Search for: rheumatoid arthritis methotrexate autoimmune disease biomarker gene expression GWAS HLA genes non-HLA genes
| ID | PMID | Title | PublicationDate | abstract |
|---|---|---|---|---|
| 3492025 | Inhibition of C1q binding to antigen-antibody complexes by a factor in rheumatoid arthriti | 1986 | The sera and synovial fluids of patients with rheumatoid arthritis (RA) contain a factor which decreases the binding of C1q to antigen-antibody complex (IC). Several lines of evidence suggest that this factor is distinct from the documented C1q inhibitor which is a chondroitin sulphate. It binds to IC rather than to C1q. It is resistant to digestion with chondroitinase ABC. The addition of chondroitin sulphate to serum does not inhibit the binding of IC to C1q. The observation that three purified IgM and IgG rheumatoid factors (RF) did not reduce C1q binding to IC indicates that the factor is not RF. The ability of RA sera to reduce IC binding to C1q was inversely correlated with their ability to prevent immune precipitation (PIP), and directly with levels of an inhibitor of PIP. These data suggest that the factor which binds to IC and reduces C1q binding may be responsible for the excessive immune precipitation which occurs in RA sera. | |
| 2049583 | The occurrence and significance of hand deformities in early rheumatoid arthritis. | 1991 Jun | One hundred rheumatoid arthritis patients (38 men, 62 women), with mean age of 53 years and mean disease duration of 11.5 months, were followed. Standardized clinical, biochemical, and radiographic evaluation was performed regularly. After 2 years the prevalence of ulnar deviation, buttonhole deformity, and swan neck deformity was 13%, 16%, and 8%, respectively. Altogether, 31 patients had developed one or more deformities. There was no difference in age or gender distribution and no predominance of the dominant hand. Each patient with a deformity was matched according to age, sex, and disease duration with another early RA patient without deformity. The deformity group had more active disease, less grip strength, more disability, and markedly more severe radiographic changes. When studied retrospectively at a time point 3 months prior to the detection of deformity, synovitis of relevant joints was as common in the group who developed deformities as in the control group. This suggests that joint inflammation may contribute to the genesis of deformity but additional factors are needed. Hand deformities were found to be common in early RA. | |
| 2335055 | Overlap syndrome with multiple calcifications of the spleen. | 1990 Mar | A woman with overlapping features of rheumatoid arthritis and systemic lupus erythematosus presented with multiple small asymptomatic calcifications of the spleen. The absence of any other origin suggests that these calcifications are directly related to the connective tissue disease. | |
| 2625048 | [Endoprosthesis of the knee joint]. | 1989 | Endoprosthetic replacement of the knee joint is an important, often the terminal stage of surgical treatment in patients with rheumatoid arthritis and gonarthritis. Basing on the results of the over-11-year-experience of the ward, treatment methods were analyzed and various knee prostheses were evaluated. In evaluation, the modified Gschwend's scale was used. Nineteen results were good 18 fair, and 7 poor. An especially important role of proper qualification of a patient to surgery, conditions for insertion of endoprosthesis and the choice of a proper type of endoprosthesis has been stressed. | |
| 2181669 | The pathogenesis of anemia in rheumatoid arthritis: a clinical and laboratory analysis. | 1990 Feb | Principal concepts concerning the anemia of RA are summarized in Tables 7 and 8. These concepts have been validated by our analysis of 93 anemic RA patients and by our review of the literature. The fact that anemia in RA may have one or more etiologies, occasionally in the same patient, mandates a reasoned approach to the analysis of anemia in every RA patient in whom it may occur. In particular, iron deficiency is common and determination of bone marrow iron content via an aspirate may be required for a definitive diagnosis. In those RA patients with anemia of chronic disease, the best therapy remains control of the underlying disease, most commonly with second line drugs and/or corticosteroids. The place for recombinant erythropoietin in