Abstract

The association of duodenal ulcer with blood group O (Aird et al., 1954 ; Roberts, 1957) and with salivary ABH non secretion (Clarke et al., 1956 ; Doll et al., 1961) is firmly estab lished. Thus the family studies of Doll and Kellock (1951), which showed evidence of a hereditary factor in duodenal ulcer, have been substantiated by identification of two of the respon sible genetic loci?namely, those for the genes determining ABO blood group and salivary ABH secretor status. Though the underlying mechanisms whereby these genes influence liability to duodenal ulcer remain somewhat obscure, yet the present paper throws some light on one facet of the problem. Sievers (1959), using the diagnex blue test as a screening procedure for achlorhydria in several hundred patients, found evidence of free acid in 86.1% of group O patients but in only 73.0% of group A patients. Similarly, using the serum-pepsinogen level as an index of gastric secretion, Sievers found a significantly higher mean level in group O than in group A patients. These findings suggest the possibility that the possession of group O phenotype leads to the development of a greater gastric-acid-pepsin secretory-cell mass than that in the other ABO blood-group phenotypes. Further support for this possibility exists in the work of Purohit and Shukla (1960), who related the mean acid output in response to an alcohol test meal to the ABO blood groups, and in the clinical evidence, wherein there is not only decreasing gastric acidity but also a gradual switch from preponderance, relative to the control population, of group O to that of group A, in the following series of conditions?duodenal ulcer, gastric ulcer, gastric cancer, and pernicious anaemia (Koster et al., 1955). While the present study was in progress Niederman et al. (1962), in a survey of 1,000 university intake students, stated that they found no significant differences between the mean serum-pepsinogen levels of the various ABO blood group and salivary ABH secretor phenotypic classes. Nevertheless, the mean level was higher in group O salivary ABH non-secretors than in group A salivary ABH secretors (P<0.2). For the following reasons it is felt that the negative results of Nieder man et al. (1962) cannot be fully accepted. (1) They studied a younger age-group of 16-21 years. It may be that, because the gastric secretory mass was still not fully developed, the potential differences between the phenotypes had not yet become apparent. (2) Comparison of the standard deviations for the data in the different phenotypic classes shows a disturbingly wide range of variation, from 77 to 155. (3) They conducted statistical analysis on material with a skew distribution. Similarly, the work of Sievers (1959) is open to the criticism that it was conducted on patients rather than the healthy popu lation, even though diseases known to influence gastric secretion were excluded.

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