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The salivary ABH and Lewis antigens of Polynesians were measured using a standardised red cell agglutination microplate assay and compared with the red cell defined Lewis phenotypes. Salivary ABH substances were detected in almost all saliva samples tested, with low levels (partial secretion) of ABH substances in the saliva from Le(a+b-) and Le(a+b+) individuals. Salivary Le^b substance was detected in all Le(a-b+) and Le(a+b+) samples and in almost all Le(a+b-) samples. It is evident from the results obtained that Polynesian red cell phenotypes cannot be used to predict the presence or absence of salivary substances. If the presence of a coding secretor gene is presumed responsible for salivary ABH antigens and salivary Le^b antigen expression, then the incidence of a coding secretor gene in Polynesians is 98%. These results indicate that the recessive non-secretor gene is absent or rare in a Polynesian derived gene pool. Two variants of secretor individuals are found among Polynesians, secretors with expression of normal amounts of the product of the secretor gene, similar to Caucasians, and partial secretors with weak expression of the secretor gene products.

Nonacid plasma glycolipids from Lewis-negative individuals of nonsecretor, partial-secretor and secretor phenotypes were prepared and separated by thin-layer chromatography and immunostained with radiolabelled Lewis antibodies. Lewis-positive plasma and intestinal epithelial cell glycolipids from Caucasians representing the four recognized Lewis and secretor combined phenotypes were used as controls. By presenting these purified total glycolipids in a cell-free environment to Lewis antibodies we were able to demonstrate the presence of small amounts of Lewis antigens in Lewis-negative individuals. It is shown that lactotetraosylceramide and extended precursor glycolipids are present in all Le(a-b-) nonsecretors. Le(a) was detected in 1 of the 3 Le(a-b-) nonsecretor plasmas and in the intestinal sample of the same phenotype. Lactotetraosylceramide was absent but H type 1 and Le(b) were both present in all group O Le(a-b-) secretors, and extended H type 1 reactive structures were also found in the partial secretor. These results clearly demonstrate that although the Lewis-negative phenotype exists at the serological level, this phenotype is not an 'all-or-nothing' phenomenon at the chemical level. We also show that in the presence of reduced fucosyltransferase activity, increased elongation of the precursor chain occurs, which allows us to postulate that fucosylation of the precursor prevents or at least markedly reduces chain elongation.

The presence of the rare Lewis phenotype Le(a+b+) is reported in various Polynesian groups, including Maoris, Samoans, Cook Islanders, Nuieans and Tokelau Islanders. The phenotype was found in Polynesians of all blood groups and the frequency was significantly increased in group 0 persons. The phenotype was not significantly associated with H reactivity in group A donors and showed no correlation with age or sex.

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