Subtypes in SLE Sample Clauses

Subtypes in SLE. The goal of creating the ACR criteria was to develop a “unified” classification system, but the result of the effort is actually the antithesis of a unified definition. ACR-classified SLE and physician-diagnosed SLE has a very wide variety of manifestations, presentations, and severity. Given that the etiology and outcomes of SLE are largely unknown, one possible way to make progress towards a revised disease definition is to identify homogenous groups of patients. Xxxxxx (1966) firmly espoused the idea that SLE consists of clinical subsets. Other authors have stated beliefs that there are SLE subsets based on research findings or clinical experience (Xxxxx-Xxxx et al., 1995; Petri and Magder, 2004; To and Petri, 2005). Formal investigation of subtypes. To and Petri (2005) used K-means cluster analysis to identify three autoantibody clusters in the Xxxxxxx Lupus Cohort. They described a cluster with a high percentage of members with anti-Sm and anti-RNP autoantibodies relative to the other clusters, a cluster with a high or relatively high percentags of anti-dsDNA, anti-Ro, and anti-La autoantibodies, and a cluster with high percentages of anti-dsDNA and anticardiolipin autoantibodies and relatively high lupus anticoagulant. Jurencak et al. (2009) described three antibody-based clusters of pediatric-onset SLE patients; a cluster with a high proportion of dsDNA antibodies, a cluster with high proportions of anti-dsDNA, antichromatin, antiribosamal P, anti-U1RNP, anti-Sm, anti-Ro, and anti-La antibodies, and a cluster with a high propor- tion of anti-dsDNA, anti-RNP, and anti-Sm antibodies. Patients in the cluster with low percentages of all autoantibodies except for anti-DNA was more likely to be Caucasion than other clusters.
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