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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3057927 | The ELISA-U: an enzyme-linked immunosorbent assay using urease as the enzyme marker for ra | 1988 Nov | A visual, enzyme-linked immunosorbent assay using urease (ELISA-U) as the enzyme marker was adapted for rapid detection of antibody against Plasmodium falciparum. Flat-bottom, 96-well microtiter plates were coated with P. falciparum soluble antigen obtained by saponin and NP-40 treatment of parasite cultures. Antibody was detected by successive incubations with test sera, urease-conjugated rabbit-human antibody, and urease substrate. Reactive sera developed a definite and easily visualized purple color. Sera from patients with single infections of P. vivax or P. ovale were unreactive. No cross-reactivity was noted with sera from patients with rheumatoid arthritis, filariasis, amebiasis, schistosomiasis, dengue, scrub typhus, leptospirosis, or toxoplasmosis. The procedure can be performed at room temperature and completed within 1 hr. The sensitivity of the assay is comparable to that of the indirect fluorescent antibody test at all but the lowest dilutions tested. | |
3696415 | Epidural lipomatosis simulating an epidural abscess: case report and literature review. | 1987 Nov | A case of epidural lipomatosis in a 49-year-old man presenting with paraparesis, midthoracic pain, and Staphylococcus aureus pneumonia is reported. The patient had been on low dose corticosteroid therapy for 7 years for rheumatoid arthritis. The clinical and myelographic findings suggested a diagnosis of epidural abscess, but the only abnormality discovered at operation was abundant fatty tissue in the dorsal epidural space significantly compressing the spinal cord, and this was partially removed. Postoperative neurological improvement suggested that the lipomatosis was responsible for the spinal cord compression and dysfunction. If this diagnosis had been suspected, it might have been confirmed by magnetic resonance imaging or postmyelography computed tomographic scanning. With such a diagnosis, an alternative treatment could have been to decrease the steroid dose, observe for clinical improvement, and perhaps avoid operation. | |
2434431 | Induction of an atypical interferon by bacteroides fragilis and Escherichia coli in experi | 1986 Nov | Previous reports have shown that Bacteroides fragilis may enhance the pathogenicity of coinfecting enterobacteriaceae by interfering with the host's immune response. With the present study, we have investigated the possible role of interferons (IFN) in mediating these effects. Mice injected with B. fragilis developed moderate serum levels of IFN that appeared just prior to alterations of the animals' immunity described earlier. The IFN was neutralized by treatment with anti-IFN-alpha/beta-antibodies or hydrochloric acid; hence it displayed the same "atypical" characteristics as IFN found in patients with immuno-compromising diseases such as AIDS, systemic lupus erythematosus or rheumatoid arthritis. Escherichia coli displayed the same induction patterns as B. fragilis, while gram-positive bacteria induced "regular" IFN alpha/beta and gamma. Spleen cells, peritoneal macrophages, or liver leukocytes taken from B. fragilis or E. coli-injected animals 6 h post infection were refractory to IFN induction by E. coli lipopolysaccharide in vitro; cells from mice infected with gram-positive organisms showed normal or enhanced responsiveness. | |
3707859 | Immunological abnormalities in myelodysplastic syndromes. I. Serum immunoglobulins and aut | 1986 May | The immunoglobulin levels and autoantibody profiles of 104 patients with primary myelodysplastic syndromes (MDS), classified according to the FAB criteria, were analysed. Eight patients, four with coexistent non-Hodgkin's lymphomas, three with chronic lymphocytic leukaemia and one with a lymphoplasmacytoma, were excluded from the final analysis of immunoglobulin levels. Serum protein electrophoresis and immunoelectrophoresis revealed the presence of monoclonal gammopathy in 12 patients (12.5%). Of the remaining 84 patients, a polyclonal rise in serum immunoglobulins was present in 27 (32%) while a further 16 (19%) had low immunoglobulin levels. The direct antiglobulin test was positive in eight out of 98 patients tested (8.1%), and organ and non-organ specific autoantibodies were present in 15 out of 67 patients tested (22.3%). Two patients had associated pernicious anaemia (PA), two hypothyroidism, and one PA with hypothyroidism. Three patients had sero-negative rheumatoid arthritis. These results demonstrate that there is a high incidence of immunological abnormalities in MDS. | |
