We report on two siblings who developed severe neonatal alloimmune thrombocytopenia (NAIT) due to an alloantibody against a labile component or components of the HPA-3a (Baka) antigen. The antibody reacted only with fresh, unfixed platelets by the solid-phase red cell adherence test, immunofluorescence test and mixed passive haemagglutination test. In the latter method, weakly fixed platelets also gave a weak positive reaction. Monoclonal-antibody-specific immobilization of platelet antigens and immunoblotting tests gave negative results. Our findings may possibly help to explain why in some cases of NAIT no platelet-specific antibody is demonstrable in tests with fixed or solubilized platelets.

The frequencies of six platelet-specific antigens among Chinese in Taiwan are reported, which have not previously been well studied. HPA-1a (PlA1) antigen was positive in all 1100 Chinese tested. HPA-4b (Yukb) antigen was positive in all 100 persons tested. HPA-2b (Ko(a), Sib(a)) antigen was positive in 9 percent of 100 persons tested, HPA-3a (Bak(a)) in 77 percent, and NAKa in 96 percent. HPA-4a (Yuk(a)) antigen occurred in 0 percent in this study but is estimated to be present in 0.5 percent of the Taiwanese population.

Lewis phenotyping of 487 blood samples from Chinese newborn infants and young children, revealed that 50% of cord cells were Le(a-b+) and 50% Le(a-b-). The weak Le^b antigen of Le(a-b+) cord cells is most likely produced by the newborn infant rather than of maternal origin and it appears that these infants eventually develop by way of an intermediate Le(a+b+) stage into the adult Le(a-b+) phenotype. Most infants with Le(a-b-) cord cells, but not all, appear to develop through a transitional Le(a+b-) stage, into Le (a+b+) by about 1 month of age, most likely continuing as such into adulthood. This development of Le(a-b-) cord cells into the adult Le(a+b+) phenotype is postulated to be the result of the weak secretor gene Se(i). Those infants with Le(a-b-) cord cells that do not convert to Le(a+b+) during the first month of life, most likely remain as such into adulthood. The blood of 120 adult voluntary blood donors, used as controls, reconfirmed adult Chinese phenotypic frequencies of approximately 70% Le(a-b+),22% Le(a+b+) and 8% Le(a-b-).

Lewis phenotyping of 487 blood samples from Chinese newborn infants and young children, revealed that 50% of cord cells were Le(a-b+) and 50% Le(a-b-). The weak Leb antigen of Le(a-b+) cord cells is most likely produced by the newborn infant rather than of maternal origin and it appears that these infants eventually develop by way of an intermediate Le(a+b+) stage into the adult Le(a-b+) phenotype. Most infants with Le(a-b-) cord cells, but not all, appear to develop through a transitional Le(a+b-) stage, into Le (a+b+) by about 1 month of age, most likely continuing as such into adulthood. This development of Le(a-b-) cord cells into the adult Le(a+b+) phenotype is postulated to be the result of the weak secretor gene Se omega. Those infants with Le(a-b-) cord cells that do not convert to Le(a+b+) during the first month of life, most likely remain as such into adulthood. The blood of 120 adult voluntary blood donors, used as controls, reconfirmed adult Chinese phenotypic frequencies of approximately 70% Le(a-b+), 22% Le(a+b+) and 8% Le(a-b-).

The clinical significance and correlation of anti‐native DNA antibodies and immune complex level were evaluated in the present study. Anti‐DNA antibodies were measured by radioimmunoassay using I125‐labeled DNA and immune complex was screened using the polyethylene glycol precipitation method. Anti‐DNA antibodies of higher than 40 units/ml were found exclusively in patients with systemic lupus erythematosus, especially in patients with lupus nephritis. The level of anti‐DNA antibodies was found to be directly correlated with the disease activity. Higher amounts of circulating immune complexes could be found in patients with systemic lupus erythematosus, vasculitis, and other diseases. The patients with more active lupus erythematosus also tended to have higher amounts of immune complexes, but the correlation was not so definite. There was also no reliable correlation between anti‐DNA activity and immune complex level.