C-reactive Protein In Rheumatoid Arthritis Research Articles

Peripheral CD4+ /CD8+ T cell composition distinct from healthy individuals is shared by ankylosing spondylitis and rheumatoid arthritis.

Ankylosing spondylitis (AS) and rheumatoid arthritis (RA) are chronic inflammatory joint diseases, linking to the alterations of immune cells. We attempted to assess whether the alterations in the composition of CD4+ /CD8+ T cells are different between AS and RA and identify the characteristic cells between male and female patients. The proportions of CD3+ or double positive T cells, 6 CD4+ T subsets and 9 CD8+ T cell subsets were detected by flow cytometry and compared in 30 healthy individuals, 42 AS patients and 45 RA patients. The differentially altered cells were individually analyzed for associations with disease activity parameters. In addition, their proportions were compared between different genders in the 3 groups. The proportions of CD4+ T cells, naive CD4+ T cells and central memory CD4+ T cells were lower in AS patients (P = 0.001, P = 0.002 and P = 0.007, respectively) and RA patients (P = 0.032, P < 0.001 and P = 0.016, respectively), but the proportion of effector memory ones was higher when compared with healthy populations (both P < 0.001), as were the decrease of naive/central memory CD8+ T cells in AS (P = 0.003 and P = 0.016, respectively) and RA (P < 0.001 and P = 0.006, respectively), and the increased tendency of terminally differentiated CD8+ T cells. However, these above-mentioned cells, regulatory T (Treg) cells and CD8+ T cells with different CD127 expressions between AS and RA were similar in proportion. Furthermore, naive CD4+ T cells were positively associated with C-reactive protein (CRP) in AS, whereas CD4+ T cells and terminally differentiated CD8+ T of RA patients were associated with CRP in RA. The gender-related alterations predominantly displayed the overexpressions of Treg cells and naive CD8+ T cells in female patients with AS and RA, respectively. AS patients and RA patients have some similar peripheral CD4+ /CD8+ T cell subsets but are distinct from healthy individuals, which may contribute to disease severity. Females are respectively characterized by the up-regulation of Treg cells and naive CD8+ T cells in AS patients and RA patients. The study offers an in-depth understanding of the role of T cell subsets in the similarities of the disorders and helps us to monitor disease changes and may offer a theoretical basis of developing novel therapies against common targets.

Methods for assessment of disease activity of polymyalgia rheumatica

Polymyalgia rheumatica (PMR) is the second most frequent inflammatory rheumatic disease in old age. Remission and recurrence are frequently used as endpoints in clinical trials; however, there is as yet no international consensus on the definition of these states, which limits the comparability of published studies. The PMR activity score (PMR-AS) is the only composite score specifically developed for PMR, which together with remission is used to define low, middle and high disease activity. In recent studies the PMR-AS was often used and low disease activity was established as endpoint. The most important limitation of the PMR-AS is the potential influence of the individual variables by comorbidities. The value of C‑reactive protein (CRP) and the erythrocyte sedimentation rate (ESR) are of restricted value in studies using drugs that influence the interleukin 6 (IL-6) axis. In these cases, calprotectin and osteopontin are promising alternative biomarkers, as they have already been shown to reflect disease activity independently of CRP in rheumatoid arthritis. Furthermore, imaging modalities including sonography, magnetic resonance imaging and fluorodeoxyglucose (FDG) positron emission tomography could also be helpful in monitoring disease activity; however, these techniques must first be validated in further studies. The PMR impact scale (PMR-IS) is acomposite score to assess the impact of PMR on the patients; however, it has not yet been used in clinical studies. The development of additional patient reported outcomes (PRO) for PMR and the definition of standardized criteria for documentation of remission and recurrence are important questions in the future research agenda for PMR.

