Search for: rheumatoid arthritis methotrexate autoimmune disease biomarker gene expression GWAS HLA genes non-HLA genes
| ID | PMID | Title | PublicationDate | abstract |
|---|---|---|---|---|
| 373087 | IgG-, IgM- and IgA-rheumatoid factors in healthy adults and rheumatoid patients determined | 1979 | Sera from 173 healthy adults and 55 rheumatoid patients were studied for IgG-, IgM- and IgA-rheumatoid factors (RFs) by a modification of Este's indirect immunofluorescence method. Rabbit IgG bound to smeared sheep red cells was used as antigen. With each serum tested a smear on non-sensitized cells was used as control antigen. Anti-IgG of the sera studied, binding to the antigen, was demonstrated by fluorescein-conjugated antisera, monospecific for gamma, mu and alpha chains, and not containing antibodies to sheep erythrocytes or rabbit IgG. Positive reactions were obtained with IgG as antigen, but not with the F(ab')2 fragment. The sera tested were treated with dithiothreitol before they were assayed for IgG-RF, in order to abolish false-positive reactions due to IgM-RF activity. The detection limit for IgM-RF was 1 IU per ml. IgM-RF titres of 9 occurred in 7% of healthy adults and 73% of rheumatoid patients, titres greater than or equal to 18 in 3.5% and 67% respectively. IgG-RF titres of 9 occurred in 9% of healthy adults, 21% of seronegative and 24% of seropositive rheumatoid patients. Titres of 18 occurred in 3% of healthy adults and in 14% of seronegative rheumatoid patients. Titres of greater than or equal to 18 occurred in 22% of seropositive rheumatoid patients. IgG-RF was correlated with an involvement of more than 20 joints. IgA-RF was found in 83% of seropositive, 11% of seronegative rheumatoid patients and in none of the healthy adults (serum dilution 1:9). | |
| 6460396 | T-lymphocyte subpopulations in rheumatoid arthritis. II. Definition by monoclonal antibodi | 1981 Nov | Samples of peripheral blood of 27 patients with seropositive rheumatoid arthritis (RA) and 27 healthy age- and sex-matched controls were coded and studied for lymphocyte subpopulations. Monoclonal antibodies and indirect immunofluorescence were used to analyse subpopulations of purified T cells: OKT3 reacts selectively with all peripheral human T cells, OKT4 defines the helper/inducer subpopulation and OKT8 the suppressor/cytotoxic T cells. RA patients had a significantly lower relative lymphocyte count (p less than 0.001). whereas the percentage of all T cells was similar in patients and controls, RA patients had a significantly higher proportion of helper/inducer cells (62 +/- 1.3 vs. 56 +/- 1.0, p less than 0.005) and significantly decreased suppressors/cytotoxic cells (25 +/- 1.5 vs. 32 +/- 1.0; p less than 0.001). This resulted in an increased "immunoregulatory ratio" of helper to suppressor cells in RA patients (2.68 +/- 0.17) compared to their normal controls (1.83 +/- 0.10; p less than 0.001). The proportions of T cells expressing HLA-D-like antigens (defined by a monoclonal antibody to human Ia) was not different in patients and controls. These findings confirm conclusions derived from our previous study of T cell subsets defined by the expression of Fe-receptors (Tm and Tg), that in the peripheral blood of patients with RA, helper mechanisms predominate over suppressor mechanisms. This derangement of the immunoregulatory balance may have an important role in the pathogenesis of seropositive RA. | |
| 6246573 | Partial purification and characterization of the high molecular weight latent collagenase | 1980 | Two latent collagenases whose apparent molecular weights were ca. 150 000 and 60 000 have been detected in human leukocytes and the partial purification of the high molecular weight component was accomplished by the following steps: acetone precipitation, ammonium sulphate fractionation, gel filtration on Sephacryl S-200, chromatography on DEAE-Sepharose, and a final gel filtration on Sephacryl S-200. After activation by an activator extracted from human rheumatoid synovial fluid, the enzyme was able to cleave collagen into the classical 1/4 and 3/4 fragments, and was inhibited by chelating agents and other typical collagenase inhibitors. | |
| 343970 | Gastrointestinal microbleeding after aspirin and naproxen. | 1978 Apr | Gastrointestinal bleeding is the most serious side effect encountered with the anti-inflammatory antirheumatic drugs. Using the 51Cr labeling technique, the comparative quantity of blood loss with aspirin or naproxen has been previously done on normal volunteers. With the present study, 12 rheumatoid arthritic patients were controlled in a double-blind crossover study with the same radioactive technique. There is a difference in favor of naproxen. The difference between the baseline period and naproxen administration was not statistically significant. | |