2557847 | Apparent inactivation of alpha 1-antiproteinase by sulphur-containing radicals derived fro | 1989 Dec 15 | alpha 1-Antiproteinase is the major inhibitor of proteolytic enzymes, such as elastase, in human plasma. Its elastase-inhibitory capacity can be inactivated by exposure to hydroxyl radicals (.OH) generated either by pulse radiolysis or by an Fe3+-EDTA/H2O2/ascorbic acid system. Inactivation of alpha 1-antiproteinase by radiolytically-generated .OH under anoxic conditions was decreased by adding a range of anti-inflammatory drugs to the reaction mixtures, including the thiol compound penicillamine. However, under conditions favouring formation of oxysulphur radicals, protection by thiols such as penicillamine was much decreased. It is proposed that sulphur-containing radicals resulting from attack of biologically-produced oxidants upon penicillamine in the presence of O2 can themselves inactivate alpha 1-antiproteinase, and that such radicals might contribute to the side-effects produced by penicillamine or gold thiol therapy in rheumatoid arthritis. | |
2173157 | [Serum type III procollagen N-terminal peptide in patients with collagen diseases]. | 1990 Apr | The serum concentration of type III procollagen N-terminal peptide (P III P) level is known to reflect the activity of collagen biosynthesis. To analyze the correlation between the disease activity and serum P III P levels in collagen diseases, serum P III P levels in patients with rheumatoid arthritis (RA), progressive systemic sclerosis (PSS), and other collagen diseases were measured. In some patients serum levels of prolyl++-hydroxylase, which is an intra-cellular enzyme of collagen biosynthesis, were measured. Serum P III P levels were elevated in patients with PSS and MCTD/overlap syndrome, suggesting a high rate of collagen biosynthesis by fibroblasts. Patients with RA showed no significant elevation of serum P III P compared with normal control group. But the group of RA patients with elevated ESR and/or serum CRP values showed high levels of serum P III P. The correlation between the disease activity and serum P III P levels was observed in RA patients with positive rheumatoid factor (RF), but not patients without RF. In addition we measured P III P levels in synovial fluid of RA and osteoarthritis patients. The levels were one to three hundred times higher than serum levels, and they showed the positive correlation with serum levels, suggesting that serum P III P might be originated from synovial P III P. | |
1686790 | Involvement of oxygen-derived free radicals in the pathogenesis of chronic inflammatory bo | 1991 Dec 15 | Ulcerative colitis and Crohn's disease are chronic inflammatory bowel diseases. The most widely prescribed drug for treatment of these diseases, sulfasalazine, has been shown to inhibit the activity of free radicals, as the active moiety of sulfasalazine, 5-aminosalicylic acid, is a radical scavenger. This effect of 5-aminosalicylic acid may be of clinical relevance, as a recent study has shown that 5-aminosalicylic acid reacts with oxygen-derived free radicals formed in the intestine in this disease. Reaction with free radicals does not, however, occur in patients with rheumatoid arthritis treated with the same agent. Furthermore, a significant correlation exists between the activity in the intestine of free radicals, as measured by the rate of lipid peroxidation, and the disease activity. | |
1920987 | [A case of oral gold tablet-induced interstitial pneumonitis]. | 1991 Jul | A 76-year-old woman was admitted with exertional dyspnea and chest roentgenographical abnormal shadows appearing after oral gold therapy (total 720 mg) for rheumatoid arthritis. Based on the patient's clinical course, chest roentgenograms, chest CT and pathological findings of TBLB specimens, gold pneumonitis was diagnosed. Steroid therapy improved symptoms and pulmonary function and cotton-like shadows on chest roentgenograms and chest CT scanning. However, linear and large ringed shadows on chest roentgenograms and chest CT scan remained, even after steroid therapy. This case is the first case of oral gold tablet-induced pneumonitis. Although the mechanism of oral gold tablet-induced pneumonitis is considered to be almost the same that of gold injection therapy-induced pneumonitis, this case suggested that fibrotic changes in oral gold tablet-induced pneumonitis may be delayed over a long period. | |
2026474 | Suppressive effect of anti-rheumatic drugs on interleukin-1 beta release from human periph | 1991 | We developed an ELISA system for human IL-1 alpha and -beta release from silica-stimulated monocytes from healthy volunteers and tested the effect of several anti-rheumatic drugs including nonsteroidal anti-inflammatory drug (Ibuprofen). Anti-rheumatic drugs including Auranofin and Sulphasalazine suppressed IL-1 beta release significantly at therapeutic concentrations, whereas Bucillamine, Lobenzarit, D-Penicillamine and Ibuprofen did not. These results suggest a possible immunotherapeutic effectiveness of some anti-rheumatic drugs on rheumatoid arthritis through their inhibition of IL-1 beta release. | |
