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. May not be reproduced in any form without permission from the publisher, except fair uses permitted under 28 Ana Maria Abreu Velez and Michael S. Howard

established that a polymorphism in the STAT4 gene (which is associated with lupus
susceptibility) is preferentially associated with lupus disease severe symptoms, including
renal malfunction [86]. The STAT4 finding may allow physicians to determine which patients
are at risk of severe disease, and may lead to the development of new treatments for these
patients. Scientists have also identified a gene that may confer susceptibility to lupus. They
have shown that having an alternative form of the gene Ly108 may impair the bodys ability
to keep self-destructive B cells under control [87]. The Ly108 gene is part of a gene family
(SLAM) that has been linked to a lupus-like disease in mice [87].

Biomarkers
Biomarkers represent another significant area of lupus research. Biomarkers are defined
as molecules that reflect a specific biological or pathological process, a consequence of a
process, or a response to a therapeutic intervention. Patients with SLE and metabolic
syndrome had significantly raised serum uric acid, C-reactive protein (CRP), lipid
hydroperoxides, and protein oxidation, in contradistinction to patients with SLE without
metabolic syndrome. Lipid hydroperoxides were correlated with CRP, whereas protein
oxidation was associated with waist circumference and uric acid. There was a positive
association between serum Complement C3 and C4 and glucose, as well as between C3 and
CRP [88]. Researchers have identified anti-double-stranded DNA antibodies and
Complement C3a (both of which can be identified utilizing blood tests) as biomarkers for
flares, in that they can predict that a flare will occur. They also showed that moderate doses of
prednisone can prevent flares in people possessing these biomarkers [89].

The Disease Process

Because lupus presentations differ between patients and the disease is characterized by
autoimmunity in variable organ systems, the initial presentation in a given patient can be
difficult to detect. Many symptoms may increase and decrease over time, often delaying the
diagnosis and initiation of therapy. Many researchers have reported that autoantibodies are
important in the diagnosis and classification of SLE; however, whether these autoantibodies
specifically correlate with changes in disease activity in individual patients is controversial
[51]. One group of researchers reported the association between changes in SLE global
disease activity and renal activity, vis-a-vis changes in multiple autoantibodies and cell
adhesion molecules [51]. The researchers utilized stored sera, collected during clinic visits
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from each of 49 SLE patients (91% female, 59% African-American, 31% Caucasian, 10%
other ethnicity, 38% under 30 years, 41% between 30-44 years, and 21% 45-63 years); the
sera were then were analyzed [51]. Specific patient clinic visits were further selected to
include one visit with proteinuria and one or two without proteinuria for each patient. Global
disease activity was measured by the Physician's Global Assessment (PGA), and SLEDAI
(SLE Disease Activity Index modified to exclude anti-dsDNA and complement); renal
activity assessed via urine protein (by urine dipstick) and renal activity score [51]. Sera were
assayed for anti-Complement C1q, anti-chromatin, anti-dsDNA, anti-ribosomal P protein,

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