Search for: rheumatoid arthritis methotrexate autoimmune disease biomarker gene expression GWAS HLA genes non-HLA genes
ID | PMID | Title | PublicationDate | abstract |
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9132859 | [Seroprevalence of B19 parvovirus infection in patients with acute polyarthritis]. | 1996 Dec | Over a period of 29 months, from January 1991 to December 1994, all cases of acute polyarthritis seen at the Rheumatology Service in our Institution were studied to determine the seroprevalence of parvovirus B19 (B19) infection. The variables studied included: age and sex of patients, presence of fever and rash, Anti-B19 IgM and IgE serological determinations (ELISA, Mardix Lab.), follow-up time and final diagnosis. The study included 36 patients (22 women and 14 men, mean age 34 +/- 19 years). Thirteen and seven patients had fever and cutaneous rash, respectively. Anti-B19 IgM serology was positive in 4 patients; in 2 of them IgG seroconversion was confirmed. The mean follow-up time was 14 +/- 9 months. Final diagnoses included undifferentiated polyarthritis, rheumatoid arthritis, B19 polyarthritis, systemic lupus erythematosus, and miscellaneous in 19, 7, 4, 2, and 4 patients, respectively. Seroprevalence of B19 infection in acute polyarthritis in our area was 11%, approximately. | |
1317454 | Characterization of type V collagenase (gelatinase) in synovial fluid of patients with inf | 1992 Apr | Gelatin degrading matrix metalloproteinases in synovial fluid from 21 patients with inflammatory arthritis were shown to consist of two distinct gene products, 92 and 70 kDa gelatinases. The gelatinolytic activity of 92 kDa enzyme, which is released from stimulated neutrophils, was positively correlated to neutrophil count in the fluid. By contrast, 70 kDa molecule did not correlate with neutrophil cell count. Purification of these enzymes revealed they could degrade type XI collagen, a cartilage component resistant to interstitial collagenase. The elevated levels of 92 kDa gelatinase in rheumatoid arthritis samples compared to osteoarthritis suggest a role of this enzyme in cartilage destruction. | |
7728880 | Bacterial infections: the arthritis of leprosy. | 1995 Feb | Arthritis is a common feature of leprosy and contributes to disability. Direct invasion of joints and bones by mycobacteria may lead to a destructive arthritis in lepromatous disease. The infective process may involve few or many joints. Reactional states may occur spontaneously but usually after the initiation of anti-mycobacterial treatment. In both the type 1 reaction of borderline case and the type 2 reaction of the lepromatous disease, intense inflammation may occur at sites of infection. The immunology of the reactions is different but they share clinical features including a polyarthritis which may resemble rheumatoid disease. The joint disease may be chronic or relapsing, affecting the wrists and small joints of the hands in particular. Radiological erosions may occur. Mycobacterium leprae is not found in the synovium in this pattern of arthritis. Further study of this phenomenon might yield useful information above the mechanism of joint inflammation in other rheumatic diseases. | |
8943713 | B- and T-cell autoantigens in pristane-induced arthritis. | 1996 Oct | Pristane-induced arthritis (PIA) is a murine disease resembling rheumatoid arthritis (RA) which is characterized by autoimmune responses to joint tissues. To identify the range of potential antigens targeted in PIA, proteins from arthritic or normal joint extracts were fractionated by sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) and systematically screened for the ability to react with either serum IgG, or cultured splenic T cells, obtained from healthy or arthritic mice. Extracts from both normal and arthritic animals contained multiple proteins that were capable of reacting with murine serum IgG in immunoblotting experiments. In healthy controls, more bands were identified in extracts prepared from 30-week-old mice than from 8-week-old animals, but the widest range of proteins bound were derived from arthritic joints. Furthermore, the sera from PIA-positive mice reacted with more bands from each of the extracts than did normal sera. Fractionated extracts prepared from healthy joints failed to stimulate the in vitro proliferation of splenic T cells from either normal or arthritic animals. When arthritic joint components were screened, T cells from healthy mice responded weakly to some fractions, but multiple fractions elicited strong proliferation by T cells from mice with PIA. A band of apparent molecular mass 60000 was the protein most commonly bound by serum IgG from arthritic mice, and the corresponding fraction stimulated the highest responses by T cells from PIA-positive animals. These results are consistent with the notion that the 60,000 MW mammalian heat-shock protein is an important antigen in PIA, but that the autoimmune response diversifies with the development of arthritis to target multiple joint components. | |
