ABO Blood Group Phenotypes Research Articles

Prevalence of the Rhesus-negative phenotype in Caucasian patients with small-cell lung cancer (SCLC).

We report that the Rhesus (Rh)-negative phenotype is more prevalent in patients with small-cell lung cancer (SCLC) than in the normal Caucasian population (SCLC: 25% Rh-negative vs. 15% expected, p less than 0.0001). This finding has been validated for a Central and a Northern European population (Switzerland and UK). In contrast, the Rh-negative phenotype is no more frequent in non-small-cell lung cancer patients or in heavy smokers with coronary heart disease than in the general population. There was a normal distribution of the ABO blood group phenotype in all patients studied. Whilst the significance of this observation is unclear, we hypothesize that a genetic predisposition to the development of SCLC may be linked to a hitherto unidentified gene on chromosome 1p near the Rh locus. Our observation may perhaps allow further progress to be made in understanding genetic mechanisms of SCLC carcinogenesis.

Glycosphingolipids of Human Large Intestine: Detailed Structural Characterization with Special Reference to Blood Group Compounds and Bacterial Receptor Structures1

Non-acid glycosphingolipid expression was studied in the large intestines from four individuals with the A1Le(a-b+), BLe(a-b+), and OLe(a-b+) blood group phenotypes. In the A1Le(a-b+) case, specimens were taken from the ascending and sigmoid parts of the large intestine in order to compare the expression of glycolipids in the proximal and distal regions of the intestine. In one blood group OLe(a-b+) individual, epithelial cells were isolated from the residual stroma to compare the glycolipid compositions in these two tissue compartments. GlcCer, GalCer, LacCer, Gb3Cer, and Gb4Cer were the major compounds in all three individuals, as shown by mass spectrometry, proton NMR spectroscopy, and degradation studies. The Lea-5 glycolipid was the major complex blood group glycolipid in all individuals, except in the proximal ascending part of the large intestine of the A1Le(a-b+) case, in which the Leb-6 glycolipid was predominant. There were trace amounts of blood group ABH glycolipids, in agreement with the ABO blood group phenotypes of the donors, Lewis antigens with more than six sugar residues in the carbohydrate chain, and blood group X and Y glycolipid antigens. The epithelial cells were dominated by monoglycosylceramides and the Lea-5 glycolipid, while only trace amounts of di-, tri-, and tetraglycosylceramide structures were present. No reactivity was seen in the epithelial cell fraction with Gal alpha 1-4Gal specific Escherichia coli, anti-Pk, or anti-P antibodies, indicating the absence of the glycolipid-borne Gal alpha 1-4Gal sequence in human large intestinal epithelial cells.

Cerebral malaria and erythrocyte resetting

There is increasing evidence that the ABO blood group phenotypes modulates Plasmodium falciparum rosetting and may influence the clinical manifestation of severe malaria. Whether blood group phenotypes are associated with risk of severe falciparum malaria in Odisha, we analyzed 343 adult malaria patients. The results showed high prevalence of blood group B in both mild (n = 110) and severe malaria (cerebral malaria [CM]; n = 130 and non-cerebral severe malaria [NCSM]; n = 103) categories among the non-O group and while type O is significantly associated with protection against CM, patients with type A and B group had increased risk for developing CM. Further, the strength of association for B group (p = < 0.0001) was high and has double the risk of (OR = 5.0) of developing CM compared to blood group A (OR = 2.5). Such findings may probably be due to strain specific blood group preferences of P. falciparum and high prevalence of B group. However, the ABO blood group distribution of mild malaria was comparable with that of the NCSM group of patients. The lack of association of ABO phenotypes with NCSM is evidence for the hypothesis that the underlying pathogenesis cascades are different in CM and NCSM clinical presentations.

ABO blood groups in hematologic malignancies

This article examines the genetic predisposition of individuals to lymphoma and leukemia with regard to the ABO blood groups. Blood samples from 558 patients suffering from various forms of lymphoma and leukemia were collected and typed for ABO blood groups. The ABO blood group phenotype frequencies of lymphoma patients were similar to those in control samples. Among leukemia patients, a significant increase in the frequency of the A2 phenotype was found in chronic lymphocytic leukemia. Possible mechanisms underlying the predisposition of individuals with the A2 blood group to chronic lymphocytic leukemia suggested by these preliminary results are discussed.

Association of the Lewis blood-group phenotype with recurrent urinary tract infections in women.

Blood-group antigens are found on the surface of urothelial cells and may affect bacterial adherence and thereby the susceptibility to urinary tract infection. We determined the ABO, P, and Lewis blood-group phenotypes in 49 white women with histories of recurrent urinary tract infections and compared them with those found in 49 healthy control women without recurrent urinary tract infections. There was no significant difference between the two groups in the distribution of the ABO or P phenotypes. The distribution of Lewis blood-group phenotypes among control women was similar to that in the general population: secretor phenotype (Le(a-b+)), 74 percent; nonsecretor phenotype (Le(a+b-)), 18 percent; and recessive phenotype (Le(a-b-)), 8 percent. The following distribution was noted among the women with recurrent urinary tract infections: secretor phenotype, 45 percent; nonsecretor phenotype, 29 percent; and recessive phenotype, 26 percent (P = 0.002). When the women with nonsecretor and recessive phenotypes were combined and considered collectively, the odds ratio (an estimate of relative risk of recurrent urinary tract infection) for those without the secretor phenotype was 3.4 (95 percent confidence interval, 1.5 to 7.9). We conclude that there is an increased frequency of the Lewis blood-group nonsecretor (Le(a+b-] and recessive (Le(a-b-] phenotypes among women with recurrent urinary tract infections.