the therapy of this anemia has not been defined; one specific role for erythropoietin may be in the preparation of RA patients for elective surgery, particularly hip arthroplasty, where correction of the anemia may either obviate the need for transfusion or may allow for donation of blood for purposes of autologous transfusion perioperatively. The pathogenesis of the anemia of chronic disease, as seen in RA anemia, is not completely understood. Inflammatory mediators, particularly the cytokines, appear to be important factors in the impairment of erythropoiesis. The mechanism by which these cytokines impair erythroid progenitor growth and hemoglobin production in developing erythrocytes is an important area for future study. | |
| 3473654 | Serological profiles in subgroups of patients with Sjögren's syndrome. | 1986 | The serological profiles of 54 patients with primary Sjögren's syndrome (pSS) and 92 rheumatoid arthritis (RA) patients with or without secondary SS (sSS), were retrospectively evaluated and correlated with: different subgroups of SS, degree of minor salivary gland biopsy lymphocytic infiltrates and the presence of glandular and extraglandular manifestations. Antibodies to nuclear antigens (ANA), anti-Ro(SSA) and anti-La(SSB) as well as rheumatoid factor (RF) correlate with definite pSS, while in RA, ANA and anti-Ro(SSA) are associated with the presence of sSS and anti-La(SSB) is practically absent. In pSS patients, the incidence of anti-Ro(SSA) and anti-La(SSB), as well as the titers of ANA and RF, correlate with the degree of salivary lymphocytic infiltrates in class 1+ to 3+. In class 4+, a substantial decrease of the autoantibodies is noted. In pSS patients, anti-Ro(SSA) and anti-La(SSB) correlate with earlier disease onset and longer disease duration, recurrent parotid gland enlargement (RPGE), as well as with the presence of extraglandular manifestations (extr. manif.) particularly splenomegaly/lymphadenopathy and vasculitis. Anti-Ro(SSA) correlates with positive Schirmer's test, ANA with decreased parotid flow rate and extr. manif., while RF correlates with RPGE and subjective xerostomia. In RA patients, autoantibodies were predominantly found in the presence of features of eye dryness: ANA correlate with positive Schirmer's test, Rose-Bengal stain and subjective xerophthalmia, the latter also correlated with anti-Ro(SSA). This study, re-emphasizes the diagnostic significance of autoantibodies for SS, and possibly contributes in the delineation of biological processes in this disease. | |
| 3109798 | The in vivo effect of triethylphosphine gold (auranofin), sodium aurothiomalate and azathi | 1987 Jan | Natural Killer (NK) cell activity was measured in 80 patients with rheumatoid arthritis (RA) grouped according to medication into 1) controls not in remission-inducing therapy, 2) patients treated with oral gold (auranofin), 3) parenteral gold (sodium aurothiomalate) and 4) azathioprine. Baseline, interferon (IF)-enhanced and interleukin 2 (Il-2)-enhanced NK cell activity of patients in the two gold groups did not differ from that of controls, while NK cell activity before and after exposure to IF and Il-2 was significantly suppressed in patients on azathioprine (p less than 0.01). The percentage of Large Granular Lymphocytes did not differ in the four groups while the percentage of Leu 11 positive cells and the total number of lymphocytes were significantly lower in the azathioprine group. Sixty out of 80 patients received nonsteroidal anti-inflammatory drugs (NSAID), whereas 20 did not. A comparison of these two groups showed no influence of NSAID on NK cell activity. | |
| 1647755 | Inhibition of myeloperoxidase by synovial fluid and serum. | 1991 Jun | An inhibitor of myeloperoxidase has been identified in the synovial fluids and sera from patients with rheumatoid arthritis and sera from normal subjects. Initially, these fluids were found to inhibit stimulus induced degranulation of polymorphonuclear leucocytes independently of the stimulating agent. Subsequently, the fluids were shown to inhibit the released enzyme rather than the degranulation response of polymorphonuclear leucocytes. Both rheumatoid and normal serum samples contained high concentrations of the inhibitor but the concentrations were lower in rheumatoid synovial fluids. The inhibitory activity seemed to be specific for peroxidase as the fluids did not inhibit beta-glucuronidase activity. A protein of relative molecular mass (Mr) 150 kd was purified from synovial fluid by affinity chromatography on myeloperoxidase-Sepharose. It is concluded that serum and synovial fluid contain a novel myeloperoxidase inhibitor, which acts by binding to myeloperoxidase and thereby prevents myeloperoxidase releasing oxidative products in serum. | |