7527741 | Anti-CD5 therapy decreases severity of established disease in collagen type II-induced art | 1994 Dec | Collagen-induced arthritis has been widely used as an animal model of rheumatoid arthritis. We have used this model with a view to determining potential therapeutic targets for the treatment of human disease. To do this we have attempted to modulate the progression of established arthritis over a 10-day time period following the first appearance of disease, by i.p. injection of one of three different MoAbs. These consist of a rat IgG2a specific for the CD5 antigen expressed on all T cells and a subpopulation of B cells, a mouse IgG2b recognizing the CD72 antigen, and a rat IgM specific for the B220 molecule, CD72 and B220 both being expressed on all B cells. None of the three MoAbs had depleting activity in vivo. The progression of arthritis was monitored both clinically, and histologically. The effects of treatment with anti-CD5 and anti-CD72 antibodies were compared with control antibodies of the same species class and subclass. In the case of anti-B220 antibodies, the effects of treatment were compared with administration of PBS. Of these MoAbs, only treatment with anti-CD5 resulted in disease amelioration with significant decrease in disease severity in 60% of the animals. These changes became apparent 6 days after initiation of treatment. There were no significant differences in serum levels of IgG antibodies to native bovine collagen type II between the groups of treated and control mice. Possible mechanisms underlying the modification of disease expression following treatment with anti-CD5 MoAb are discussed. | |
8130291 | Factors affecting unprescribed remedy use among people with self-reported arthritis. | 1993 Sep | OBJECTIVE: The purpose of the study is to determine the frequency and consequences of use of unprescribed remedies by people with self-reported osteoarthritis, and to find methods for predicting such use. METHODS: A random digit telephone survey was used to contact respondents. A 90-item questionnaire evaluated demographic characteristics, type of disorder, area affected, severity of problem, and symptoms encountered. RESULTS: Among 1,811 contacts, 21% had musculoskeletal complaints. Of those with self-reported musculoskeletal disorders, 84% had used at least one unprescribed remedy during the past 6 months. People with self-reported rheumatoid arthritis used more such remedies than those with self-reported osteoarthritis, and those with a greater degree of disability used more unprescribed remedies than those who were less affected. Unprescribed remedies were rated as effective as prescribed remedies. CONCLUSIONS: Unprescribed remedies are used frequently, particularly by those with painful and disabling arthritis. These remedies may be effective. Harmful and expensive remedies are used rarely. | |
7537678 | Suppression of adjuvant-induced arthritis by selective inhibition of inducible nitric oxid | 1995 Jan 24 | Adjuvant-induced arthritis is a model of chronic inflammation that exhibits several pathological changes similar to those occurring in rheumatoid arthritis, an autoimmune disease in humans characterized by chronic inflammation of the joints. We have examined the role of inducible nitric oxide synthase in producing the pathological changes associated with adjuvant-induced arthritis. Plasma nitrite concentrations were maximally elevated 14 days following adjuvant administration compared to untreated control animals. Arthritic changes in the paw were first observed between days 10-12 and were maximally elevated 21 days following adjuvant administration. Inducible nitric oxide synthase immunoreactivity was found localized in the synovial tissue from adjuvant-treated rats, while untreated controls exhibited no inducible nitric oxide synthase staining. Two selective inducible nitric oxide synthase inhibitors, aminoguanidine and N-iminoethyl-L-lysine, suppressed the increase in plasma nitrite levels and joint inflammation associated with adjuvant-induced arthritis in a dose-dependent manner. N-Iminoethyl-L-lysine attenuated the inducible nitric oxide synthase immunoreactivity in adjuvant-treated rats. Blood pressure was not affected by the highest dose of N-iminoethyl-L-lysine administered in the drinking water, indicating a lack of inhibition of constitutive nitric oxide synthase. | |
