- Email: [email protected]
No correlation between H. pylori and blood groups in gastric cancer
March 1998
secretion by omeprazole is related to H. pylori status (abstr). Gastroenterology 1997;112:A126. 3. Ruiz B, Correa P, Fontham ET, et al. Antral atrophy, Helicobacter pylori colonization, and gastric pH. Am J Clin Pathol 1996;105:96– 101.
No Correlation Between H. pylori and Blood Groups in Gastric Cancer Dear Sir: We read with much interest the article by Clyne and Drumm reporting the absence of effect of Lewis A and B expression on adherence of Helicobacter pylori to primary human gastric cells.1 Bore´n et al.2 reported the involvement of the Lewis blood group antigen in the attachment of H. pylori to the gastric mucosa and suggested that there is a reduction in the availability of fucosylated receptors in individuals with blood group A and B. Epidemiological studies of patients in the Western world show a higher prevalence of A blood group in gastric adenocarcinoma and O blood group in gastric ulcer.3 These data suggest a possible association between O or A blood groups and H. pylori infection in gastric carcinoma. If H. pylori is a causative agent in gastric carcinoma and uses blood group antigens as receptors, this might be reflected by a distinct distribution of H. pylori infection in relation to the blood group phenotype in patients with gastric carcinoma. To evaluate this hypothesis, we studied the prevalence of H. pylori infection in a series of French patients who underwent gastric resection for gastric adenocarcinoma from 1989 to 1992, before the intensive use of antibiotics for the treatment of H. pylori infection. Criteria for inclusion included tumor without a component of linitis plastica or squamous cell carcinoma, surgical resection specimen including gastric tumor, and nontumoral gastric mucosa. Thirty-eight patients were included in this study. H. pylori infection was detected by pathological analysis on the resected specimens. Detection was performed in the area of the tumor and in normal mucosa by standard pathological examination of H&E-Giemsa–stained paraffin sections. The result of the blood group typing for each patient was not available to the pathologist. In our study, no increased frequency of any of the four blood groups was observed. The four blood groups, A, B, O, and AB, were present in our 38 patients according to the following distribution: A, 17 of 38 (45%); B, 5 of 38 (13%); O, 16 of 17 (42%); and AB, 0 of 38 (0%). This is similar to what was observed in healthy French blood donors. The overall frequency of H. pylori infection was 45% (17 of 38): 41% in A blood group (7 of 17), 60% in B blood group (3 of 5), and 44% in O blood group (7 of 16). As reported by Clyne and Drumm, although our study included a small number of patients, our data do not support the hypothesis that gastric adenocarcinoma occurs more frequently in patients with blood group A. H. pylori infection was noted in 45% of our patients. Previous studies have show that H. pylori infection rate ranges between 60% and 95%. Our lower rate of H. pylori infection could in part be explained by the technique used, which is probably less sensitive than the serological detection method used in the other study.4 Other possible explanations include the presence of atrophic gastritis with diffuse intestinal metaplasia (in 6 patients of the series), in which no H. pylori infection is usually found, and epidemiological factors, as our study included only French patients. However, comparison between the different blood groups remains valid. In conclusion, our clinical data suggest as human research data1 that in patients with gastric adenocarcinoma, the susceptibility to H. pylori infection seems not to be influenced by the host blood group antigen.
CORRESPONDENCE
621
The potential role of H. pylori infection in gastric cancer carcinogenesis warrants further investigation. MARC POCARD YVES PANIS PATRICE VALLEUR Department of Surgery DIDIER SARAZIN Department of Pathology Lariboisie`re Hospital Paris, France 1. Clyne M, Drumm B. Absence of effect of Lewis A and Lewis B expression on adherence of Helicobacter pylori to human gastric cells. Gastroenterology 1997;113:72–80. 2. Bore´n T, Falk P, Roth KA, et al. Attachment of Helicobacter pylori to human gastric epithelium mediated by blood group antigens. Science 1993;262:1892–1895. 3. 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;106:221–229. 4. Lee WJ, Lin JT, Shun CT, et al. Comparison between resectable gastric adenocarcinomas seropositive and seronegative for H pylori. Br J Surg 1995;82:802–805.
Reply. We thank Dr. Pocard and colleagues for their interest in our paper. Despite the reported association between blood group antigens and peptic ulcer disease, it is very unlikely that a blood group antigen functions as the sole mucosal receptor for H. pylori. As is shown in our study, blood group antigen expression on the gastric mucosa varies greatly between individuals and may not even reflect the blood group antigens on the red blood cells of the same individual. Despite great variation in mucosal blood group antigen expression, up to 80% of children are infected with H. pylori by 10 years of age in developing countries. It is likely that multiple bacterial adhesins and several mucosal receptors are involved in the mediation of H. pylori adhesion to the gastric mucosa. It is still not clear how important adhesion to the gastric mucosa is, because relatively small numbers of organisms are seen adhering to the mucosa in comparison to the overall number of H. pylori present on the mucosa. It must also be stressed that the majority of people who become infected with H. pylori do not develop either peptic ulcer disease or gastric cancer. Therefore, there are likely to be host and/or environmental cofactors that are essential for these conditions to develop in association with H. pylori infection. Identification of these cofactors is essential if we are to identify subpopulations at risk for the development of gastric cancer and ulcer disease. MARGUERITE CLYNE BRENDAN DRUMM Department of Paediatrics University College Dublin The Children’s Research Center Our Lady’s Hospital for Sick Children Dublin, Ireland
Exocrine Pancreatic Insufficiency in Celiac Disease Dear Sir: We read with interest the recent article by Carroccio et al.1 in which they showed in a cross-sectional design that 37% of children with newly diagnosed celiac disease had a reduced pancreatic secretory capacity. In a longitudinal assessment, they also showed evidence that
secretion by omeprazole is related to H. pylori status (abstr). Gastroenterology 1997;112:A126. 3. Ruiz B, Correa P, Fontham ET, et al. Antral atrophy, Helicobacter pylori colonization, and gastric pH. Am J Clin Pathol 1996;105:96– 101.