| 3006976 | Monocytes and granulocytes in rheumatoid arthritis (RA): phagocytic activity and superoxid | 1985 Dec | It is suggested by many tests that phagocytic cells were implied in inflammation which occurred during rheumatoid arthritis (RA). Further, three subject populations were selected for this study: Rheumatoid arthritis patients diagnosed according to American Rheumatism Association criteria (ARA mean = 6) and treated with gold compounds. Control subjects treated with the same non-steroidal anti-inflammatory drug (NSAID), diclofenac (75 mg per day). Normal subjects without disease or treatment. Blood granulocytes and monocytes were separately tested for ingestion of three different particle species (opsonized zymosan, immunoglobulin G sheep red cells, glutaraldehyde-treated sheep red cells) and stimulation of superoxide anion production by these particles. All phagocytic cells in RA patients have normal phagocytic response and superoxide anion production. Autologous serum does not inhibit the activity of these cells. In addition the NSAID (diclofenac) does not act upon phagocytosis and oxidative burst of control cells. | |
| 6975631 | Detection and quantitation of fibronectin in synovial fluid from patients with rheumatic d | 1981 Oct | Fibronectin, a high molecular weight glycoprotein that binds to glycosaminoglycans, fibrinogen or fibrin, and collagen, was identified and quantitated in synovial fluid from patients with various rheumatic diseases. Fibronectin concentration was significantly higher in synovial fluids from patients with rheumatoid arthritis (RA) (697 microgram/ml) than in other synovial fluids. In RA, synovial fluid fibronectin concentration exceeded that in plasma and did not directly correlate with synovial fluid concentrations of albumin, total protein, or fibrinogen. Synovial fluid fibronectin concentration correlated directly with synovial fluid white blood cell count (r = 0.50, P less than 0.005). Fibronectin was present in cryoprotein formed from four rheumatoid synovial fluids. | |
| 7307254 | "Sandwich" enzyme immunoassay for placental alkaline phosphatase. | 1981 Dec | Alkaline phosphatase of the placental type in serum has been suggested as a "marker" for malignancy and pregnancy. We describe a highly sensitive enzyme-linked immunosorbent assay (ELISA) for the measurement of this enzyme in serum and ascitic fluid. The assay will detect as little as 0.4 microgram/L, significantly less than with a radioimmunoassay performed with the same reagents. It is highly specific; it does not measure even above-normal concentrations of the intestinal and liver isoenzymes of alkaline phosphatase. The assay is technically simple and allows the processing of many samples in less than 10 h. We measured this isoenzyme in serum of an adult control population. The upper limit of normality is 1.85 microgram/L. Interference by rheumatoid factor was eliminated. Concentrations of the analyte were increased in all pregnancy sera tested. Concentration and activity as measured by two different catalytic assays correlated well. Samples from cancer patients also showed a good correlation, with some exceptions. Possible reasons for these exceptions are discussed. The high sensitivity, specificity, and simplicity of this assay should make it a useful adjunct in monitoring cancer and pregnancy. | |
| 6356308 | [Humoral and cellular anticollagen autoimmunity in rheumatic pathology]. | 1983 Jul | Using an immuno-enzymatic technique, the authors studied the production of anti-collagen I and II auto-antibodies in 171 cases of rheumatoid arthritis (RA), 40 cases of systemic lupus erythematosus (SLE) and 21 cases of overriding syndrome. Cellular immunity to native collagen II was tested in a group of 26 patients with RA and 27 control subjects, by studying the production of LIF (Leukocyte Inhibitory Factor) in response to this antigen. The anti-collagen I and II antibodies are present in 15.2% and 17.5% of RA patients respectively and also in 15% and 15.5% of the SLE patients studied. Anti-collagen I antibodies are associated with RA with extra-articular signs and anti-collagen II antibodies are associated with early RA, but no association could be found with the clinical or radiological course of the disease. Cellular reactivity to collagen II was found in 30% of the cases of RA studied and was associated with the early forms of the disease. Complementary studies on the association of certain HLA antigens with cellular or humoral reactivity to collagen should allow a better approach to the clinical relationships of certain cases of chronic inflammatory rheumatism with anti-collagen auto-immunization. | |