8853166 | Plasma lipids and lipoproteins in juvenile chronic arthritis. | 1996 Jul | Altered levels of high density lipoprotein (HDL), low density lipoprotein (LDL), and very-low density lipoprotein (VLDL), as well as apolipoproteins have been previously described in rheumatoid arthritis patients. We have attempted to evaluate the serum triglyceride, total cholesterol, cholesterol in DHL, LDL, apolipoprotein A1 (apo-A1) and apolipoprotein B (apo-B) levels in juvenile chronic arthritis (JCA) and to correlate them with CRP and ESR in the active and non-active stages of JCA. A total of 37 children no fulfilled ARA criteria for the diagnosis of JCA were studied. There were 18 girls and 19 boys. Age range was 2.5-16 years with a mean of 9.5. The mean duration of disease was 1.8 years. Nineteen patients were accepted to have active disease. Eighteen age and sex matched healthy children served as controls. Apo-A1 was significantly lower in the active JCA group when compared to inactive patients and healthy controls (both p < 0.05). There were significant inverse correlations between apo-A1 and both ESR and CRP levels in these patients (r = 0.67, p < 0.05 and r = -0.61, p < 0.-05, respectively). Although mean LDL levels were numerically lower in the JCA patients (67.2 mg/dl in the active and 68.6 mg/dl in the inactive patients) the difference with healthy controls (91.7 mg/dl) was not statistically significant. There was no significant differences in regard to triglyceride, total cholesterol, cholesterol in HDL, and apo-B levels between neither of the groups. We conclude that JCA patients have a dyslipoproteinaemic state with already altered metabolism of lipids at different stages of the chronic inflammation from active to inactive disease. | |
8222316 | Critical role of peripheral blood phagocytes and the involvement of complement in tumour n | 1993 Nov | Studies have implicated tumour necrosis factor-alpha (TNF-alpha) in type-II collagen (CII)-induced arthritis (CIA), a well established animal model of human rheumatoid arthritis. Precisely how TNF is involved in CIA is not yet clear. In this study the effects of TNF on CIA were examined, independent of its potential effects on the immune response, by performing peri-articular injection of TNF in combination with passive immunization of rats. A sub-arthritic dose (5 mg) of affinity-purified anti-CII IgG, which alone was insufficient to induce spontaneous clinical arthritis, was used throughout the study. Obvious clinical arthritis that persisted for several days was rapidly induced by injections of 100 ng TNF into hindpaws of rats that were passively immunized shortly before the TNF injection. Injections of TNF in non-immunized control rats did not induce clinical arthritis, nor did buffer-only injections in passively immunized controls. The clinical arthritic response was a local phenomenon, limited only to the TNF-injected hindpaws. No swelling was observed in the opposite, buffer-injected hindpaws, indicating the effects of TNF were not systemic. Depletion of peripheral blood phagocytes with anti-rat neutrophil antiserum before passive immunization completely abolished the ability of TNF to induce clinical arthritis, identifying phagocytic cells as the essential target cells in evoking this arthritic response. A role for complement activation was also demonstrated in this model through the use of a soluble recombinant version of CD35, the cell surface complement receptor type-1 (sCR1, BRL55730), which significantly reduced TNF-induced arthritis in phagocyte-replete rats. | |
8488398 | STAR complexes: febrile illnesses associated with sore throat, arthritis, and rash. | 1993 May | Between January 1990 and February 1991 we evaluated the cases of 20 patients for a symptom complex consisting of Sore throat, elevated Temperature, migratory Arthritis, and a pruritic urticarial Rash (STAR). The patients ranged in age from 3 1/2 to 48 years; most were from central Texas. Duration of illness varied from 2 weeks to longer than 1 year. Results of laboratory studies included the following abnormal findings: elevated erythrocyte sedimentation rate, leukocytosis, anemia, and thrombocytosis. Eleven of 18 (61%) patients had low antinuclear antibody titers. HLA-A2 was noted in 8 of 10 (80%) of those tested. Test results were positive in eight cases for IgM antibodies to parvovirus and in six cases for IgM antibodies to rubella, suggesting that these entities may represent an underdiagnosed cause of STAR complex. In six cases no specific cause of disease was found; these cases may be attributable to other infectious agent(s) yet to be identified. Here we present a description of the cases, a discussion of the differential diagnosis, and an evaluation of STAR complex. | |