No Correlation Between H. pylori and Blood Groups in Gastric Cancer Dear Sir: We read with much interest the article by Clyne and Drumm reporting the absence of effect of Lewis A and B expression on adherence of Helicobacter pylori to primary human gastric cells.1 Bore´n et al.2 reported the involvement of the Lewis blood group antigen in the attachment of H. pylori to the gastric mucosa and suggested that there is a reduction in the availability of fucosylated receptors in individuals with blood group A and B. Epidemiological studies of patients in the Western world show a higher prevalence of A blood group in gastric adenocarcinoma and O blood group in gastric ulcer.3 These data suggest a possible association between O or A blood groups and H. pylori infection in gastric carcinoma. If H. pylori is a causative agent in gastric carcinoma and uses blood group antigens as receptors, this might be reflected by a distinct distribution of H. pylori infection in relation to the blood group phenotype in patients with gastric carcinoma. To evaluate this hypothesis, we studied the prevalence of H. pylori infection in a series of French patients who underwent gastric resection for gastric adenocarcinoma from 1989 to 1992, before the intensive use of antibiotics for the treatment of H. pylori infection. Criteria for inclusion included tumor without a component of linitis plastica or squamous cell carcinoma, surgical resection specimen including gastric tumor, and nontumoral gastric mucosa. Thirty-eight patients were included in this study. H. pylori infection was detected by pathological analysis on the resected specimens. Detection was performed in the area of the tumor and in normal mucosa by standard pathological examination of H&E-Giemsa–stained paraffin sections. The result of the blood group typing for each patient was not available to the pathologist. In our study, no increased frequency of any of the four blood groups was observed. The four blood groups, A, B, O, and AB, were present in our 38 patients according to the following distribution: A, 17 of 38 (45%); B, 5 of 38 (13%); O, 16 of 17 (42%); and AB, 0 of 38 (0%). This is similar to what was observed in healthy French blood donors. The overall frequency of H. pylori infection was 45% (17 of 38): 41% in A blood group (7 of 17), 60% in B blood group (3 of 5), and 44% in O blood group (7 of 16). As reported by Clyne and Drumm, although our study included a small number of patients, our data do not support the hypothesis that gastric adenocarcinoma occurs more frequently in patients with blood group A. H. pylori infection was noted in 45% of our patients. Previous studies have show that H. pylori infection rate ranges between 60% and 95%. Our lower rate of H. pylori infection could in part be explained by the technique used, which is probably less sensitive than the serological detection method used in the other study.4 Other possible explanations include the presence of atrophic gastritis with diffuse intestinal metaplasia (in 6 patients of the series), in which no H. pylori infection is usually found, and epidemiological factors, as our study included only French patients. However, comparison between the different blood groups remains valid. In conclusion, our clinical data suggest as human research data1 that in patients with gastric adenocarcinoma, the susceptibility to H. pylori infection seems not to be influenced by the host blood group antigen.
CORRESPONDENCE
621
The potential role of H. pylori infection in gastric cancer carcinogenesis warrants further investigation. MARC POCARD YVES PANIS PATRICE VALLEUR Department of Surgery DIDIER SARAZIN Department of Pathology Lariboisie`re Hospital Paris, France 1. Clyne M, Drumm B. Absence of effect of Lewis A and Lewis B expression on adherence of Helicobacter pylori to human gastric cells. Gastroenterology 1997;113:72–80. 2. Bore´n T, Falk P, Roth KA, et al. Attachment of Helicobacter pylori to human gastric epithelium mediated by blood group antigens. Science 1993;262:1892–1895. 3. 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;106:221–229. 4. Lee WJ, Lin JT, Shun CT, et al. Comparison between resectable gastric adenocarcinomas seropositive and seronegative for H pylori. Br J Surg 1995;82:802–805.
Reply. We thank Dr. Pocard and colleagues for their interest in our paper. Despite the reported association between blood group antigens and peptic ulcer disease, it is very unlikely that a blood group antigen functions as the sole mucosal receptor for H. pylori. As is shown in our study, blood group antigen expression on the gastric mucosa varies greatly between individuals and may not even reflect the blood group antigens on the red blood cells of the same individual. Despite great variation in mucosal blood group antigen expression, up to 80% of children are infected with H. pylori by 10 years of age in developing countries. It is likely that multiple bacterial adhesins and several mucosal receptors are involved in the mediation of H. pylori adhesion to the gastric mucosa. It is still not clear how important adhesion to the gastric mucosa is, because relatively small numbers of organisms are seen adhering to the mucosa in comparison to the overall number of H. pylori present on the mucosa. It must also be stressed that the majority of people who become infected with H. pylori do not develop either peptic ulcer disease or gastric cancer. Therefore, there are likely to be host and/or environmental cofactors that are essential for these conditions to develop in association with H. pylori infection. Identification of these cofactors is essential if we are to identify subpopulations at risk for the development of gastric cancer and ulcer disease. MARGUERITE CLYNE BRENDAN DRUMM Department of Paediatrics University College Dublin The Children’s Research Center Our Lady’s Hospital for Sick Children Dublin, Ireland
Exocrine Pancreatic Insufficiency in Celiac Disease Dear Sir: We read with interest the recent article by Carroccio et al.1 in which they showed in a cross-sectional design that 37% of children with newly diagnosed celiac disease had a reduced pancreatic secretory capacity. In a longitudinal assessment, they also showed evidence that