The incidence of HL—A3 among 94 patients with a diagnosis of multiple sclerosis (MS) was significantly higher than for 871 normal persons. In addition, some increase in Te58 and decrease in HL—A2 and Te60 frequencies was noted. The well‐known higher incidence of MS among Caucasians than among Orientals is paralleled by the higher incidence of HL—A3 and Te58 among Caucasians and a lower incidence of Te60.

We studied the quantitative and qualitative characteristics of lipoprotein(a) [Lp(a)] as a function of apolipoprotein(a) [apo(a)] phenotypes in 152 patients (123 males, 29 females) undergoing maintenance hemodialysis (HD) with or without diabetes mellitus (DM), in 101 patients with diabetes mellitus without hemodialysis (58 males, 43 females), and in 421 normal controls (333 males, 88 females). Serum Lp(a) levels were significantly (P < 0.01) higher in patients than in controls (26.2 +/- 18.3 mg/dl in HD with DM, 26.4 +/- 22.0 mg/dl in HD without DM, 27.1 +/- 27.3 mg/dl in DM without HD, and 14.9 +/- 13.7 mg/dl in controls, respectively). Apo(a) phenotyping was performed by a sensitive, high resolution technique using SDS-agarose/gradient (3 to 6%) PAGE. In normal controls, the molecular weights of apo(a) isoforms were inversely correlated with plasma Lp(a) levels, and the same tendency was found in patients who were undergoing hemodialysis and/or who had diabetes mellitus. We assumed the differences in apo(a) phenotypes detectable with our method reflected consecutive differences in molecular weights of apo(a). The results of an analysis of covariance and a least square means comparison indicated that the regression lines between serum Lp(a) levels [log Lp(a)] and apo(a) phenotypes in patient groups were significantly (P < 0.01) elevated for every apo(a) phenotype, as compared to the regression line of the control group. Even after the low molecular weight apo(a) phenotypes (A1-A8) were omitted, the same tendency was observed. However, no differences were observed between the patient groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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SUMMARY Systemic lupus erythematosus (SLE) has shown associations with the major histocompatibility complex (MHC) class II DR antigens and class III complement components C2 and C4 in previous studies. The primary susceptibility locus has been difficult to identify, however, on account of linkage disequilibrium within the MHC. We have studied C4A and C4B distributions in 63 Caucasoid, 75 Chinese and 51 Japanese SLE patients. All three populations showed a statistically significant increase in C4A*Q0 (null) alleles when compared with 323 ethnically matched controls. We conclude that complete or partial deficiency of C4A is a genetic determinant of SLE common to these three ethnically distinct populations.