Occurrence Of Rheumatoid Factor Research Articles

Predictors of flare in rheumatoid arthritis patients with persistent clinical remission/low disease activity: Data from the TARAC cohort.

To identify predictors of rheumatoid arthritis (RA) disease activity flare in RA patients who achieved low disease activity (LDA) or persistent remission from the observational Thai Army Rheumatoid Arthritis Cohort study.RA patients with persistent clinical remission, defined by disease activity score 28 (DAS28) < 2.6 and LDA defined by DAS28 ≤ 3.2 for 3 consecutive months, were recruited and followed-up for at least 2 years. The flare was defined by an escalation of DAS28 ≥ 1.2 plus their physicians’ decision to enhance RA treatment. Differences between sustained remission/LDA and flare groups were analyzed, by Chi-square test and unpaired Student t test. Multivariate Cox proportional hazard regression analysis was conducted to determine flare predictors.From 199 RA patients, female were 82.9%. Anticitrullinated peptide antibodies (ACPA) or Rheumatoid factor (RF) were found in 69.8% of patients. Flares occurred in 69 patients (34.9%). Multivariate analysis found that the timescale from symptoms emergence to DMARD commencement, the timescale from DMARD commencement to when RA patients showed remission/LDA, the occurrence of RF or ACPA, LDA (in contrast to remission) and the increased DAS28 score when remission/LDA was achieved and tapering DMARDs promptly when persistent remission/LDA was achieved were predictors of RA flares with hazard ratios of (95% confidence interval [CI]) of 1.017 (1.003–1.030), 1.037 (1.015–1.059), 1.949 (1.035–3.676), 1.926 (0.811–4.566), 2.589 (1.355–4.947), and 2.497 (1.458–4.276), respectively.These data demonstrated that early and aggressive DMARDs treatment approach could maintain remission espcially in seropositive patients. Tapering should be applied minimally 6 months after reaching remission.

Interaction between Mesenchymal Stem Cells and the Immune System in Rheumatoid Arthritis.

Rheumatoid arthritis (RA) is an autoimmune disease that causes damage to joints. This review focuses on the possibility of influencing the disease through immunomodulation by mesenchymal stem cells (MSCs). There is an occurrence of rheumatoid factor and RA-specific autoantibodies to citrullinated proteins in most patients. Citrulline proteins have been identified in the joints of RA patients, and are considered to be the most suitable candidates for the stimulation of anti-citrulline protein antibodies production. Fibroblast-like proliferating active synoviocytes actively promote inflammation and destruction in the RA joint, in association with pro-inflammatory cells. The inflammatory process may be suppressed by MSCs, which are a population of adherent cells with the following characteristic phenotype: CD105+, CD73+, CD90+, CD45−, CD34− and HLA DR−. Following the stimulation process, MSCs are capable of immunomodulatory action through the release of bioactive molecules, as well as direct contact with the cells of the immune system. Furthermore, MSCs show the ability to suppress natural killer cell activation and dendritic cells maturation, inhibit T cell proliferation and function, and induce T regulatory cell formation. MSCs produce factors that suppress inflammatory processes, such as PGE2, TGF-β, HLA-G5, IDO, and IL-10. These properties suggest that MSCs may affect and suppress the excessive inflammation that occurs in RA. The effect of MSCs on rheumatoid arthritis has been proven to be a suitable alternative treatment thanks to successful experiments and clinical studies.

Immunological comparison of patients with rheumatoid arthritis with and without nephropathy.

