Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Synovial fluid samples (139) from 121 patients with rheumatoid arthritis, osteoarthritis, pseudogout, chronic pyrophosphate arthritis, gout, and reactive arthritis were analysed for cartilage proteoglycan components. Keratan sulphate (KS) epitope was determined by a competitive radioimmunoassay, and total sulphated glycosaminoglycans (S-GAG) were determined after papain digestion by a specific dye binding assay. Increased concentration of both KS epitope and S-GAG were found in synovial fluid from joints with acute inflammatory arthropathy (gout, pseudogout, and reactive arthritis). Analysis of consecutive samples from the same joint at different stages showed that the concentration of KS epitope or total S-GAG varied with acute inflammatory activity. In samples from patients with chronic conditions during active and inactive inflammatory phases concentrations were much lower and not distinguishable among these disease groups. The detection of raised concentration of proteoglycan components may reflect the rapid depletion or greatly increased turnover of proteoglycan in the articular cartilage during acute inflammation in the joint. This did not appear to be sustained in most patients with chronic joint diseases.
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PMID:Increased concentrations of proteoglycan components in the synovial fluids of patients with acute but not chronic joint disease. 246 86

In order to avoid inappropriate therapy and prolonged morbidity, it is important to recognise when a patient's rheumatic complaints are due to drugs. However, this is often difficult because of the large number of drugs that have been implicated and the diversity of clinical presentations. Arthropathy may be seen with several different syndromes, including drug-induced lupus erythematosus (DILE), serum sickness and gout. The most widely reported of these is DILE, which usually develops after some months or even years of drug therapy. While many authors do not specifically require their presence for the diagnosis of DILE, antinuclear antibodies have been detected in the great majority of reported patients with DILE, whatever the causative drug. In contrast, patients who develop arthropathy soon after commencing a drug rarely have antinuclear antibodies and appear to be distinct from patients with DILE. Apart from arthropathy, a number of other syndromes that appear to have an immunological basis may be induced by drugs. Cutaneous vasculitis is not uncommon and drugs are frequently considered to be the aetiological factor. Whether drugs may cause larger vessel systemic vasculitis is less certain. Rarely, polymyositis and scleroderma-like syndromes have been associated with drug therapy. Corticosteroid-induced osteoporosis is a complication of all the corticosteroid preparations that are widely used at present. However, the development of deflazacort, a so-called 'bone-sparing' steroid, has raised the possibility that the effect of corticosteroids on bone may be separable, at least in part, from the other actions of these drugs. Data have been conflicting with regard to whether there is a 'safe' dose of corticosteroid. Similarly, it is unclear whether prophylactic therapy with agents such as calcium, fluoride and vitamin D is beneficial. Nonetheless, recent findings suggest that approaches will be developed to minimise the risk of osteoporosis in patients who require corticosteroids. There are a number of other ways in which drugs may affect bones. Osteomalacia is a well-known but uncommon complication of treatment with anticonvulsants and occasionally other drugs. The mechanism probably relates to the induction of hepatic enzymes and the consequent increased metabolism of vitamin D in patients with borderline levels initially. Osteosclerosis may also result from drug therapy; usually with fluoride or retinol (vitamin A) and its analogues. With continued research, the true spectrum of drug-induced rheumatic syndromes should become more clearly defined.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Drug-induced rheumatic syndromes. Diagnosis, clinical features and management. 249 Jan 48