| 3208453 | In vivo and in vitro evidence of cell recovery from complement attack in rheumatoid synovi | 1988 Sep | In the previous article we have demonstrated, by quantifying terminal complement complexes in synovial fluid, that membrane attack complex activation occurs in the joint in rheumatoid arthritis. Here we describe evidence of synoviocyte resistance to complement attack in vivo and in vitro. Gel filtration of terminal complement complex positive synovial fluid on Sepharose 2B revealed two forms of terminal complement complex: one form, eluting coincident with the column void, did not react with antibody to the fluid-phase inhibitor of complement membrane attack, the S-protein, suggesting that it was composed of membrane attack complexes, the other form, eluting in the included volume, did react with the anti-S-protein antibody, suggesting that it was composed of functionally inactive SC5b-9 complexes. The high molecular weight membrane attack complex peak was demonstrated by electron microscopy to be composed of membrane vesicles bearing many lesions having the typical appearance of complement membrane attack complexes. No discernible structures were present in the lower molecular weight peak. The effects of non-lethal complement membrane attack on human synoviocytes in culture were also investigated. Synoviocytes were relatively resistant to killing by autologous complement, end-point lysis of optimally antibody-sensitized cells never exceeding 60% even at a serum dilution of 1:2. At serum dilutions of 1:20 or less, no significant cell killing occurred despite a high degree of membrane attack pathway activation, suggesting the existence of resistance and recovery mechanisms. Non-lethal complement membrane attack stimulated the release of toxic reactive oxygen metabolites from synoviocytes. These, and other reactive species released during non-lethal complement attack in vivo, may play a significant role in the pathogenesis of rheumatoid arthritis. | |
| 2421737 | Alpha 2-macroglobulin-proteinase complexes as correlated with alpha 1-proteinase inhibitor | 1986 Mar | The levels of alpha1-proteinase inhibitor-elastase and alpha 2-macroglobulin (alpha 2M)-proteinase complexes were measured in synovial fluids from arthritis patients by use of specific immunosorbent assays. Both types of proteinase inhibitor-proteinase complexes were significantly correlated with each other as well as with the total neutrophil count in synovial fluids of rheumatoid arthritis patients but were discordant in synovial fluids of patients with osteoarthritis. One synovial fluid sample showed active (inhibitory) alpha 2M as well as active collagenase. We purified alpha 2M from pooled synovial fluids obtained from patients with rheumatoid arthritis. This alpha 2M retained approximately 90% of its proteinase binding (inhibiting) capacity, compared with that of normal plasma alpha 2M. We found no evidence that alpha 2M was inactivated by means other than proteinases. | |
| 3708236 | Stanford Health Assessment Questionnaire modified to assess disability in British patients | 1986 May | The Stanford Health Assessment Questionnaire was modified for use amongst British patients by the substitution of colloquial expressions. Completion of the modified questionnaire was shown to be simplified compared with the original. Results correlated well with scores obtained at interview and were shown to be more sensitive to patients' functional changes than the Steinbrocker grading. | |
