Mild elevations of CRP have been seen in chronic autoimmune diseases like systemic lupus erythematosus (SLE), and CRP has been linked to an increased risk of cardiovascular events.
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.
Multiple genes may be involved and identifying them will provide an insight into pathways regulating CRP expression, highlight potential cardiovascular disease and SLE candidates and improve the ability of basal CRP to predict cardiovascular risk.
Among clinical parameters, concentrations of C3/C4 were lower and erythrocyte sedimentation rate, C-reactive protein, anti-double-stranded DNA (anti-dsDNA) antibodies, and SLE Disease Activity Index-2000 (SLEDAI-2K) were higher in LN patients than in SLE patients without LN.
In comparison with non-infectious SLE patients (387.9±261.6/μL), CD4+T cells count decreased significantly in infectious SLE patients (217.8±150.4/μL) (P<0.05), and it was negatively correlated with infection-related indicators including PCT (r=-0.573, P=0.041) and CRP (r=-0.596, P=0.032) levels.
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.
The purpose of this study was to characterize pharmacokinetics (PK) of PF-04236921, a novel anti-interleukin-6 monoclonal antibody, and its pharmacokinetic/pharmacodynamic (PK/PD) relationship on serum C-reactive protein (CRP) in healthy volunteers and patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and Crohn's disease (CD).
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.
Factors, such as enlarged liver, spleen and lymph nodes, digestive system involvement, low hemoglobin, leukopenia, CRP, decreased albumin, anti-dsDNA antibody, glucocorticoids, and cyclophosphamide, were independent risk factors for noninfectious fever in SLE.
NLR was positively correlated with the SLE Disease Activity Index 2000 (SLEDAI-2K), erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), whereas it was not correlated with C3 or C4.
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.