Synovial fluids from patients were examined, including 15 cases of rheumatoid arthritis (RA); 9 cases of sero-negative arthropathy (3 cases of ankylosing spondylitis, 6 cases of reactive arthritis); 1 case of gout arthritis; and 5 cases of osteoarthritis. The synovial fluids contained 330-72600 white blood cells/mm3, 9-97% of which were granulocytes, in RA patients. Other physical features of RA fluids were: straw green color, cloudy or unclear; moderate viscosity; fair or poor mucin clotting; lack of crystals and bacteria. Synthesis of the above may contribute to the diagnosis of RA. We also found that IgG, IgA and IgM of serum and IgG of synovial fluids in 15 cases of RA were higher than in the other arthritis groups; the IgM-RF positive rates of RA synovial fluids and sera were 20% and 35.7% respectively, while all were negative in the other groups. Immunoglobulins and complement levels in the synovial fluids of all the tested arthritis cases were about half of those in the serum.
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PMID:[The clinical significance of synovial fluid examination]. 253 73

Crystal-related joint diseases are often associated with systemic inflammatory manifestations, including increased levels of acute-phase proteins, leukocytosis, and fever. Recently, interleukin-6 (IL-6) has been identified as a pluripotent mediator of inflammatory and immunologic responses and the major hepatocyte-stimulating factor. In this study, we demonstrated that monosodium urate (MSU) and calcium pyrophosphate dihydrate (CPPD) crystals, and to a lesser extent, hydroxyapatite crystals, increased IL-6 production by synoviocytes and monocytes in vitro. Immunoprecipitation experiments showed that MSU and CPPD crystals, but not hydroxyapatite crystals, were able to increase the release of newly synthesized IL-6. Crystal-induced IL-6 stimulated acute-phase protein synthesis, immunoglobulin production, and hybridoma cell proliferation, which was neutralized by a specific antibody to IL-6. High levels of IL-6 were found in synovial fluid from patients with gout and pseudogout. These results demonstrate that MSU and CPPD crystals can induce IL-6 production in synoviocytes and monocytes, and that synovial fluid from patients with gout and pseudogout contains high levels of IL-6. Crystal-induced IL-6 is likely to be an important mediator of inflammatory responses in acute gout and pseudogout.
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PMID:Inflammatory microcrystals stimulate interleukin-6 production and secretion by human monocytes and synoviocytes. 255 32

Safe, effective treatment is available for acute crystal-associated arthropathy. It is time for some older remedies, phenylbutazone and perhaps colchicine, to give way to more modern regimens of combined NSAID therapy and intra-articular steroid injection. Hypouricaemic agents have revolutionised the management of gout but are not without their dangers, and there is a need for re-emphasis on the value of dietary measures and control of alcohol and diuretic use. At present only symptomatic management is available for chronic pyrophosphate- and hydroxyapatite-associated disease.
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PMID:Crystal-associated rheumatic disease. Current management considerations. 266 Nov 99

Cryptococcal arthritis remains a rare entity. Crystalline arthropathy has been described in association with bacterial infection, but no similar association has been described for crystalline joint disease and fungal infection. We have described a renal transplant patient with concurrent gout and cryptococcal arthritis that responded favorably to treatment. Joints with crystalline arthropathy should be cultured for both bacteria and fungi.
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PMID:Cryptococcal pyarthrosis complicating gouty arthritis. 268 33

Less than 30 years ago, McCarty and others first described a syndrome which presented with gout-like attacks of arthritis but was due to CPPD crystals instead of urate crystals. They termed the condition "pseudogout." It was noted that this was often associated with chondrocalcinosis and it was commonly held that cartilage calcification had to be present if the diagnosis was to be suggested on the basis of the radiographic findings. Subsequently, a clinical and radiographic pattern has emerged in which the diagnosis of CPPD deposition disease can be suggested in the absence of chondrocalcinosis. This condition is termed pyrophosphate arthropathy and is differentiated from degenerative disease by the pattern and distribution of the joint disease. It is important to recognize CPPD deposition disease because of its association with other diseases, such as hemochromatosis and hyperparathyroidism. Although painful periarticular tendinous calcification (peritendinitis calcarea) resulting from the deposition of calcium HA crystals has long been recognized, it has only recently been discovered that intra-articular HA can be associated with an acute inflammatory synovitis. Additionally, patients are now being identified who have CPPD deposition at one anatomic location and HA deposition at another. Differentiation of these various types of crystal-induced arthropathies should lead to more effective therapy in the future.
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PMID:Chondrocalcinosis and other calcifications. 284 68

