We confirmed associations between PTPN22 SNPs with selected autoantibody sub-phenotypes and with malar rash in independently associated SNPs. We avoided inter-laboratory variation by only considering data from OMRF testing laboratory. When analyzing subgroups of SLE cases based upon clinical criteria, there is usually a loss of power due to the smaller sample size relative to all SLE. Alternatively, we can increase statistical power by analyzing more homogenous groups when clinical phenotype is more strongly associated compared to SLE. Because of these issues using P-values alone is unreliable; therefore we look for an increasing magnitude of the OR. In this report EA patients positive for IgG anti-cardiolipin antibodies (aCL IgG) were enriched for the risk allele (A) and effect sizes increased (OR = 1.30 for SLE cases vs. controls, OR = 1.62 for case-only). This was especially true for those with moderate to high anticardiolipin antibodies (aCL IgG>40) as well as a subset of APS patients who also were aCL positive (see above). This effect was not detected in patients with low titer aCL or presence of only lupus anticoagulant. ACL