2089024 | [Castleman tumor, lichen ruber and pemphigus vulgaris: paraneoplastic association of immun | 1990 Dec | In a 45-year-old patient with an unusual clinical course of wide-spread cutaneous and oral lichen planus as well as pemphigus vulgaris of the oral cavity, both refractory to standard therapy, a Castleman tumour was suspected. Computer tomography disclosed a solid retroperitoneal tumour in the pelvis. After its surgical removal both dermatoses regressed substantially within a matter of weeks. In 1954 and again in 1956, Castleman described a thymoma-like lymph node hyperplasia, for which various synonyms are used. Castleman tumours are classified into the common hyalin-vascular type (80-90%), the rarer plasma cell type (10-20%) and the intermediate type. It is usually a benign lymphoma of variable location, but mostly intrathoracic. There is a remarkable association of Castleman tumours with skin diseases (lichen planus, pemphigus vulgaris, Kaposi sarcoma), neurological diseases (POEMS syndrome, myasthenia gravis, arteritis temporalis, Guillain-Barré syndrome), and internal diseases (nephrotic syndrome, amyloidosis, plasmacytoma, rheumatoid arthritis, thrombotic thrombocytopenic purpura). The coincidence of Castleman tumours with various immune phenomena and immunological diseases is higher than could be expected by chance, presenting a challenging pathophysiological model of antibodies and variable immunodeficiencies. | |
2216989 | Medical treatment and prevention of peptic ulcer disease. | 1990 Oct | Many agents seem to be equally effective for the treatment of peptic ulcer disease. This is true despite the drugs' varied mechanisms of action, and this observation has caused investigators to shift their focus from aggressive to defensive factors when studying ulcer pathogenesis. Patients with a healed ulcer are always at risk for recurrence, and guidelines are available for management of these patients. Ulcer prevention becomes a crucial issue in intensive care units where critically ill patients have many known risk factors. Maintaining a gastric pH above 4.0 appears to reduce the morbidity and mortality associated with such stress-induced ulcers. Use of nonsteroidal anti-inflammatory drugs increases ulcer risk and complications in the elderly, in women with rheumatoid arthritis, and in smokers and abusers of alcohol. Prophylaxis with the synthetic prostaglandin analogue misoprostol (Cytotec) appears to reduce this risk. | |
2196872 | Anti-neutrophil cytoplasm antibodies (ANCA). | 1990 Jun | Circulating antibodies directed against cytoplasmic constituents of granulocytes and monocytes (anti-neutrophil cytoplasm antibodies, ANCA) are found in about 80% of active cases of Wegener's granulomatosis and microscopic polyarteritis. Antibodies are detected by indirect immunofluorescence on normal peripheral blood leucocytes, or by ELISA or radio-immunoassay using a neutrophil cytoplasm extract. There are 2 patterns of staining seen on indirect immunofluorescent examination of leucocytes and a number of different molecules recognised on Western blots. In Wegener's granulomatosis diffusely granular cytoplasmic staining (cANCA) is associated with a 29KD molecule that has recently been identified as neutrophil proteinase 3. A finely granular pattern may also be seen in microscopic polyarteritis. A perinuclear pattern (pANCA) is present in some other cases of segmental necrotising glomerulonephritis and occasionally in rheumatoid arthritis but almost never in Wegener's granulomatosis. This pattern is often associated with the presence of anti-myeloperoxidase and anti-elastase antibodies. Levels of anti-neutrophil cytoplasm antibodies usually reflect disease activity but a pathogenetic role for these antibodies in the development of small vessel vasculitides is, as yet, unproven. | |
