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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2285737 | The impact of JRA on children, adolescents, and their families. Current research and impli | 1990 Mar | This article focusses on the impact of Juvenile Rheumatoid Arthritis (JRA) on children, adolescents, and their families. Investigations reported in the literature that consider the etiologic role of psychopathology and JRA, psychologic adjustment/maladjustment of adolescents with JRA, family adaptation to chronic illness, and changes in the family that affect health outcomes and treatment compliance are critically reviewed. Methodologic and research design issues are discussed in relation to previous investigations, and implications for future research are presented. | |
1951415 | The rheumatoid factor: an analysis of clinical utility. | 1991 Nov | The rheumatoid factor (RF) is a frequently ordered diagnostic test, yet it possesses significant limitations in sensitivity, specificity, and predictive value. Recognition of these limitations could improve the test's utility by encouraging more selective test ordering and more circumspect interpretation of test results. An analysis of 563 requests for RF from a teaching hospital revealed a positive predictive value of only 24% to 34%. The RF performs best under conditions of moderate pretest likelihood of rheumatoid arthritis, and otherwise has rather limited clinical utility. | |
18415238 | [What do pain scales measure in patients with rheumatoid arthritis?]. | 1990 Dec | In this study carried out in a sample of 80 patients suffering from rheumatoid arthritis (RA) tried an attempt was made to answer the following questions: 1. are there pain factors with a wider range that are more generally applicable than those covered by current German questionnaires? 2. To what extent can somatic parameters predict pain factors? 3. To what extent can a patient's pain behavior (a patient's activity scores) predict pain factors? The study was based on data collected by means of the Pain Experience Questionnaire (PEQ), the McGill Pain Questionnaire MPQ, the West Haven-Yale Multidimensional Pain Inventory WHYMPI, the Measurement Of Patient Outcome Scale MOPO, as well as six different clinical parameters. By means of factor analysis, two second-order factors were extracted, representing 1. the patient's impairment due to intensive pain and 2. socio-emotional consequences of pain. At a statistically significant level, the first factor can be predicted by the clinical variables. Regression of the activity scores on the factor "socio-emotional consequences" suggests a close correlation between the two variables, although the results failed to reach statistical significance. On the whole, the results strongly support the notion of integrating clinical, behavioral and cognitive findings in the diagnostic assessment of chronic rheumatoid pain patients. | |
3416569 | Juvenile rheumatoid arthritis: clinical characteristics in 100 Thai patients. | 1988 Jun | The clinical characteristic of 100 patients diagnosed for JRA at the Department of Pediatrics, Ramathibodi Hospital, Bangkok, Thailand during 1968-1984 are reported. There were 64 male and 36 female patients with a respective ratio of 1.7:1. In ninety-one percent the age of onset was over the age of five, the most common type being polyarticular onset (77%) followed by pauciarticular onset (13%) and systemic onset (10%). Twenty percent had a positive rheumatoid factor and 4% had cardiac complications. Over half of the patients (58%) responded to salicylate and other supportive treatment. The overall remission was 36 percent with a mean follow-up of 3.8 years. The highest remission rate was found in the polyarticular type of onset (43%) followed by systemic onset (33%) and pauciarticular onset (23%). Only 11 percent of the patients responded poorly to the treatment. As opposed to Western reports differences occurred in the type of onset, sex, and eye complications. | |
2027121 | Macromolecular markers in joint disease. | 1991 Feb | Cartilage contains a number of matrix macromolecules not present in other connective tissues. In tissue processes in disease and in normal turnover of the matrix these molecules are fragmented and released into surrounding fluids, in the case of joints into the synovial fluid. Immunoassay techniques have been developed to quantify these fragments. It appears that increased levels in synovial fluid (SF) correlate to a process in the joint cartilage. With successful therapy the level returns to normal. Interestingly, in early rheumatoid arthritis, i.e., with no discernible cartilage damage by radiography, a high SF level of one major cartilage component (proteoglycan aggrecan/fragments) is prognostic for future extensive cartilage destruction. There are major differences in the levels of proteoglycan fragments between different disease groups. Thus, patients with acute reactive arthritis have high SF levels, while patients with late rheumatoid arthritis with extensive cartilage destruction not surprisingly have subnormal values. Patients with osteoarthritis, even those with fairly extensive cartilage destruction, have elevated levels of proteoglycans/fragments in their SF, perhaps indicative of a more pronounced reparative phase. | |