ABO genes are differentially distributed in socio-economic groups in England.

No direct evidence is available concerning what average genetic differences, if any, characterize the segments of socially stratified human populations, although theoretical considerations suggest that genetic differentiation within such populations is to be expected. We have now analysed two large samples of data from blood donors in England to test whether the distributions of the ABO and Rhesus blood group phenotypes are random with respect to socio-economic groups as determined by occupational classification. We have found that in both native and migrant sections of the populations of two widely separated regions (south-west England and part of Yorkshire) and in both sexes, the A phenotype is highly significantly more, and the O phenotype significantly less, frequent than expected in social classes I and II, while the converse is seen in social classes III-V. An individual of the A phenotype has thus about 15% greater probability than chance would dictate of being placed in classes I and II. The distribution of the Rh+ and Rh- phenotypes does not differ significantly between classes. It seems unlikely that this nonrandom distribution of the ABO phenotypes among socio-economic groups results from sampling, historical or migrational effects and we conclude that the observed association is likely to result from pleiotropic effects of the ABO alleles (or genes closely linked to them) on attributes influencing occupational type, social mobility and social class.

Alpha-L-fucosyltransferases in human serum from donors of different ABO, secretor and Lewis blood-group phenotypes.

The presence of α‐l‐fucosyltransferases in human serum of different ABO, secretor and Lewis blood‐group phenotypes was investigated with guanosine diphosphate fucose as the sugar donor and low‐molecular‐weight oligosaccharides, or a macromolecular glycoprotein, as acceptors. In contrast to the α‐2‐l‐fucosyltransferases in human milk, submaxillary glands and stomach mucosa that occur only in ABH secretors, an enzyme that transfers l‐fucose to the C‐2 position of non‐reducing β‐galactosyl residues was found in the serum of all normal ABO donors irrespective of their ABH secretor‐nonsecretor status. The only sera in which the α‐2‐l‐fucosyltransferase was not demonstrable were three examples of the blood group Bombay Oh phenotype and one example of the Bh phenotype. An a‐3‐l‐fucosyltransferase that conveyed L‐fucose to the C‐3 position in N‐acetyl‐d‐glucosamine or d‐glucose occurred in all the sera examined including those from donors of the Bombay Oh and Bh phenotypes. a‐4‐l‐Fucosyltransferase activity was virtually absent from the sera, irrespective of the Lewis blood group of the donors.

The genetic characteristics of South-Moravian twins.

A total of 400 DZ and 76 MZ twin pairs were studied for: maternal age, in which no significant differences were found; birth order, which was significantly higher in DZ twins; weight at birth; frequency of ABO blood-group phenotypes, where no significant differences were found; and, lastly, frequency of twinning in relatives, where, there was significantly higher occurrence, namely in siblings of probands.

The influence of abo blood groups, secretor status and fat ingestion on serum alkaline phosphatase

Two experiments have been performed in an attempt to clarify the relationship between liver and intestine alkaline phosphatase iso-enzymes and ABO blood group and secretor phenotype. In the first experiment 6 subjects, each of phenotype O secretor, O non-secretor, A secretor and A non-secretor, were studied on two occasions. On the first occasion a fasting sample was followed by ingestion of a non-fat meal, and blood was taken 2 and 4 h thereafter. A similar procedure was followed on the second occasion except that a fatty meal was ingested. The serum samples had determinations performed of total alkaline phosphatase activity and percentage inhibition thereof by l-phenylalanine which gives a measure of the intestinal contribution. The sera were also all subjected to starch gel electrophoresis. A second intestinal electrophoretic band was found in all sera from O secretors and in none of the sera from the other 3 phenotypes. Males had significantly higher mean fasting alkaline phosphatase levels than females. There was a significant increase in total alkaline phosphatase activity 4 h after a fatty meal in O secretors, as compared with a non-fat meal. O secretor subjects had significantly higher values for percentage inhibition of alkaline phosphatase activity by l-phenylalanine than did the other 3 phenotypes, indicating a larger intestinal contribution to total serum alkaline phosphatase activity. The percentage l-phenylalanine inhibition did not change after either non-fatty or after fatty food. In order to assess the last point a second experiment was performed on a further 12 O secretor subjects. Blood was drawn fasting and 7 sol1 2 h following a synthetic fat meal. Total serum alkaline phosphatase, percentage l-phenylalanine inhibition and percentage urea inhibition (which gives a measure of liver and bone iso-enzyme contributions to total activity) were determined. A considerable variation was observed between individual O secretors, the effect of fat in elevating total serum alkaline phosphatase being much more marked in some individuals than in others. The results again indicated that the proportional contribution of the intestinal iso-enzyme remained constant. This last observation suggests that the mechanism of release of alkaline phosphatase iso-enzymes from parenchymal cell into serum is influenced in a similar manner in both liver and intestine by the O and secretor genes.

HEREDITARY ASPECTS OF DUODENAL ULCERATION: SERUM-PEPSINOGEN LEVEL IN RELATION TO ABO BLOOD GROUPS AND SALIVARY ABH SECRETOR STATUS.

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.