2183526 | [Generalized tendomyopathy. II: Pathogenesis and therapy]. | 1990 Jan | Many factors are known to play a role in the pathogenesis of generalized tendomyopathy (GTM), or fibromyalgia. While the secondary forms develop along with known diseases, particularly rheumatoid arthritis, the cause of primary GTM is often not well understood. The fact that this disorder usually appears first at a single site, e.g., as low-back pain or cervical syndrome in which poor posture or malformation of the spine can be observed, gives rise to the theory that local changes in the spine or the joints are particular underlying causes of the initial manifestation. As the disorder becomes generalized, however, psychological causes predominate. Psychosocial factors in particular seem to further the process of generalization. Therapy can take many forms. Above all, it calls for an understanding attitude on the part of the managing physician and, whenever, possible, elimination of likely causal factors. Analgesics and antiinflammatories are often inadequate; antidepressants and neuroleptics provide more effective relief. Moreover, intensive physiotherapy and psychotherapy are necessary. GTM in many cases is resistant to treatment despite intensive management, although it often subsides naturally after age 60. Recognizing GTM is of great importance in order to initiate appropriate treatment promptly, avoid incorrect diagnoses and their consequences, e.g., repeat surgery, and to prevent premature disability. | |
2789113 | Reversible interleukin-2 response defects in systemic lupus erythematosus. | 1989 Aug | Limiting dilution analysis techniques were used to determine precursor frequencies for interleukin-2 (IL-2) responsive cells among the peripheral blood lymphocytes of patients with systemic lupus erythematosus (SLE) and rheumatoid arthritis compared with healthy subjects. Response defects in SLE were found, but were of two types: reduced precursor frequencies with normal pattern of response (single-hit kinetics); and abnormal multi-hit responsiveness. These abnormalities were not more frequent statistically in those with active disease. Precursor frequencies of SLE peripheral blood lymphocytes were enhanced by resting the cells for up to 72 h prior to activation, and by adding exogenous IL-2 during the initial activation step. The IL-2 response defects of SLE are therefore reversible and may in part be secondary to other in vivo abnormalities, such as deficient IL-2 production. | |
2472810 | MS: a CNS and systemic autoimmune disease. | 1989 Mar | Multiple sclerosis (MS) is an inflammatory disease which exclusively affects the white matter of the central nervous system (CNS). Although there is a localized immune response within the CNS, immune abnormalities that correlate with disease activity are also found in the peripheral immune compartment of MS patients. These abnormalities primarily involve immunoregulatory defects in T-cell function that are associated with T- and B-cell hyperactivity. In this review, David Hafler and Howard Weiner discuss the evidence that there are T-cell abnormalities in MS similar to those observed in other autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis, and that the immunoregulatory defects in the blood of MS patients appear to be accompanied by the rapid migration of activated T cells from the peripheral blood to the CNS. That immunotherapy directed at the peripheral immune compartment affects the disease process supports their argument. Specifically, total lymphoid irradiation of the peripheral immune compartment ameliorates progressive MS whereas systemic treatment with IFN-gamma makes the disease worse. They conclude that the CNS inflammatory response is closely linked to, and in some ways dependent upon, the peripheral immune compartment. | |
2786180 | Prevalence of diabetes mellitus in common rheumatic diseases. | 1989 Jan | Association between diabetes and some rheumatic diseases have been proposed. The aim of our work is the evaluation of the prevalence of diabetes mellitus (DM) in a population of patients affected by some common rheumatic disease. We evaluated 356 consecutive out-patients [205 (71.66%) women and 101 (28.34%) men] attending the Rheumatology Unit of the Dept. of Internal Medicine of the Catholic University of Rome. The control group consisted of 200 out-patients, age and sex matched, who were examined in the Dept. of Surgery. The diagnosis of rheumatic patients were osteoarthritis (OA) (45.5%), rheumatoid arthritis (RA) (34%) and periarthritis (PA) (20.5%). The prevalence of diabetes mellitus in our rheumatic population was 5.78% in RA, 6.17% in OA, 10.9% in PA. The prevalence of DM in the control group was 4%. Our data suggest that the prevalence of DM in OA and RA patients is similar to that of general population, while it is significantly higher in PA patients probably for an active role of microangiopathy and hyperglycemia in the genesis of such disease. | |