1586252 | Effect of iron complexes on adjuvant arthritis in rats. | 1992 Apr | When a total dose infusion of iron dextran is given to anaemic rheumatoid patients an exacerbation of inflammatory synovitis in previously affected joints is observed. The adjuvant arthritis model of inflammation in rats has been used to investigate the mechanism of iron promoted synovitis. Either iron dextran (5 mg injected intravenously) with a dextran C control, or iron sorbitol (7.5 mg injected intramuscularly) with a sorbitol citrate complex control was given at the onset of clinical joint inflammation. Iron dextran significantly increased joint inflammation (assessed by joint scoring) at days 12, 13, 14, and 16 after injection. Similarly, iron sorbitol produced a significant increase in the joint score at days 17, 18, 19, and 21. In addition, extensive osteoporosis was observed in the rats treated with iron sorbitol. These pro-inflammatory effects of iron coincide with the presence of positive results for synovial iron (III) using Perl's test and neutrophil infiltration. The results of this study suggest that the iron induced increase in synovitis in adjuvant arthritis is a result of iron promoted oxidative damage and is not likely to be due to the dextran C or the sorbitol citric acid components. It is suggested that a similar mechanism may occur in rheumatoid patients given iron supplements. | |
19078029 | Marked eosinophilia in the pleural fluid associated with pleural rheumatoid nodules. | 1996 Feb | We report a case of a 39-year old African-American man with an eosinophilic (86%) pleural effusion. The finding of rheumatoid nodules in the pleura, with positive assays for rheumatoid factor in both the pleural fluid and blood, suggests rheumatoid disease as the etiology, although the patient did not have any articular manifestations. After the removal of the fluid, no reaccumulation occurred during 6 months of follow-up, and arthritis had not yet appeared. | |
1408116 | [Current status of diagnostic and surgical hip arthroscopy]. | 1992 Aug | Due to the anatomy and topography of the hip, clinical diagnostic procedures are often not very significant. Even the use of highly technical examination methods mostly does not allow differentiation of specific hip problems and do not give exact information about the extent and stage of the lesion. This applies specifically for rheumatoid diseases. Arthroscopy of the hip joint, like other big joints of the extremities, closes this diagnostic gap. Directly visualized findings on the joint, in addition to the results of joint aspiration and histological biopsies, give one security in finding the right diagnosis and planning adequate therapy. The conventional surgical approach to the hip joint leads to large wounds and to corresponding risks and damage to the patient. The advantages of arthroscopy are obvious. It was shown that arthroscopic surgery can be used very efficiently in cases with loose-body, osteochondrosis dissecans, scattered cartilage fragments, or septic arthritis. The other therapeutic application is in cases with rheumatoid arthritis where an arthroscopically assisted synovectomy to the hip achieves a high rate of success without temporary luxation. Diagnostic arthroscopy and arthroscopic surgery to the hip have been used in the Orthopedic Department of the University of Ulm since autumn of 1984. The possibilities and limitations of this surgical procedure have been evaluated in more than 100 cases. Based on our experience with arthroscopy on hip joints, we think that this procedure is very helpful for making a diagnosis and administering therapy. | |
8673810 | Enzyme immunoassay in the diagnosis of Lyme borreliosis. | 1996 | Comparison of serological EIA tests available in Poland, used in diagnostics of Lyme borreliosis: VIDAS Lyme Screen II (LYT II)-bioMérieux (France), Lyme Borreliosis-Dako (Denmark), Borrelia Recombinant-Biomedica (Austria) was carried out in sera of 112 persons: 39 inhabitants of Białowieza area-Lyme borreliosis endemic region, 43 persons with Lyme borreliosis (first of all erythema migrans and neuroborreliosis), 27 healthy persons (control group), 3 persons with serologically confirmed rheumatoid arthritis. Compatibility of results in all tests was 73%, and it was the highest in control group (78%) and in neuroborreliosis patients (76%). Sensitivity of all tests was similar and varied from 77% (Dako) up to 81% (Biomedica). The highest specificity (93%), positive (94%) and negative (74%) predictive values demonstrated bioMérieux test. The lowest error of method for positive results showed bioMérieux (2,48%) and Dako-IgG (2,94%), whereas for negative Biomedica-IgG (0). There were no positive (false) results in sera of patients with rheumatoid factor dependent on cross reaction. | |
