PATHBASE
A database of blood group correlations to common diseases



Total number of records: 145 Matching records: 1

Ulcer, H. pylori


Description:In the early1950's it was first discovered that Type O seemed to predominate over the other types in the occurrence of all types of stomach ulcers at a rate of approximately two to one. These findings have been reproduced so many times--over 25 studies in the last 20 years alone--with the same consistent result (Type O getting more ulcers than the other blood types) that the conclusions are virtually unquestionable.

In several studies, non-secretors of ABO substances have been found to have a significantly higher rate of gastric and duodenal ulcers. Because of the increased prevalence of ulcers among non-secretors, it should come as no surprise that researchers have suggested that secretor status might influence bacterial colonization density or the ability of H. pylori to attach to gastroduodenal cells.

Because non-secretors are limited in their ability to secrete blood type antigens into the mucus secretions of their digestive tract, it has been proposed that they be at a competitive disadvantage from preventing H. pylori attachment. In other words, a non-secretor's lack of antigens in mucosal fluids might indirectly contribute to colonization by H. pylori.

In a simplified sense, when specific antigens are free-floating in the mucus, it probably acts to bind up some of the H. pylori before it can contact and attach to your tissues. In essence, being a secretor provides you with an ability to put some biological decoys or metabolic false targets (in the United States Navy, false targets are referred to as "chaff," and they are deployed as a part of the counter measures against incoming missiles or torpedoes) out into your secretions. Non-secretors, as a general rule, also show a significantly higher proportion of the H. pylori-seronegative subjects and a lower IgG (H. pylori immunoglobulin G (IgG) antibody) immune response to H. pylori antigens as compared with the individuals of the secretor phenotype.

This might indicate that non-secretors are unable to mount an aggressive immune response against this organism in comparison with their secretor brethren. Evidence does suggest that both bacterial colonization and the ensuing inflammatory response are influenced, at least in part, by the ability to secrete blood group antigens. This relationship is strongest among Blood Type O non-secretors.

The genetics of the ABH secretor/non-secretor system interact to alter an individual's risk for ulcers. In several studies, non-secretors of ABH substances have been found to have a significantly higher rate of duodenal and peptic ulcers.

In fact the Copenhagen study found that the lifetime prevalence of peptic ulcer in men who were ABH non-secretors was 15% (statistically 15% of ABH non-secretors will have an ulcer at some point in their lives). And, the attributable risk of peptic ulcer in men who were Lewis (a + b-) or ABH non-secretors, with blood group O or A phenotypes was 37%.

Overall, the relative risk of gastroduodenal disease for non-secretors compared with secretors is 1.9 (95% confidence interval). Duodenal ulcer patients are more likely to be non-secretors, and being a non-secretor acts as a multiplicative risk factor with the gene for hyperpepsinogenemia I to impact the risk of duodenal ulcer.

Because of the increased prevalence of ulcers among non-secretors researchers have suggested that secretor status might influence bacterial colonization density or the ability of H. pylori to attach to gastroduodenal cells. With regards to the overall interaction with H. pylori infection, non-secretor status is generally considered to be a separate independent risk factor for gastroduodenal disease in addition to H. pylori infection; however, there is more to this story, and, in fact some interesting interactions between secretor status, Lewis genetics, and H. pylori.

Because non-secretors are limited in their ability to secrete the Lewis (b) blood group antigen into the mucus secretions of their digestive tract, it has been proposed that they be at a competitive disadvantage from preventing H. pylori attachment. In fact, the Lewis (b) antigens have been found to act as somewhat of a preferential target for H. pylori attachment. Thus, lack of Lewis (b) in mucosal fluids of ABH non secretors might indirectly contribute to colonization by H. pylori.

In a simplified sense, when the Lewis (b) antigen is free floating in the mucus, it probably acts to bind up some of the H. pylori before it can contact and attach to host tissue. In essence, being an ABH secretor provides an ability to put some biological decoys or metabolic chaff out into the gastric secretions that is very specific for H. pylori. Also, in ABH non-secretors the immune response against H. pylori appears to be lower and H. pylori appears to attach with higher aggressiveness and cause more inflammation.

Individuals with Lewis (a+b-) ABH non-secretor phenotype also show a significantly higher proportion of the H. pylori-seronegative subjects and a lower IgG (H. pylori immunoglobulin G (IgG) antibody) immune response to H. pylori antigens as compared with the individuals of Lewis (a-b+)/secretor phenotype.

Evidence also indicates that 100% of non-secretors with duodenal ulcers culture positive for H. pylori infection. However, among non-secretors with gastric ulcer, H. pylori is found in only about 12.5% of the cases. This is not observed among secretors, who are nearly equally likely to have H. pylori infection in either gastric or duodenal ulcer. (52)
References:1. Suadicani P, Hein HO, Gyntelberg F. Genetic and life-style determinants of peptic ulcer. A study of 3387 men aged 54 to 74 years: The Copenhagen Male Study. Scand J Gastroenterol 1999 Jan;34(1):12-7

2. Hein HO, Suadicani P, Gyntelberg F. Genetic markers for stomach ulcer. A study of 3,387 men aged 54-74 years from The Copenhagen Male Study. Ugeskr Laeger 1998 Aug 24;160(35):5045-46

3. Dickey W, Collins JS, Watson RG, et al. Secretor status and Helicobacter pylori infection are independent risk factors for gastroduodenal disease. Gut 1993 Mar;34(3):351-3

4. Sumii K, Inbe A, Uemura N, et al. Multiplicative effect of hyperpepsinogenemia I and non-secretor status on the risk of duodenal ulcer in siblings. Gastroenterol Jpn 1990 Apr;25(2):157-61

5. Dickey W, Collins JS, Watson RG, et al. Secretor status and Helicobacter pylori infection are independent risk factors for gastroduodenal disease. Gut 1993 Mar;34(3):351-3

6. Oberhuber G, Kranz A, Dejaco C, et al. Blood groups Lewis(b) and ABH expression in gastric mucosa: lack of inter-relation with Helicobacter pylori colonisation and occurrence of gastric MALT lymphoma. Gut 1997 Jul;41(1):37-42

7. Su B, Hellstrom PM, Rubio C, et al. Type I Helicobacter pylori shows Lewis(b)-independent adherence to gastric cells requiring de novo protein synthesis in both host and bacteria. J Infect Dis 1998 Nov;178(5):1379-90

8. Alkout AM, Blackwell CC, Weir DM, et al. Isolation of a cell surface component of Helicobacter pylori that binds H type 2, Lewis(a), and Lewis(b) antigens. Gastroenterology 1997 Apr;112(4):1179-87

9. Klaamas K, Kurtenkov O, Ellamaa M, Wadstrom T. The Helicobacter pylori seroprevalence in blood donors related to Lewis (a,b) histo-blood group phenotype. Eur J Gastroenterol Hepatol 1997 Apr;9(4):367-70

10. Mentis A, Blackwell CC, Weir DM, et al. ABO blood group, secretor status and detection of Helicobacter pylori among patients with gastric or duodenal ulcers. Epidemiol Infect 1991 Apr;106(2):221-9





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PathType is a searchable database of blood group and disease associations, clinical correlates and citations.
By Peter D'Adamo. Copyright 2001-2011.