3271571 | Lymphocytosis of large granular lymphocytes in splenectomized subjects. | 1988 | Lymphocytosis of large granular lymphocytes (LGL) has been observed in 6 patients splenectomized for various pathological conditions. In all of them the LGL count was higher than 3.5 x 10(9)/l. No patient showed neutropenia nor suffered from rheumatoid arthritis. A surface markers heterogeneity was observed by immunophenotypic studies. A reversal of the CD4/CD8 ratio was observed in all patients, indicating that LGL are in the majority CD8+. Three patients showed the phenotype CD2+ CD3+ CD4- CD8+ indicating the T-lineage derivation of LGL; patient 6 showed a non-T non-B phenotype (CD2- CD3- CD4- CD8+/-). The percentage of lymphocytes presenting LGL-related markers (HNK-1, CD16, CD11b) was higher than that observed in normal subjects in 4 out of 5 examined patients. However, the percentage of cells bearing these markers was inferior to the LGL counts indicating that not all LGL express them. NK cytotoxic activity was similar to that of normal subjects in the three examined patients. Our data suggest that lymphocytosis of LGL in splenectomized subjects is a reactive process favoured by the asplenic state. | |
3597495 | Occipitocervical fusion. Indications, technique, and long-term results in thirteen patient | 1987 Jul | Thirteen patients who underwent occipitocervical fusion that was performed using the same operative technique were followed for an average of 3.6 years (range, two to seven years). The indications for surgery were occipitocervical instability, neurological deficit, or intractable pain that was not responsive to non-operative treatment. Of the thirteen patients, eight had rheumatoid arthritis, two had atlanto-axial osteomyelitis, and one patient each had trauma, ankylosing spondylitis, and atlanto-occipital osteoarthritis. At follow-up, all of the thirteen patients had a solid arthrodesis and relief of severe pain in the neck. Of the ten patients who had had myelopathy preoperatively, all improved, but of four patients who had been unable to walk preoperatively because of severe motor involvement, only one was considered to be able to walk. Of the thirteen patients, ten had a satisfactory result. Occipitocervical arthrodesis using iliac grafts and the wiring technique that is described herein achieves immediate stable fixation, allowing early mobilization with a successful arthrodesis, and it should be undertaken before severe myelopathy occurs in patients who have instability of the cervical spine. The operation may optimize the patient's chances of neurological recovery. | |
3498034 | Prevalence of anti-SSA (Ro) antibodies in a Mexican population of patients with various sy | 1987 Jun | The prevalence of anti-SSA (Ro) antibodies was investigated in 126 patients with various systemic rheumatic diseases and in 77 normal subjects. Also, we studied the relationship between these autoantibodies and the clinical features of our patients with SLE. Anti-SSA (Ro) occurred with a frequency of 14% in SLE but was not associated with specific clinical features of the disease. In Sjögren's syndrome the frequency was 25%, in rheumatoid arthritis 20.3% and in mixed connective tissue disease 15.4%. Finally, in the control group anti-SSA (Ro) antibodies were not present. We believe that the presence of this antibody is not specific to any rheumatic disease in our Mexican population, and should not be used as a "marker antibody" of some clinical features in patients with SLE. | |
3317810 | Diagnostic methods for evaluation of activity in inflammatory rheumatic disease. | 1987 | Inflammation is one of the cardinal clinical signs of rheumatic disease, although the pathogenesis of inflammation may differ from one such disease to another. The role played by inflammation in the diverse irreversible changes in the structure of the musculoskeletal system is probably also quite different. Despite this proviso, one of the prime tasks of clinical rheumatology is precise measurement of inflammation, because the information so acquired makes it possible to draw conclusions about the activity of the disease and assess the effect of therapeutic measures. Measurement of inflammation consists, fundamentally, of quantifying the classic symptoms of pain, swelling, heat, redness and limitation of movement. All attempts to measure inflammation by means of a single parameter, for instance of a humoral type (acute phase proteins), or by a single method (scintiscanning with radionuclides or thermography) have failed sooner or later. The only practical approach is to measure a number of subjective and objective parameters. With all these methods, sensitivity and reproducibility are crucial to success. In rheumatoid arthritis, the major rheumatic disease, various authors have compiled indices on the basis of individual parameters: number of painful joints, number of swollen joints, grip strength, duration of morning stiffness, a number of function tests, erythrocyte sedimentation rate (or other humoral inflammation parameters), a special pain measurement (pain scale) and subjective evaluation of the rheumatic condition by the physician and the patient. |