Serum immunoglobulins IgG, IgA, and IgM, serum complement components C3 and C4, circulating immune complexes, antinuclear antibodies, and rheumatoid factor were measured in 56 patients with rheumatoid arthritis (RA) and nephropathy (23 with mesangial glomerulopathy; 13 with membranous glomerulonephritis; and 20 with amyloidosis) and 35 patients with RA without nephropathy (controls). Renal immunofluorescence findings in patients with mesangial glomerulopathy were compared with the serologic data. There were no differences in the occurrence of rheumatoid factor, antinuclear antibodies, and circulating immune complexes and the concentrations of serum complement C3 and C4 between various RA nephropathy groups and controls. Serum IgA and IgM concentrations were significantly higher in patients with mesangial glomerulopathy and amyloidosis than in controls. In patients with mesangial glomerulopathy glomerular IgM, IgA, and C3 were the most prominent findings in immunofluorescence examination. The serum IgA concentration was significantly higher in those patients with mesangial glomerulopathy with mesangial IgA deposits than in those without (4.97 (SD 1.03) g/l v 2.07 (1.21) g/l). The highest serum IgA concentrations (5.08 (1.39) g/l) were seen in the four patients with IgA glomerulonephritis. The prevalence of IgA glomerulonephritis in the renal biopsy material of the patients with RA was 5%, which possibly differs little from that seen in the general population. The results suggest that circulating immune complexes may not have any major role in the pathogenesis of various nephropathy types in patients with RA, contrary to their role in most extra-articular manifestations of RA.

Smooth-muscle antibodies in rheumatoid arthritis.

Smooth-muscle antibodies (SMA) detected by the indirect immunofluorescence method were found more often in rheumatoid arthritis (RA) patients (15.3%) than in normal controls (7.6%) (0.02 > p > 0.01). The increased frequency was due to IgG-antibodies which occurred in 12.2% of RA patients, in 4.1% of normal controls and in 7.3% of patients with other arthritic diseases. Eight of 9 IgG-SMA-positive RA sera reacted with F-actin, and one serum contained non-actin antibodies. In RA, ANA were found in 35.7%, glomerular antibodies in 1.0%, parietal cell antibodies in 4.1% and mitochondrial antibodies in 2.0%. SMA were associated with the occurrence of rheumatoid factors and mitochondrial antibodies (0.02% > p and 2p = 0.04, respectively). In the SMA-positive group the erythrocyte sedimentation rate was higher and elevated serum alkaline phosphatase values were found more often than in the SMA-negative group.

Rheumatoid factor in melanoma patients:Alterations of humoral tumor immunity in vitro

Rheumatoid factors (RF) were associated with alterations of antibody reactions to melanoma cells in vitro by two serologic assays. Removal of RF from melanoma patients' sera by absorption with Cohn's Fraction II coated latex particles enhanced seroreactivity in the Immune Adherence (IA) assay and diminished IgM detection by the Indirect Membrane Immunofluorescence (IMI) assay. The addition of serum with high titers of RF to these assay systems led to diminution of IA reactivity and enhancement of IgM detection by IMI. Since these factors are found in cancer patients' sera and can alter humoral immune reactions directed against antigens on the membranes of tumor cells, their presence should be recognized when performing assays with tumor target cells. RF may be of significance in the host-tumor relationship in vivo.

The pattern of anti-immunoglobulin activities in serum, pleural, and synovial fluids.

Abstract A number of surveys on the occurrence of rheumatoid factors (RF) in nonrheumatoid sera, pleural, and synovial effusions suggests a lack of diagnostic specificity in many of the commonly employed RF test systems. Sera matched with effusion fluids of 70 patients were tested in 4 commonly used RF test systems standardized against an International RF Reference Standard. Although there were significant positive results in both the rheumatoid and nonrheumatoid specimens, the pattern of reactivity suggested classical RF in the former, but a high incidence of anti-antibody in the latter. Inhibition tests confirmed this impression. Anti-antibody was responsible for 88 per cent of our nonrheumatoid RF-positive tests and of these, 79 per cent occurred in our pleural effusion patients. Moreover, this study shows that the diagnostic specificity of RF testing is improved when agglutination inhibition techniques are used to differentiate RF from other immune, non-RF, antiglobulin agglutinators such as anti-Gm factors and anti-antibodies. Thus, in addition to eliminating nonimmune agglutinations by heat decomplementation of all specimens and hyaluronidase treatment of the most viscous synovial effusions, agglutination specificity challenges for RF and non-RF immune factors using pooled native and heat-aggregated γ-globulin aid in further characterizing the source as rheumatoid or nonrheumatoid.

The LE factor in rheumatoid arthritis. Clinical and serological studies.

