For inclusion, patients must have had a diagnosis of diabetes mellitus, moderate or severe infection, ESR and CRP values within 72 hours of admission, either advanced imaging (MRI or single-positron emission computed tomography/computed tomography [SPECT/CT]) or bone biopsy during admission and must not have had comorbidities that could affect ESR and CRP, such as autoimmune disorders.
We conducted multivariable logistic regression analysis adjusted for age, sex, randomization, body mass index, MMSE, ASA status, infection/autoimmune disease/malignoma and types of surgery to determine associations between CRP with POD and post-operative NCD, respectively.
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.
However, CRP may also mediate tissue damage in various human diseases like atherosclerosis, acute myocardial infarction, dilated cardiomyopathy, stroke, and potentially autoimmune disease.
Biomarkers to differentiate infection from disease activity are scarce, but the combination of procalcitonine and C-reactive protein seems to have higher specificity and sensibility to identify infections in patients with AIDs.
In this paper, we will first summarize the findings on immune dysfunction in schizophrenia, including (1) genetic, prenatal, and premorbid immune risk factors and (2) immune markers across the clinical course of the disorder, including cytokines; C-reactive protein; immune cells; antibodies, autoantibodies and comorbid autoimmune disorders; complement; oxidative stress; imaging of neuroinflammation; infections; and clinical trials of anti-inflammatory agents and immunotherapy.
Additionally, an RF association with tender joints and elevated CRP levels suggests that autoantibodies are a valid intermediate marker of RA-related autoimmunity in this cohort.
We selected 46 variants: (1) eight variants known to alter circulating levels of inflammatory proteins, including those in the IL18, IL1RN, IL6R, MIF, PAI1 (also known as SERPINE1) and CRP genes; and (2) 38 variants known to predispose to autoimmune diseases, including type 1 diabetes.
The pentraxin C-reactive protein (CRP), an innate immune system opsonin which binds nuclear debris and apoptotic bodies, may protect against autoimmunity.
Comparison of the main clinical and laboratory findings suggestive of a systemic autoimmune disease (e.g., acute-phase reactants, constitutional symptoms, other autoimmune diseases associated with CP) between the HLA-DRB1*03-positive and the HLA-DRB1*03-negative patients showed that the former group had significantly higher levels of C-reactive protein (P = 0.045) at disease onset, although this difference was not statistically significant after correction for multiple tests (P(corr) = 0.369).
Here, we analyzed the levels of circulating nucleosomes, caspases, and C-reactive protein in sera of 244 individuals with various autoimmune diseases (155 with autoimmune hepatic disorders, 25 with ANCA-associated vasculitis, and 64 with various connective tissue diseases), and 32 healthy controls.
Protective molecules--C-reactive protein (CRP), serum amyloid P (SAP), pentraxin3 (PTX3), mannose-binding lectin (MBL), and apolipoprotein A1 (Apo A1), and their autoantibodies: prevalence and clinical significance in autoimmunity.
We provide a description of recent studies, which suggest that CRP acts through FcgammaR to reduce inflammation and protect from certain autoimmune diseases.