| 2575080 | Expression of Leu M1 antigen on a monoclonal B cell line established from a patient with r | 1989 Nov | The purpose of this study is to show that anti-Leu M1 antibody (anti-CD15), which has different staining characteristics in lymphoid and non-lymphoid cells, reacted against the surface antigen of a defined monoclonal B cell line. This antibody recognizes the sugar moiety, lacto-N-fucopentaose (LNF-III), which is linked to the cell membrane protein in several kinds of cells, but not in B cells. However, a human monoclonal B-cell line (TKS-1) which was established from the peripheral blood of a patient with rheumatoid arthritis, expressed the Leu M1 antigen spontaneously. The analysis of surface markers using a fluorescence-activated cell sorter (FACS) has revealed that the surface markers of TKS-1 were anti-mu, delta, kappa, HLA-DR, DQ, Leu 12 (CD19) and Leu M1 (CD15). TKS-1 cells were not reactive with any of the following antibodies: anti-OK M1 (CD11b), Leu M2, Leu M3 (CD14), Leu M4, Leu 1 (CD5), Leu 2 (CD8), Leu 3 (CD4), Leu 4 (CD3), Leu 7 and Leu 11 (CD16). In addition, TKS-1 was positive to Epstein-Barr nuclear antigen, weakly positive to non-specific esterase without staining inhibition by NaF, and negative to peroxidase. TKS-1 cells produced IgM in the culture supernatant and have kappa-light chain rearrangement in its DNA. As shown in other studies, distribution of Leu M1 is very wide. This antigen is not a specific immunodiagnostic marker to distinguish the cell type. We conclude that it is possible to express Leu M1 antigen on the membrane of a B-cell lineage cell. | |
| 3656331 | Possible origin of synovial lining cell hyperplasia in rheumatoid arthritis. | 1987 Aug | A perplexing feature of rheumatoid arthritis is the increase in the number of synovial lining cells with no mitotic activity. This feature has been investigated in the rabbit model. Rabbits with the established condition were injected into the affected joint with tritiated thymidine and killed either up to 24 hours later, or at 3 or 7 days. The location of labelled cells, detected by autoradiography, showed the label predominantly in the stroma in the former, and mainly in the lining cells in the latter, indicating that the lining cells were derived by recruitment from active cells deep in the stroma. | |
| 3668977 | The impact of rheumatoid arthritis and osteoarthritis: the activities of patients with rhe | 1987 Aug | We measured the impact of rheumatoid arthritis (RA) and osteoarthritis (OA) by comparing the activities of patients with these illnesses to controls matched for age, sex, and community of residence. Our results indicate that patients with RA experience more losses than controls in every domain of human activity and that patients with OA experience more losses in the performance of household chores, shopping and errands, and leisure activities. The methods described here provide a simple, reliable way to assess the impacts of illness in the same terms for all dimensions of human activity. | |
| 3592785 | Measurement of radiographic changes occurring in rheumatoid arthritis by image analysis te | 1987 Apr | We have applied image analysis techniques to serial measurements of bone contour in standard radiographs of single small joints of the hands in subjects with rheumatoid arthritis (RA) and controls. Adequate reproducibility was shown in 20 controls radiographed twice over a six month period. The technique showed significant changes in a proximal interphalangeal joint of 13 of 15 patients with RA studied over periods of three to 10 months. In further serial studies in selected small joints of RA hands significant changes could be shown as early as four months. These results justify further development of these techniques to allow their full scale evaluation in multiple joints in patients with RA receiving long term drug therapy. | |
| 2169654 | Bronchoalveolar lavage in patients with mild and severe rheumatoid lung disease. | 1990 Aug | The reported prevalence of interstitial lung disease in patients with rheumatoid arthritis has varied from 10% to 50%, yet less than 5% of patients with arthritis develop severe fibrosing interstitial lung disease. This suggests that subclinical disease may not always presage progressive disease. Bronchoalveolar lavage fluid from patients with rheumatoid arthritis and either clinically evident interstitial lung disease or subclinical disease was examined for the presence of factors with a putative role in the development of interstitial fibrosis. Patients with subclinical disease were identified by prospective radiographic and lung function screening of 93 patients with rheumatoid arthritis. Fourteen patients were identified in this manner and an association between subclinical disease and smoking history was noted. Eleven patients with established interstitial lung disease had increased neutrophils (p less than 0.05), collagenase, and