2658071 | The use of quinacrine (Atabrine) in rheumatic diseases: a reexamination. | 1989 May | Atabrine has been available for nearly 60 years. It has a variety of actions and has been administered to millions of individuals. Its antirheumatic properties have been well documented but have not been exploited optimally for a variety of reasons. The drug is generally quite safe and could be used in low doses in lupus and rheumatoid arthritis patients as a steroid-sparing agent or synergistically with hydroxychloroquine. Its bothersome side effects should not deter the clinician from using it, because they are easy to deal with or prevent (Table 5). Future studies should attempt to better characterize the immunosuppressive actions of this powerful drug, particularly in the treatment of lupus erythematosus and rheumatoid arthritis. Studies of the role of combination or single-agent antimalarial therapy in combination with other "remittive" drugs could be of great potential benefit. | |
2021895 | [Sjögren's syndrome and differential diagnosis of parotid gland hypertrophy]. | 1991 Feb | Some auto-immune systemic pathologies can first be detected through a very characteristic symptomatology which must be known for an early diagnosis. This is particularly the case with primary Sjögren syndrome (sicca syndrome). Based on a well documented case, this article is a review of the etiopathogenesis, symptomatology and investigation of the Sjögren syndrome. The differential diagnosis of the parotid gland hypertrophies is also discussed, based on a systematic approach. | |
2235472 | [Primary Sjögren's syndrome--more than a dry mouth and dry eyes]. | 1990 | Primary Sjögren's syndrome is an autoimmune disease mainly affecting exocrine glands. The cardinal symptoms are keratoconjunctivitis sicca and xerostomia, the sicca complex, in addition to extraglandular manifestations. The diverse clinical picture and the therapeutic aspect of the syndrome are discussed. | |
2590806 | Sjögren's syndrome: association with type-1 diabetes mellitus. | 1989 Dec | This study of 102 unselected type-1 diabetic patients has shown that sicca symptoms affect 55% of the patients, although sometimes only during hyperglycaemic phases. While these symptoms might be attributable to the diabetes, the frequency of antinuclear antibodies in those suspected of having Sjögren's (25% by HEp-2) and particularly anti-Ro antibodies (32% by ELISA) reinforces the suspicion that Sjögren's syndrome may underlie their presence. | |
2136584 | Prevalence of primary Sjögren's syndrome in patients with multiple sclerosis. | 1990 May | Sixty-four consecutive patients with clinically or laboratory-supported definite multiple sclerosis (MS) were evaluated prospectively for evidence of primary Sjögren's syndrome (SS). This diagnosis was established when a patient had objective keratoconjunctivitis sicca, xerostomia, or both together with positive labial salivary gland biopsy. We found 2 patients (3.1%) with clinical evidence of primary SS. Whether this association is fortuitous or whether there is pathogenetic linkage between MS and primary SS remains to be established. | |
3301125 | Immunopathological features of primary Sjögren's syndrome. | 1987 Apr | When the immunopathological features of primary Sjögren's syndrome (SS) are outlined, three questions may be asked. Firstly, how is auto-immunity triggered off? The arguments which suggest that viruses play a role are discussed and the key role of the genetic background is emphasized. Secondly, why does the auto-immune vicious circle operate? Lymphocyte proportions, activation markers and functions are analysed in the peripheral blood and in the salivary glands. Thirdly, how do SS lesions occur? Although their physiopathological role is not well defined, a myriad of organ-specific or non organ-specific autoantibodies are observed. In addition to this B-lymphocyte polyclonal activation, apparently there is an early monoclonal proliferation in the course of the disease. | |
2785287 | [Value of anti-Ro antibodies in 2 cases of Sjögren's disease with multisystem involvement | 1989 Jan 21 | In 2 patients the finding of anti-Ro antibodies led to the diagnosis of Sjögren syndrome, which explained a succession of various autoimmune diseases, viz. glomerulonephritis, orbital lymphoma and hemolytic anemia in case 1; primary biliary cirrhosis, subacute cutaneous lupus erythematosus and subclinical autoimmune thyroiditis in case 2. | |
1813522 | Keratoconjunctivitis sicca. | 1991 Mar | Keratoconjunctivitis sicca (KCS) is one of the dry eye syndromes characterized by a deficiency of the aqueous layer of the tear film. The disorder may occur as an isolated entity or in association with a variety of local and systemic conditions affecting aqueous production. Often it follows a mild course but in severe cases, complications resulting in blindness may occur. In this paper, the clinical features, diagnostic strategies, and current treatment of KCS will be covered. Etiologies, including a discussion of the Sjögren syndrome, will also be presented. | |
3701742 | The inheritance of Felty's syndrome in a family with several affected members. | 1986 Feb | A family in which 3 siblings had Felty's syndrome is described. All affected family members shared the common haplotype HLA-A2, B15, Cw3 and DR4. In addition, all affected siblings possessed the A2 and ABO phenotype. Four unaffected siblings possessed either the HLA-A2, B15, Cw3 and DR4 haplotype or the A2 ABO phenotype or neither but not both. We believe our data support the hypothesis that multiple genetic factors are involved in the predisposition of family members to Felty's syndrome. | |
