibility factor in the spondylarthropathies. Br Med J 1987; 294: 208–10.CrossRefGoogle Scholar
12.Buck, GE. Campylobacter pylori and gastric duodenal disease. Clin Microbiol Rev 1990; 3: 1–12.CrossRefGoogle Scholar
13.Pateraki, E, Mentis, A, Spiliadis, C et al. , Seroepidemiology of Helicobacter pylori infection in Greece. FEMS Microbiol Immunol 1990; 64: 129–36.Google Scholar
14.Merikas, G, Christakopoulos, P, Petropoulos, E. Distribution of ABO blood group in patients with ulcer disease; its relationship to gastroduodenal bleeding. Am J Digest Dis n.s. 1986; 11: 790–5.CrossRefGoogle Scholar
15.Hirszfeld, L, Hirszfeld, H. Serological differences between the blood of different races. The result of researches on the Macedonian front. Lancet 1919; ii: 675—9.CrossRefGoogle Scholar
16.Langman, MJS, Doll, R. ABO blood group and secretor status in relation to clinical characteristics of peptic ulcers. Gut 1965; 6: 270–3.CrossRefGoogle ScholarPubMed
17.McCarthy, DM. Smoking and ulcers – time to quit. N Engl J Med 1984; 311: 726–8.CrossRefGoogle ScholarPubMed
18.Rauws, EIAJ, Longenberg, W, Howthoff, HJ, Zanen, HC, Tytgat, GNJ. Campylobacter pyrloridis-associated chronic antral gastritis. Gastroenterol 1988; 94: 33–40.CrossRefGoogle Scholar
19.Lomberg, H, Cedergren, B, Leffler, H, Nilsson, B, Carlstrom, AS, Svanborg-Eden, C. Influence of blood group on the availability of receptors for attachment of uropathogenic Escherichia coli. Infect Immun 1986; 51: 919–26.CrossRefGoogle ScholarPubMed
20.May, SJ, Blackwell, CC, Weir, DM. Lewisa blood group antigen, a receptor for Candida species. FEMS Microbiol Immunol 1989; 47: 407–10.CrossRefGoogle Scholar
21.Darwazeh, AMG, Lamey, P-J, Samaranayake, LP et al. , The relationship between colonisation of secretor status and in vitro adhesion of Candida albicans to buccal epithelial cells from diabetics. J Med Microbiol 1990; 33: 43–50.CrossRefGoogle ScholarPubMed
22.Lark, D. Protein-carbohydrate interactions in biological systems. London: Academic Press, 1986.Google Scholar
23.Kallenius, G, Mollby, R, Svensson, SB et al. , The pk antigen as receptor for the haemagglutinin of pyelonephritic Escherichia coli,. FEMS Microbiol Lett 1980; 7: 297–302.CrossRefGoogle Scholar
24.Miller, LH, Mason, SJ, Dvorak, JA, McGinniss, MH, Rothman, IK. Erythrocyte receptors for (Plasmodium knowlesi) malaria: Duffy blood group determinants. Science 1975; 189: 561–3.CrossRefGoogle ScholarPubMed
25.Race, RR, Sanger, R. Blood groups in man, 6th ed., Oxford: Blackwell Scientific Publications, 1975.Google Scholar
26.Marcus, DM, Cass, LE. Glycosphingolipids with Lewis blood group activity: uptake by human erythrocytes. Science 1969; 164: 553–5.CrossRefGoogle ScholarPubMed
27.Ogata, M, Nakasoro, I, Iwasaki, M. Two familial cases of dissociation of saliva Lea levels and erythrocytes Lewis type. Hum Hered 1988; 38: 303–7.CrossRefGoogle Scholar
28.Oriol, R, Danilous, J, Hawkins, BR. A new genetic model proposing that the Se gene is a structural gene closely linked to the H gene. Am J Hum Genet 1981; 33: 421–31.Google Scholar
29.Rahat, A, Stewart, J, Blackwell, CC, Weir, DM. Semi-quantitative determination of H type 1 and type 2 antigens on buccal epithelial cells and in saliva of secretors and non-secretors. Vox Sang 1990; 59: 101–5.Google ScholarPubMed
30.Lingwood, CA, Law, H, Pellizzari, A, Sherman, P, Drumm, B. Gastric glycerolipid as a receptor for Campylobacter pylori. Lancet 1989; ii: 238–41.CrossRefGoogle Scholar
31.Evans, DG, Evans, DJ, Moulds, JJ, Graham, DY. N-acetyl-neuraminyl-lactose-binding fibrillar hemagglutinin of Campylobacter pylori: a putative colonization factor antigen. Infect Immun 1989; 56: 2896–906.CrossRefGoogle Scholar
32.Nakazawa, T, Ishibashi, M, Konishi, H, Takemoto, T, Shigeeda, M, Kochiyama, T. Haemagglutination activity of Campylobacter pylori. Infect Immun 1989; 57: 989–91.CrossRefGoogle ScholarPubMed
33.Mentis, A, Tzouvelekis, L, Spiliadis, C, Blackwell, CC, Weir, DM. Inhibition of Helicobacter pylori haemagglutination activity by human salivary mucin. FEMS Microbiol Immunol 1990; 64: 125–8.Google Scholar