The prevalence of thyroid dysfunction and thyroid autoantibodies among patients with rheumatoid arthritis

Background and objective: Rheumatoid arthritis is a chronic and inflammatory autoimmune systemic disease of unknown cause that may affect many tissues and organs. Rheumatoid arthritis and thyroid disorders may occur in the patient simultaneously. The main antigens that give rise to thyroid antibodies are thyroglobulin, thyroid peroxidase, anti-cyclic citrullinated protein, and thyroid hormone receptor. This study aimed to determine the frequency of thyroid dysfunction and seroprevalence of anti-thyroid antibody in patients with rheumatoid arthritis and its association with inflammatory marker C-reactive protein. Methods: A cross-sectional study was performed at Rizgari Teaching Hospital and CMC private hospital, Erbil, Iraq. From 15 January to15 October 2020. A hundred patients with rheumatoid arthritis were included in the study, in addition to 70 controls. The serum levels of biomarkers were determined by the chemiluminescent immunoassay method. Results: Patients with rheumatoid arthritis had 6% of thyroid dysfunctions. Regarding the prevalence of thyroid autoantibodies in patients with rheumatoid arthritis, 9% had positive anti-thyroid peroxidase, 13% had positive anti-thyroglobulin, and 6% were positive for a combination of both. There was a statistically significant (P &lt;0.001) high level of serum anti-cyclic citrullinated protein and C-reactive protein in rheumatoid arthritis than in control. Euthyroid profiles were 73% inrheumatoid arthritis patients and 82.9% in control. Conclusion: The study delineated the co-existence of thyroid disorder in rheumatoid arthritis patients with or without autoimmune origin, besides the increased prevalence of auto-thyroid antibody among rheumatoid arthritis with thyroid dysfunction.

Association between severity of periodontitis and rheumatoid arthritis

ABSTRACT Many studies have shown a correlation between periodontitis and rheumatoid arthritis, and both areinflammatory diseases that cause damage to their surrounding tissues and have similar characteristics. Periodontitiscan cause an increased erythrocyte sedimentation rate and C-reactive protein in rheumatoid arthritis (RA) patientsand can cause systemic inflammation in RA. This review aims to assess the association between the severity ofperiodontitis and rheumatoid arthritis. The method of this study is scoping review. PRISMA method is used as aguideline for searching and selecting articles using four electronic databases with criteria (P: Population)periodontitis and rheumatoid arthritis patients, (C: Concept) Relationship between periodontitis and rheumatoidarthritis, (C: Context) periodontal medicine. Articles selection based on the inclusion criteria: journals published in2011-2020, research methods using case-control, cohort, or RCT, subjects diagnosed with RA and Periodontitis, andsubjects age at least 18 years old and exclusion criteria are subjects were pregnant and issues diagnosed with otherdiseases. Six articles included one cohort study and five case-control studies. The result showed a positivecorrelation between periodontitis and RA. There is an association between the severity of periodontitis andrheumatoid arthritisKEYWORDS: Periodontitis, periodontal disease, rheumatoid arthritis

The Relationship Between Serum Pentraxine 3 Levels and Hematological Markers in Patients With Rheumatoid Arthritis.

This study aims to investigate the association of pentraxin 3 (PTX3) with neutrophil/lymphocyte ratio (NLR) rather than the disease activity score 28 using C-reactive protein in rheumatoid arthritis (RA). The study included 59 RA patients (11 males, 48 females; mean age 53.79±13.55 years; range 40 to 66 years) and 20 healthy controls (5 males, 15 females; mean age 50.41±6.11 years; range 43 to 56 years). Complete blood count tests were recorded and NLR and platelet/ lymphocyte ratio were calculated. PTX3 and interleukin-6 levels were examined in serum samples. Disease activity of RA patients was assessed by disease activity score 28. Demographic characteristics were similar between the two groups, with no statistically significant difference in terms of sex, age, and body mass index (p>0.05). NLR, PTX3 and interleukin-6 levels were higher in patients with RA than the control group (p<0.05). While erythrocyte sedimentation rate had a positive correlation with mean platelet volume, we found no correlation between NLR and other parameters of disease activity, PTX3, and interleukin-6. We found no correlation between PTX3 and disease activity score 28 or NLR, although PTX3 levels were higher in RA patients than the controls. As a result, we were unable to establish a relationship between PTX3 and disease activity, directly or indirectly. To our knowledge, our study was the first to investigate the relationship between PTX3 and NLR.