2789650 | Personality structure disturbances and psychiatric manifestations in primary Sjögren's sy | 1989 Aug | It has been recently suggested that primary Sjögren's syndrome (SS) patients present with a variety of personality structure disturbances and psychiatric symptoms. To evaluate this finding further, we assessed hostility structure and psychiatric symptoms in 33 Sjögren's syndrome patients and compared the results with those of 33 healthy women, and 41 women with solid malignant tumors. The utilized psychometric instruments were the hostility and direction of hostility questionnaire (HDHQ) and the symptom checklist 90R (SCL-90R). High levels of introverted hostility were reported by SS patients in relation to the other two groups. Cancer and SS patients reported higher scores on anxiety and depressive symptoms compared to the healthy women, but the differences were not significant. In addition, high scores on paranoid ideation, somatization and obsessive compulsive symptoms were found in SS patients compared to the cancer and healthy controls. The results strongly suggest that psychiatric disorders are common in primary SS patients, who may need appropriate therapy. | |
1780096 | [Sweet's syndrome (acute febrile neutrophilic dermatosis) associated with Sjögren's syndr | 1991 Dec | A case of Sweet syndrome associated with Sjögren syndrome is reported. After a review of the literature, the clinical and pathologic patterns of the disorder are described. The possible underlying or associated diseases, and the problems on diagnosis and prognosis are discussed. In spite of the several etio-pathogenetic problems still unsolved, the syndrome can be considered as a primary, immuno-mediate disorder. | |
1848431 | Induction of neutrophil-mediated cartilage degradation by interleukin-8. | 1991 Mar | Neutrophil influx into the inflamed joint is a characteristic feature of disease flares in patients with rheumatoid arthritis. Recently, a protein produced by monocytes and fibroblasts that has chemoattractive/activating properties for neutrophils has been identified and characterized. This protein has been called interleukin-8 (IL-8). In this study, we cocultured neutrophils with 35S-sulfate-labeled cartilage and found that the addition of recombinant human IL-8 (rHuIL-8) caused rapid, neutrophil-mediated cartilage degradation that was the result of induction of neutrophil degranulation by the cytokine. With 10(-7)M rHuIL-8, 23% of the radiolabel was released into the culture medium in 4 hours, compared with a 9% release without the factor. At concentrations of up to 10(-6)M, rHuIL-8 had no direct effect upon cartilage breakdown. These findings indicate that IL-8 may participate in the pathogenesis of rheumatoid arthritis through the induction of neutrophil-mediated cartilage damage. | |
3264507 | Human cathepsin B and cysteine proteinase inhibitors (CPIs) in inflammatory and metabolic | 1988 May | Synovial fluid of patients with different inflammatory and metabolic joint diseases contains low-molecular CPIs (stefins and cystatins) and high-molecular CPIs (kininogens). An additional inhibitory fragment with a molecular mass of about 20 kDa, which is a part of the kininogen molecule, has been detected. Cathepsin B and cystatin C were determined by ELISA test in 47 patients with rheumatoid arthritis, seronegative spondylarthritis, osteoarthritis, undifferentiated arthritis and gout. A significantly higher amount of cathepsin B was found in patients with rheumatoid arthritis. The elevation of cathepsin B was accompanied by an increased amount of cystatin C. | |
3476907 | Intraosseous rheumatoid nodule. | 1987 | The authors present a case of an intraosseous rheumatoid nodule in the rib of a 9-year-old boy. | |
2549699 | Epstein-Barr virus (EBV). V. Incidence of EBV antibodies in patients with rheumatic diseas | 1989 Jan | Serum samples from 95 patients with rheumatoid arthritis, 24 patients with other various rheumatic diseases, 50 patients with diabetes mellitus, 34 patients with acute viral infections, 6 patients with infectious mononucleosis, 77 patients with lymphomas and leukemia and 110 blood donors and 24 healthy subjects as normal controls, respectively, were tested by indirect immunofluorescence (IF) reaction for the presence of specific antibodies against Epstein-Barr virus determined viral capsid antigen (anti-VCA) and Epstein-Barr active viral infection. The IF test carried out in acetone-fixed smears of EB-3 cell line revealed EB antibodies anti-VCA in 83.3% of infectious mononucleosis, 61.0% lymphomas and leukemia, 58.0% diabetic patients. The frequency of anti-VCA antibodies in rheumatic patients was 31.4%, and 3.6% and 25% in sera from blood donors and healthy subjects, respectively. Incidence of active EBV infection was 5.7% of rheumatic diseases, 17.7% of acute virus infections, 50.0% of infectious mononucleosis, and 31.1% of lymphomas and leukemia patients. Active EBV infection was not found out in blood donors (0/110) and healthy subjects (0/24) groups as control. Rheumatoid arthritis with or without rheumatoid factor patients had serological evidence of active EBV infection 6/26 and 4/26 respectively. |