One hundred consecutive patients admitted to an acute geriatric unit were examined for evidence of peripheral arthritis with recognised criteria used to define osteoarthritis, rheumatoid arthritis, pyrophosphate arthropathy, gout, and disorders of the shoulder joint. The presence of arthritis and its severity were related both to functional independence and to a recognition by the patient that joint problems were impairing independence. Seventy six patients had clinical peripheral arthritis; 48 had arthritis contributing to loss of function, and 19 of these did not volunteer evidence of their joint disease. The common occurrence of arthritic conditions in the elderly, with consequential disability and dependency, suggests that increased medical awareness may be required to prevent unnecessary morbidity. Our findings need confirmation in community based studies.
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PMID:Peripheral arthritis in the elderly: a hospital study. 293 Feb 78

A 31 year old man with Down's syndrome presented with a 10 year history of an inflammatory polyarthritis resembling juvenile chronic arthritis. This case was similar to those already reported of an arthropathy associated with Down's syndrome but was eventually found to be gout. This emphasised the importance of serum uric acid estimation in patients with Down's syndrome and coexistent arthritis.
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PMID:Arthritis in Down's syndrome. 296 56

The monoclonal antibodies anti-2H4 and anti-4B4 identify the suppressor-inducer (CD4+2H4+) and helper-inducer (CD4+4B4+) subpopulations of CD4 (T4+) lymphocytes, respectively. The cell surface phenotype of peripheral blood lymphocytes and synovial fluid lymphocytes in patients with rheumatoid arthritis and other inflammatory joint diseases was analyzed by use of these and other well-characterized anti-T-cell monoclonal antibodies. In the synovial fluid of patients with rheumatoid arthritis, there was a markedly decreased percentage of T4+2H4+ suppressor-inducer cells (3.1 +/- 1 percent) and an increased percentage of T4+4B4+ helper-inducer cells (29.1 +/- 9 percent) as compared with the proportions found in the peripheral blood of normal individuals (T4+2H4+: 19.0 +/- 6 percent, T4+4B4+: 23.0 +/- 7 percent). Moreover, patients with other chronic and acute inflammatory joint diseases exhibited highly similar synovial T-cell findings to those of the patients with rheumatoid arthritis (T4+2H4+: 4.2 +/- 3 percent, T4+4B4+: 33.1 +/- 9 percent). In contrast, there were no significant differences between the normal control subjects and patients with rheumatoid arthritis in the percentage of T4+2H4+ cells in peripheral blood lymphocytes, nor were there significant differences between normal control subjects, patients with rheumatoid arthritis, and patients with other joint diseases (osteoarthritis, gout, B27+ spondyloarthropathy, and psoriatic arthritis) in the number of T4+4B4+ cells or in the T4/T8 ratio of peripheral blood lymphocytes. However, very low numbers of T4+2H4+ (suppressor-inducer) peripheral blood lymphocytes were seen in a subgroup of patients, including five of seven with Reiter's syndrome and several patients with systemic rheumatic disease syndromes. In addition, although the percentage of T4+2H4+ cells in peripheral blood lymphocytes of patients with osteoarthritis (13.7 +/- 7 percent) and gout (14.3 +/- 7 percent) was decreased compared with that of normal controls (19.0 +/- 6 percent) (osteoarthritis versus normal controls p less than 0.025), this difference appeared to reflect alterations due to age rather than disease. Consistent with the phenotypic changes observed, synovial T cells were also functionally defective, since autologous mixed lymphocyte reaction-activated T4 cells from the synovial fluid of patients with rheumatoid arthritis failed to exhibit suppressor-inducer activity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Abnormalities in CD4+ T-lymphocyte subsets in inflammatory rheumatic diseases. 296 79


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