| 819459 | C3b inactivator in the rheumatic diseases. Measurement by radial immunodiffusion and by in | 1976 Jun | C3b inactivator (C3bINA) has been measured in biologic fluids by radial immunodiffusion using a monospecific antiserum prepared in rabbits, and by a hemolytic assay which measures the reduction in the capacity of EAC43 cells bearing limited C3b sites to form C3B, the alternative pathway C3 convertase. The radial immunodiffusion and hemolytic assays show a good correlation (r = 0.86 P less than 0.001). Measurement of C3bINA concentrations in the sera of patients with systemic lupus erythematosus showed that during exacerbations of disease activity C3bINA concentrations tended to be lower, usually in association with reductions in C4, C3, factor B, and properdin, and sometimes with reductions of the alternative pathway proteins, factor B, and properdin alone. Supranormal values for C3bINA were found in the sera of 14 of 20 patients with seropositive rheumatoid arthritis and 3 of 9 seronegative patients, but none of 7 patients with degenerative joint disease. Synovial fluid concentrations of C3bINA, after correction for total synovial fluid protein and serum concentration of the enzyme, were significantly reduced in patients with rheumatoid arthritis compared to patients with degenerative joint disease (P less than 0.05). In both serum and synovial fluid from patients with rheumatoid arthritis, there was a good correlation between the concentrations of C3bINA and those of C3, factor B, and properdin, but not that of C4, suggesting that levels of C3bINA may serve to modulate recruitment of the properdin amplification loop in this disease. | |
| 6431808 | Mechanism of action of nonsteroidal anti-inflammatory agents. | 1984 Jul 13 | Recent data from several laboratories, which suggest that generally accepted concepts relating to the mechanism of action of nonsteroidal, anti-inflammatory drugs (NSAIDs) in rheumatoid arthritis may be incorrect, are reviewed. Over the past decade, most researchers have espoused the idea that NSAIDs act by inhibiting cyclooxygenase, thereby removing prostaglandins, which are thought to be responsible for pain and inflammation. Recent studies demonstrating that prostaglandins have important immunomodulating properties and that NSAIDs actually provide partial correction of several immunoregulatory dysfunctions in patients with rheumatoid arthritis are described. In addition, some NSAIDs inhibit migration along with other monocyte and polymorphonuclear leukocyte functions. Data suggest that these actions are not related to inhibition of cyclooxygenase. | |
| 529249 | The clinical significance of protein-bound hydroxyproline fractions in sera of patients wi | 1979 Nov | Clq levels in sera of adult patients with rheumatoid arthritis (RA) were found to be significantly higher than corresponding levels of normal subjects (p less than 10(-3)) The increase in Clq observed in RA was not seen in systemic lupus erythematosus, chronic polyarticular gouty arthritis, ankylosing spondylitis, Paget's disease of bone, or Hodgkin's disease. Clq levels were determined both chemically (calculated) from the protein-bound hydroxyproline content of the euglobulin fraction) and by radial immunodiffusion. Although the estimates of Clq by these 2 methods did not agree, the increase of Clq in RA was found by the use of either method. | |
| 6603315 | T-cell subpopulations in the peripheral blood of patients with connective tissue diseases | 1983 Jun | We studied by flow cytometry using monoclonal antibodies the T3, T4, and T8 subpopulations of T cells in the peripheral blood of 109 patients with various connective tissue diseases who were not receiving any treatment. Comparison of the results was made with those obtained with normal controls matched for age and sex with each connective tissue disease group. When compared as disease groups, patients with systemic lupus erythematosus (n = 41) had decreased T8 cells, but patients with active disease (n = 17) had all three T-cell subpopulations lower than their controls, whereas those with inactive disease (n = 24) showed no differences. Patients with rheumatoid arthritis (n = 23) had decreased T3 and T8 cells, whereas patients with scleroderma (n = 22) only had decreased T3 cells, and patients with primary Sjögren's syndrome (n = 15) had lower proportions of all three T-cell subpopulations than their matched controls. Patients with mixed connective tissue disease (n = 8) had proportions of all three T-cell subpopulations akin to those of their matched controls, but showed a tendency to have decreased T8 cells that reached statistical significance when compared to the entire control group. Although our findings tend to support the notion that the abnormalities in immunoregulatory T-cell circuits leading to autoimmunity are different in each connective tissue disease, the great variability found in both patients and controls seems to preclude the use of these determinations in individual patients for clinical purposes. | |