8633094 | Systemic versus cartilage-specific expression of a type II collagen-specific T-cell epitop | 1996 Apr 30 | Immunization of mice with rat type II collagen (CII), a cartilage-specific protein, leads to development of collagen-induced arthritis (CIA), a model for rheumatoid arthritis. To define the interaction between the immune system and cartilage, we produced two sets of transgenic mice. In the first we point mutated the mouse CII gene to express an earlier defined T-cell epitope, CII-(256-270), present in rat CII. In the second we mutated the mouse type I collagen gene to express the same T-cell epitope. The mice with mutated type I collagen showed no T-cell reactivity to rat CII and were resistant to CIA. Thus, the CII-(256-270) epitope is immunodominant and critical for development of CIA. In contrast, the mice with mutated CII had an intact B-cell response and had T cells which could produce gamma interferon, but not proliferate, in response to CII. They developed CIA, albeit with a reduced incidence. Thus, we conclude that T cells recognize CII derived from endogenous cartilage and are partially tolerized but may still be capable of mediating CIA. | |
8635287 | Superantigen-mediated proliferation and cytotoxicity of T cells isolated from the inflamma | 1996 Jun | Superantigens are thought to play a role in acute infections and in the pathogenesis of autoimmune diseases that are believed to have an infectious etiology. The effect of the superantigens staphylococcal enterotoxin A, staphylococcal enterotoxin B, and streptococcal M type 5 protein on T cells derived from inflammatory tissues and peripheral blood (PB) of arthritis patients was studied in seven rheumatoid arthritis (RA), two psoriatic arthritis, two reactive arthritis, and one ankylosing spondylitis patient. Superantigen-reactive T cells and T cell lines derived from the PB, synovial fluid (SF), and synovial membrane (SM) of all 12 arthritis tissues recognized the superantigens in an MHC-unrestricted manner. Heterogeneities in proliferation and superantigen-directed T cell cytotoxicity were observed in E+ T cells and the T cell lines. Four SF-CD4+ mycobacteria heat-shock protein 65-kDa specific T cell clones generated from an RA patient could recognize and lyse each other when pulsed with staphylococcal enterotoxin A and used as targets. From another RA patient, four SF-CD4+ T cell clones that specifically recognize autoantigens were generated with human IgG fragments or collagen type II fragments. Heterogeneities of such superantigen-mediated specific lysis were also demonstrated. The data presented by us suggest a model in which superantigens do not have to be involved in triggering the initial disease because autoreactive T cells elicited by antigen can, in the presence of superantigen, lyse cells that express MHC class II molecules, including activated T cells. | |
1414694 | Interaction studies of tilomisole, aspirin, and naproxen in acute and chronic inflammation | 1992 May | The effect of combination NSAID therapy of tilomisole with aspirin or naproxen was studied in rats with carrageenan-induced paw edema and established adjuvant arthritis. Inflamed paws were measured using mercury plethysmography and the arthritic paws were X-rayed to determine any bony/soft tissue changes. The gastrointestinal tract was also examined for bleeding and ulceration. Tilomisole had a less potent acute anti-inflammatory effect than aspirin or naproxen, but produced no significant gastrointestinal damage. A significant reduction in anti-inflammatory activity was observed with the tilomisole/aspirin combination in acute inflammation. Only additive interactions were observed with the naproxen inhibition. In the established arthritis assay, a significant synergistic anti-inflammatory response, i.e. both inhibition of paw edema and bone erosion, was also observed with the 80 and 93% tilomisole/naproxen combinations. The gastric ulcerogenic effect of the combination paralleled its increased activity. The synergism between tilomisole and naproxen in this chronic arthritic model may be due to enhanced cyclooxygenase inhibitory activity. These drug interaction studies suggest possible interactions in human clinical trials of rheumatoid arthritis. | |