SummaryEighty-nine patients with rheumatoid arthritis and LE factor were compared to 181 LE-negative patients. The LE-positive group had a significantly higher mean serum gamma globulin level, and the mean ESR was significantly higher in anatomical stage III—IV. No difference was found in the occurrence of rheumatoid factor or subcutaneous nodules. An increased incidence of thyroid antibodies and positive Coombs' direct test occurred among the LE positives as compared to the normal population. Two patients with LE cells had massive renal involvement. Patients with LE factor also had a slight increase in extra-articular manifestations of rheumatoid arthritis. No difference was observed in complications of gold treatment.

THE OCCURENCE OF RHEUMATOID FACTOR IN ASSOCIATION WITH ANTIBODY RESPONSE TO INFLUENZA A2(ASIAN) VIRUS.

AbstractAnalysis of sera from persons exposed to the 1957 Asian influenza epidemic demonstrated the appearance of rheumatoid factor in 14.8 per cent of 27 post‐epidemic sera showing viral antibody response and in only 1.3 per cent of 79 corresponding sera which did not show viral antibody response. The factor was associated with either clinical infection or vaccination. Rheumatoid factor activity was demonstrated in both the latex FII agglutination and sensitized sheep cell tests and was abolished by mercaptoethanol treatment.

THE LACK OF RHEUMATOID FACTOR IN PSORIATIC ARTHRITIS.

Summary104 cases of psoriasis arthropathy were compared serologically with 140 cases of rheumatoid arthritis and with 80 cases of uncomplicated psoriasis. Rheumatoid factor was present much more seldom in cases of P.A. than in R.A. and could be demonstrated in only one case of uncomplicated psoriasis. Study of the occurrence of rheumatoid factor in association with various types of roentgenological abnormalities showed that cases of psoriasis with typically localized erosions in the distal joints of the fingers and/or the interphalangeal joints of the lateral toes, with at the same time a total lack of rheumatoid factor, can be classified as psoriatic arthritis. Additional studies are required to throw light on the cause of the low values of macroglobulins in psoriasis.

The occurrence of rheumatoid factor in synovial fluid

The concentration of gamma globulin and the latex agglutination reaction of synovial fluid have been compared to serum values in eighty-three patients with various forms of rheumatic disease. In the majority of patients with active rheumatoid arthritis and a positive agglutination reaction in serum, the reaction of synovial fluid also was positive, usually in a somewhat lower titer. This discrepancy may be related to the lower protein content of synovial fluid compared to serum. There were a number of cases, however, in which the agglutination reaction of synovial fluid was negative despite strongly positive agglutination reactions of the serum. It is possible that in some cases this may have been the result of recent intra-articular steroid treatment. There were several patients with suspected (possible or probable) rheumatoid arthritis in whom the agglutination reactions of the serum were negative and of the synovial fluid positive. The course of these subjects must be carefully followed before any conclusions can be drawn concerning the possible value of this observation in the early diagnosis of rheumatoid arthritis. This finding is compatible, however, with the belief that production of the rheumatoid factor in such cases may be confined to the tissues of one or a few joints. The synovial fluid from a small group of patients with a variety of other rheumatic diseases showed negative reactions with the exception of two patients with ankylosing spondylitis and peripheral arthritis. The study of synovial fluid samples, which have a strong positive agglutination reaction, by means of immunoelectrophoresis and ultra-centrifugationand the effects of mercaptoethanol treatment indicate that the factor responsible for latex agglutination is a macroglobulin.

The occurrence of rheumatoid factor and other abnormalities in families of patients with agammaglobulinemia.

AbstractThe incidence of rheumatoid agglutinating activity (RAA) in parents and siblings of patients with acquired agammsglobulinemia was found to be considerably higher than the incidence of RAA in the normal population. Elevated γ‐globulin levels were also occasionally present, as well as alterations in the β2A and β2M proteins in such relatives. Laboratory findings suggestive of lupus erythematosus were observed in two instances. The high incidence of serum γ‐globulin abnormalities in relatives of patients with idiopathic “acquired” agammaglobulinemia suggests that this is a genetically determined disorder.