| 4009166 | Gas chromatographic-mass spectrometric determination of myo-inositol in human cerebrospina | 1985 Aug | The concentration of free myo-inositol in CSF was determined with a gas chromatographic-mass spectrometric method using deuterated myo-inositol as an internal standard after conversion to the hexa-O-acetyl derivative with acetic anhydride and pyridine. Twenty microliters of CSF is sufficient for the analysis which has a coefficient of variation of 9%. Identical analytical results were obtained on two different mass numbers. Schizophrenic patients were compared with healthy control persons. In addition, patients with rheumatoid arthritis or with neurological illnesses were studied. No consistent differences related to the illness could be found. The mean concentration of myo-inositol was about 25 micrograms/ml. Treatment of schizophrenic patients with chlorpromazine or sulpiride had no significant effect on the concentration of myo-inositol in CSF. | |
| 6637187 | [Morphology and pathogenesis of penicillamine-induced nephropathy]. | 1983 | Histological, immunohistological and electron microscopical investigations on the glomerular renal lesions in penicillamine-induced nephropathy were carried out by studying biopsy material of eight patients with rheumatoid arthritis (4 cases), allergic alveolitis (3 cases) and systemic scleroderma (1 case) under the treatment with D-penicillamine. Summarizing all the findings, the characteristic pattern of immune complex nephritis as membranous type glomerulonephritis on the one hand and proliferative type glomerulonephritis (mesangioproliferative GN, focal proliferative GN or minimal proliferative GN) on the other hand could be demonstrated. The different types of glomerular alterations in penicillamine nephropathy obviously depend on the kind and duration of the primary main disease and on the individual immune reactivity of the body was a whole by this determined. The possible pathogenesis related to definite effects of the D-penicillamine is discussed and compared with the communications in the literature. | |
| 7299765 | Persistent hypouricemic effect of longterm diflunisal administration. | 1981 Jul | Diflunisal, a salicylic acid derivative, caused a significant fall in serum uric acid concentration from 0.29 +/- 0.02 to 0.20 +/- 0.02 mmol/l (mean +/- SEM) during chronic administration of 750 mg daily in 18 patients with rheumatoid arthritis. There was a significant correlation between plasma diflunisal concentration and fall of serum uric acid concentrations (p less than 0.01) at week 14. Diflunisal concentrations were statistically higher in females (p less than 0.05) at week 24. | |
| 7432153 | Nodular regenerative hyperplasia of the liver in hematologic disorders: a possible respons | 1980 Sep | Nodular regenerative hyperplasia was found in nine patients who had hematological disease including polycythemia vera, agnogenic myeloid metaplasia, primary thrombocythemia, rheumatoid arthritis with thrombocytosis, multiple myeloma, and erythrocytosis associated with polycystic renal disease. Portal hypertension was suspected in three and features of hypersplenism were present in four. 2. Nodular regenerative hyperplasia occurred in livers which had widespread obliteration of portal vein radicals (obliterative portal venopathy). Morphometric analysis indicated that the portal vein lesions were predominately located in veins up to 0.2 mm in diameter and were significantly more frequent than similar lesions occurring in elderly persons. 3. The following pathogenesis of nodular regenerative hyperplasia is proposed: Thrombi, perhaps largely composed of platelet aggregates formed in the portal venous circulation or spleen, embolize to the liver and results in obliterative vascular lesions. Atrophy and regenerative nodule formation occur in response to the interruption of the portal blood supply. | |
