Recommendations to adjust citrate concentration for blood coagulation specimens with high hematocrit values are based on indirect experimental studies and not direct studies of patient samples with high hematocrit values. We compared the effect of adjusted and non-adjusted citrate concentrations on coagulation test results in samples from 28 patients with high hematocrit values (55%-72% [0.55-0.72]). Prothrombin time (PT) and activated partial thromboplastin time (aPTT) results from nonadjusted and adjusted samples were statistically different and exponentially increased with increasing hematocrit values. Results for fibrinogen, factor VIII, and protein C activity were statistically different and increased linearly with increasing hematocrit values; however, the difference was not as clinically significant. The protein C antigen value increased with increasing hematocrit values but was not significant. The effects on PT and aPTT are due to a dilutional effect of plasma and an interference effect of the higher final citrate concentration on the clotting test result. For patients with high hematocrit values, citrate concentrations must be adjusted for accurate results.

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Primary Sjögren's syndrome is an autoimmune disease characterized clinically by dryness of the eyes and mouth. The use of different classification criteria for primary Sjögren's syndrome has led to dramatically different estimates of prevalence and incidence. Despite this, several genetic and environmental factors are thought to play a role in the susceptibility to primary Sjögren's syndrome, as is the current conceptual formulation of the pathogenesis of many other autoimmune maladies. Primary Sjögren's syndrome appears a complicated polygenic disorder with many genes interacting with environmental factors. Similar to many other polygenic autoimmune rheumatic diseases, human leukocyte antigen associations have been reported and confirmed. Additionally, other non-human leukocyte antigen candidate genes have been reported to reveal association with primary Sjögren's syndrome, but, in general, these effects are not confirmed. The authors review the human leukocyte antigen and non-human leukocyte antigen genetic associations herewith, knowing that new technologies are providing access to the entire genome for association studies. No doubt a much more comprehensive description of the genetics of this disorder will soon emerge.

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