type III procollagen N terminal peptide levels (p less than 0.01) in the bronchoalveolar lavage fluid. Preliminary characterisation of the bronchoalveolar lavage collagenase suggested that it originated from neutrophils. Ten patients with subclinical interstitial lung disease underwent bronchoalveolar lavage. Of these, one had increased neutrophils and two had increased collagenase concentrations--abnormalities associated with advanced interstitial lung disease and a poor prognosis. These results suggest that in arthritis patients with evidence of subclinical pulmonary interstitial disease bronchoalveolar lavage might be useful in identifying those who may require careful monitoring in the hope that early treatment will prevent severe fibrosis. | |
| 3260951 | Interleukin-2 abnormalities in systemic lupus erythematosus and rheumatoid arthritis. A ro | 1988 Apr | Interleukin-2 (IL-2) production in systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) was assessed at varying cell densities from 3 X 10(3)-1 X 10(5) cells/culture in response to mitogen stimulation, using a cellular interleukin assay in which IL-2 responsive CTLL-2 indicator cells were added directly to stimulated peripheral blood lymphocyte cultures. It was found that in both RA and SLE there was a significant overproduction of IL-2 demonstrable at low cell densities. At high cell densities, IL-2 production was decreased in SLE but remained enhanced in RA. The former abnormality appears to be related to disease activity and was not reversed by irradiation, suggesting that it is not the result of the actions of a radiation sensitive suppressor cell population. The possibility is discussed that a local hyper-production of IL-2 could induce disturbances of the immune response, resulting in the breaking of normal tolerance. | |
| 2565227 | Life stress and lymphocyte alterations among patients with rheumatoid arthritis. | 1989 | The relation between life stress and immune parameters was investigated for 33 female rheumatoid arthritis (RA) patients interviewed during three routine monthly clinic checkups. Life stress from major and minor events, coping efficacy, and self-reported psychological distress were assessed, and immunofluorescence of T-cells and B-cells was performed on the blood drawn during each visit. Small stressful events were positively related to the proportion of circulating B-cells, psychological distress was inversely related to proportion of circulating T-cells, and major life events were associated with lower T-helper/T-suppressor cell ratios. | |
| 3114875 | Reduced production of interferon alpha and interferon gamma in leukocyte cultures from pat | 1987 | Tests for lymphoproliferation and interferon induction in normal blood donors and patients with rheumatoid arthritis (RA) were performed in a whole-blood assay. Patients with high inflammatory RA showed significantly reduced lymphoproliferation and interferon gamma production after stimulation with phytohemagglutinin (PHA) and concanavalin A (Con A) when compared with patients with low inflammatory activity, or with normal control individuals. Similarly, patients with high and low inflammatory RA exhibited a significantly reduced interferon alpha production after stimulation with Newcastle Disease Virus (NDV) when compared with normal blood donors. Our findings may point to an important immunodeficiency of the circulating lymphocytes of RA patients and may explain some of the in vitro immunoregulatory abnormalities reported in this disease. | |
| 3022861 | Effect of corticosteroid therapy on blood monocyte superoxide generation in rheumatoid art | 1986 Nov | Rates of superoxide (SA) generation by blood monocytes stimulated ex vivo were studied before and during corticosteroid treatment of rheumatoid arthritis (RA) patients, in control patients and in healthy controls. The direct effect on stimulated SA production of pre-incubating cells with prednisolone in vitro was also studied. Significant inhibition of monocyte SA output stimulated with IgG-treated zymosan (ITZ) and fluoride ion (F), but not serum-treated zymosan (STZ) was demonstrated following steroid therapy in RA. No inhibitory effect of prednisolone could be demonstrated in vitro, using ITZ, STZ and F as stimuli. Our data on blood monocyte yields, size and cytochemistry suggest that the in vivo effect is due to a shift in blood monocyte traffic. |