Comparison of the Disease Activity Score-28 Based on the Erythrocyte Sedimentation Rate and C-reactive Protein in Rheumatoid Arthritis

Comparison of the Disease Activity Score-28 Based on the Erythrocyte Sedimentation Rate and C-reactive Protein in Rheumatoid Arthritis

Deletion of C-reactive protein exacerbates collagen-induced arthritis: A role for CRP in immune tolerance? (96.23)

Abstract Heightened C-reactive protein (CRP) blood level associates with inflammation and tissue damage in rheumatoid arthritis (RA), and so CRP is assumed to have a detrimental effect. However, the exact role of CRP in RA remains unknown. To ascertain the contribution of CRP in RA we subjected wild type mice (WT) and CRP deficient mice (moCRP-/-) to collagen-induced arthritis (CIA). To our surprise, disease developed 14 days earlier in moCRP-/- than WT, achieving a threefold higher clinical score. The beneficial effect of CRP in CIA appears to be linked to the protein’s ability to dampen the activation state of dendritic cells (DCs). For example, incubation of bone marrow-derived CD11c+ DCs (BMDCs) with 10 μg/ml purified human CRP reduced display of MHC class II and CD80/86 compared to BMDCs exposed to media alone (8 ± 4% lower and 5 ± 5.5% lower, respectively). This effect was observed whether BMDCs were derived from WT or moCRP-/- but was lost if cells were from mice lacking expression of FcγRIIB, the latter showing increased activation in response to CRP. Based on these observations we suggest that CRP binding to the inhibitory FcγRIIB conveys a signal leading to reduced display of DC activation markers. Accordingly, in the absence of CRP or FcγRIIB this pathway is disrupted, thereby de-inhibiting DCs and rendering moCRP-/- more prone to CIA. Experiments now underway are investigating whether a CRP→FcγRIIB pathway on DCs contributes to maintenance of immune tolerance.

Serum ADA and C-reactive Protein in Rheumatoid Arthritis

Immunological and inflammatory reactions play a pivotal role in the initiation and perpetuation of rheumatoid arthritis. The present study is an attempt to estimate the levels of adenosine deaminase (ADA) activity, a marker for cell mediated immunity and C-reactive protein a marker for inflammation in patients with rheumatoid arthritis.75 cases presenting rheumatoid arthritis and same number of age and sex matched healthy controls were included in the study. Serum ADA activity was measured spectrophotometrically at 630 nm and serum C-reactive protein was detected using Avitex CRP kit, which is a rapid latex agglutination test. The mean ADA levels were 59.79 ± 21.09 in patients and 20.71 ± 5.63 in controls, significant at p< 0.01. CRP test was found to be positive in 69/75 cases of RA and none of the controls. The present study observed the importance of ADA as a serum marker in addition to CRP for better therapeutic management of RA.