| 3918827 | Amyloid 'degrading factor activity': a non-specific calcium-mediated effect. | 1985 Mar | The clarification of turbid AA-amyloid-fibril-containing agarose gels by serum has been ascribed to degradation of the fibrils and designated as 'amyloid degrading factor'. In the present study, sera of 32 healthy blood donors and 32 patients with rheumatoid arthritis all showed 'degrading factor activity' against both AA amyloid fibrils and a non-fibrillar reticulin preparation of normal liver in an agarose plate assay. AL amyloid fibrils were not affected. The 'degrading activity' of serum was correlated with the serum albumin concentration, and the effect was also given by purified human and bovine serum albumin, although it was not seen with other serum proteins. The 'degrading activity' of serum against AA amyloid and reticulin was significantly correlated: both substrates showed low levels in a chronic disease such as rheumatoid arthritis, and reticulin inhibited 'degrading activity' against AA amyloid and vice versa. These results suggest the same process involves both substrates. 'Degrading activity' was also given by EDTA and a specific calcium chelator, and was inhibited by calcium and magnesium. An enzyme inhibitor showed only partial inhibition of the 'degrading activity' of serum, purified albumin, and EDTA. These results suggest that serum 'degrading factor activity' is a non-specific calcium-mediated effect against AA amyloid and reticulin preparations dispersed in agarose. It may represent a change in the degree of aggregation of these proteins rather than being an effect of proteolytic degradation. This confirms the conclusions of other workers that amyloid 'degrading factor activity' is an phenomenon in vitro of doubtful pathophysiological significance. | |
| 6425865 | Modification of prostaglandin generation by L-histidine--possible pathogenetic implication | 1984 Feb | The effect of l-histidine on arachidonic acid metabolism was studied in rabbit splenic fibroblast cultures and human platelets. The noradrenaline-stimulated generation of PGE2 in fibroblast cultures was inhibited by l-histidine dose dependently. In the same way l-histidine diminished the aggregation-induced synthesis of TXB2 in human platelets. In contrast to this, after incubation with l-histidine the generation of PGE2 in activated platelets increased in a dose dependent way up to 240% of pretreatment values. The further increase of l-histidine concentration resulted in an inhibition of platelet PGE2 synthesis. The present results demonstrate a differential influence of the amino acid l-histidine on cell arachidonic acid metabolism. It is concluded that the supposed anti-rheumatic property of l-histidine is caused by its effect on the synthesis of prostaglandins which are known to be mediators of inflammation. | |
| 6333945 | Cytokines and the chronic inflammation of rheumatic disease. II. The presence of interleuk | 1984 Nov | Sera and synovial fluids from patients with a variety of rheumatic diseases were assayed for interleukin-2 (IL-2) activity in a system utilizing the proliferative response of cultured human phytohaemagglutinin (PHA) T cell blasts. The synovial fluids from 14 rheumatoid arthritis, eight ankylosing spondylitis, three psoriatic arthritis and 11 osteoarthritis patients, all showed IL-2 activity. The amounts of IL-2 present in the fluids from different diseases were compared and ranged from 4.2 to 140.0 units/ml. | |
| 6345166 | Piroxicam--a literature review of new results from laboratory and clinical studies. | 1983 | Piroxicam is a chemically unique, long-acting, potent antiinflammatory/analgesic agent now available for the treatment of arthritis and other inflammatory diseases in over 80 countries around the world. The literature of the last 2 years on preclinical and clinical results with piroxicam has been reviewed. Recent laboratory experiments have given insights into additional actions of piroxicam which may play a role in its broad spectrum of antiinflammatory activity. In various animal models, piroxicam inhibits cell migration into an inflamed site. In vitro, piroxicam inhibits both superoxide anion production and lysosomal enzyme release from human neutrophils and also inhibits IgM-rheumatoid factor production by human lymphocytes. The safety and excellent toleration of piroxicam in animals has been reconfirmed. Extensive clinical trials in over 66,000 patients have demonstrated the high efficacy and excellent toleration of piroxicam in rheumatoid arthritis, osteoarthritis, gout, various musculoskeletal disorders and pain of varied etiology. Patient preference and compliance has consistently been higher for patients on piroxicam therapy. A single 20 mg, daily oral dose produces 24 hour control of symptoms. Piroxicam has been shown to be a useful addition to the physicians armamentarium. |