1628358 | [Recombinant erythropoietin--a fundamental change in the treatment of anemia?]. | 1992 Apr | The authors summarize in the submitted review recent findings on erythropoietin (EPO) and recombinant EPO (rHuEPO), a new therapeutic preparation which changed fundamentally the clinical picture of many diseases associated with anaemia. The authors discuss the physiology of EPO, regulation of its secretion, mechanism of action on bone marrow and its importance in the pathogenesis of polycythaemia and in particular anaemia. They emphasize in particular the use of rHuEPO in the treatment of different forms of anaemia. They analyze the pathogenesis of renal anaemia and the importance of treatment with rHuEPO for improvement of the haemogram as well as the general condition of the patients, their adaptability, improved psychic condition and reduced need of transfusions. The authors draw attention to the great importance of treatment with rHuEPO in the treatment of anaemias associated with inflammatory diseases (rheumatoid arthritis, AIDS, Crohn's disease and others), anaemia associated with malignancies, in the treatment of surgical diseases and in autotransfusions, in anaemias of premature infants and in some congenital heart diseases. The introduction of rHuEPO into the treatment of anaemia is a great advance of modern pharmacotherapy, which moreover opened new vistas on the role of anaemia in the clinical picture of many diseases. | |
8838528 | A killing defect of natural killer cells as an underlying immunologic abnormality in child | 1996 Jan | OBJECTIVE: To elucidate the nature of the natural killer (NK) cell system in children with systemic lupus erythematosus (SLE), we performed phenotypic and functional studies of circulating NK cells during the course of childhood SLE. For comparison, similar examinations were undertaken in juvenile rheumatoid arthritis (JRA). METHODS: Twenty-five children with SLE and 27 children with JRA were studied; 5 of these children with SLE were examined 6 to 67 months before the overt progression to SLE. The number and cytolytic function of NK cells were determined, using flow cytometry, 51Cr release, and single-cell cytotoxicity assays. RESULTS: At the diagnosis of SLE, a decrease in NK cells defined as CD16+ or CD56+ was the most prominent of the numerical changes in lymphocyte subsets. In regard to cytolytic function, NK activity in children with SLE was greatly reduced at diagnosis: at the single cell level, their NK cells were defective in killing and recycling abilities. Although the relative number of NK cells and their recycling capacity returned to normal with the improvement of active SLE, the killing defect persisted during the inactive phase; there was no persistent NK cell abnormality in JRA. Reduced NK activity due to a killing defect was demonstrable early in the course of SLE: the NK activity and killing capacity values were profoundly decreased in 5 children before the overt progression to SLE. CONCLUSION: It would appear that NK cell functional abnormality, characterized by a killing defect, is an underlying immunological abnormality during the course of childhood SLE. | |
7704463 | Chronic nephrotoxicity of anti-inflammatory drugs used in the treatment of arthritis. | 1995 Feb | We determined the consumption of non-steroidal anti-inflammatory drugs (NSAIDs) and the prevalence of chronic renal impairment and renal papillary necrosis (RPN) in patients with various types of arthritis. Ninety-four patients with chronic arthritis who had consumed more than 1000 capsules and/or tablets of NSAIDs were studied. Renal profiles and radiological investigations such as intravenous urogram (IVU), ultrasonography (US) and computed tomography (CT) were performed to look for evidence of RPN. Twelve patients did not complete the study. Ten of the 82 patients who had completed the study (12.2%) had radiologic evidence of RPN. Five out of 53 patients (9.4%) with rheumatoid arthritis, three out of 11 patients (27.3%) with gouty arthritis and two out of seven patients (28.6%) with osteoarthritis had RPN. Renal impairment (serum creatinine levels of 125-451 mumol/l) was found in 20 patients (24.4%). The patients had consumed 1000-26,300 capsules and/or tablets over a period ranging from 1 yr to more than 30 yr. Patients with chronic arthritis who consume excessive amount of NSAIDs are at risk of developing RPN and chronic renal impairment. |