Serum ADA and C-reactive Protein in Rheumatoid Arthritis

Serum ADA and C-reactive Protein in Rheumatoid Arthritis

Galectin-3 and galectin-3 binding protein in rheumatoid arthritis

Galectin-3 (Gal-3) is one of the soluble lectins that has key functions in inflammation, chemotaxis, cell adhesion and apoptosis. We examined the role of Gal-3 and Gal-3 binding protein (Gal-3BP) in rheumatoid arthritis (RA). Localization of Gal-3 and Gal-3BP in rheumatoid synovium was examined by immunohistochemistry and in situ hybridisation. Gal-3 and Gal-3BP concentrations in plasma and synovial fluid were measured by ELISA. Gal-3 protein and mRNA stained throughout the synovial membrane, and Gal-3BP expressed at the site of erosion in RA. Lower and scattered expression of both Gal-3 and Gal-3BP were detected in osteoarthritis synovium and normal synovium. ELISA revealed a marked increase of Gal-3 and Gal-3BP in synovial fluid of patients with RA compared with osteoarthritis patients and normal controls. Furthermore, the level of Gal-3 in serum correlated with the level of C-reactive protein in RA. In vitro, Gal-3 can induce the production of matrix metalloproteinase (MMP)-1, MMP-3, and MMP-9 in synovial fibroblasts in a dose-dependent manner. Our data indicate that Gal-3 and Gal-3BP represent novel markers of disease activity in RA. Moreover, Gal-3 might contribute to the destruction of bone/cartilage in RA by the induction of MMPs.

PLASMA LACTOFERRIN AND NEUTROPHIL ELASTASE IN RHEUMATOID ARTHRITIS AND SYSTEMIC LUPUS ERYTHEMATOSUS

In order to assess lactoferrin (LF), stored in specific granules of neutrophils, as a marker of inflammation, LF was measured in plasma and serum samples of patients with active rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). In active RA, the median plasma LF level (800 ng/ml) was significantly higher than in normal individuals (220 ng/ml) (P less than 0.00001) and patients with active SLE (235 ng/ml) (P less than 0.00001). Median plasma elastase-proteinase inhibitor complex (EPIC) and C-reactive protein (CRP) levels were also significantly higher in patients with RA than in normal individuals (P less than 0.00001) and active SLE (P less than 0.00001 for both EPIC and CRP). Elevations of LF, EPIC and CRP in RA were independent of rheumatoid factor titres. Plasma lactoferrin in RA correlated significantly with EPIC (Rs = 0.7, P less than 0.0001), CRP (Rx = 0.72, P less than 0.0001) and absolute neutrophil counts (Rs = 0.483, P less than 0.02), but surprisingly not with the Ritchie index, with which CRP showed a weak but significant correlation (Rs = 0.27, P less than 0.05 greater than 0.025). Thus plasma LF and EPIC are markers of inflammation in RA and their levels may reflect release of mediators of inflammation into the joint space and periarticular tissue.

Relationship between urinary sialylated saccharides, serum amyloid A protein, and C-reactive protein in rheumatoid arthritis and systemic lupus erythematosus.

The urinary excretion of sialic-acid-containing oligosaccharides, total sialic acid, serum amyloid A protein (SAA), and C-reactive protein (CRP) has been studied in 48 patients with rheumatoid arthritis (RA) and in 17 patients with systemic lupus erythematosus (SLE). Linear regression analysis revealed a close positive correlation between serum SAA and CRP levels in both RA (r = 0.71, p less than 0.001) and SLE (r = 0.86, p less than 0.001). The urinary excretion of sialyl lactose showed a positive correlation with the serum levels of SAA and CRP in RA (r = 0.45 and r = 0.45, respectively, p less than 0.01) but not in SLE (r = 0.05 and r = 0.10 respectively). Changes in serum total sialic acid levels paralleled those in CRP and SAA in RA as well as in SLE. Patients with very active RA had higher urinary sialyl oligosaccharide excretion (p less than 0.001), higher CRP levels (p less than 0.01), and higher SAA levels ( p less than 0.05) than those with moderately active disease.

Relationship between erythrocyte sedimentation rate and serum C-reactive protein in rheumatoid arthritis.

Serum C-reactive protein (CRP) and the erythrocyte sedimentation rate (ESR) were compared in 241 patients with rheumatoid arthritis (RA). There was a positive linear correlation between the 2 measurements with a high degree of variability. Neither age nor duration of RA had a detectable influence. The relationship between CRP and ESR was, however, altered by treatment with gold, penicillamine, or high doses of prednisone. It is suggested that serum CRP is the more sensitive measurement, but that CRP and ESR do not have identical clinical significance.