When an SLE patient presents with pre-existing arthritis and suddenly develops asymmetric oligo- or large-joint swelling and pain with elevated CRP levels and low disease activity, joint infections should be considered.
The results show that in SLE patients, the finding of a relative increase in Con A-bound serum alpha 1-acid glycoprotein is a more sensitive indicator of intercurrent infection than is the finding of increased levels of CRP.
C-reactive protein (CRP) is an acute-phase protein with therapeutic activity in mouse models of systemic lupus erythematosus and other inflammatory and autoimmune diseases.
Conclusions The ratio of ESR:CRP may provide diagnostic value beyond individual ESR and CRP levels in distinguishing flare vs infection in SLE patients presenting with fever.
Increased s-BAFF levels in SLE patients are associated with the acute-phase responses, CRP and haemoglobin, but probably not dependent on BAFF genotype or expression.
It is not yet known how this genetic polymorphism mediates its effect on CRP expression, and it probably is not a systemic lupus erythematosus susceptibility factor.
In this study, we investigated the presence of anti-chloride intracellular channel 2 (anti-CLIC2) and anti-high mobility group box 1 (anti-HMGB1) autoantibodies in SLE patients (n = 43) versus healthy controls ([HCs] n = 43), and their association with serological parameters (antinuclear antibody [ANA], anti-double-stranded DNA [anti-dsDNA], and C-reactive protein [CRP]) and disease activity using Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) score (active or inactive).
Interferon (IFN)-α is typically elevated during SLE flares, and inhibits hepatocyte production of the pentraxin 'C-reactive protein' (CRP), partly explaining the poor correlation between CRP levels and SLE disease activity.
Initial CRP level was not significantly associated with regular corticosteroid or immunosuppressant use in SLEs patients during a bacterial infection episode, and CRP level was not dose-dependently related to daily corticosteroid use.
Patients with CNS infections also had a larger prednisone dose at the time of symptom onset, larger cumulative dosages over the preceding year, lower SLE Disease Activity Index (SLEDAI) scores, higher rate of nephritis, lower albumin levels, higher C-reactive protein (CRP) levels, higher 24-h-urine protein levels, higher cerebrospinal fluid (CSF) white blood cell levels, and lower protein and glucose levels than those with NPSLE.
Interestingly, the combination of nCD64 index, CRP, WBC, C3 and C4 improved significantly the diagnostic potential of SLE infection (AUC 0.783 (interquartile range 0.672, 0.871), p < 0.001; sensitivity 85.29% specificity 62.50%).
Our study was done to confirm the reported association in an independent population-based case-control cohort, and also to investigate the influence of 3 additional CRP tagSNP (-861, -390, +90) on SLE risk and serum CRP concentrations.
Erythrocyte sedimentation rate and C-reactive protein were elevated, an autoimmune workup was consistent with a new diagnosis of systemic lupus erythematosus and triple-positive antiphospholipid antibodies.
Elevated levels of Sema5A were correlated positively with 24-h proteinuria excretion (r = 0·558, P < 0·0001), SLE disease activity index (SLEDAI) (r = 0·278, P = 0·0006) and C-reactive protein (CRP) (r = 0·266, P = 0·002), but negatively with planet (PLT) (r = -0·294, P = 0·0003) and complement 3 (C3) (r = -0·287, P = 0·0004) in SLE patients.