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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Arthritis, which can be acute, chronic or asymptomatic, is caused by a variety of crystal deposition in joints. The three main types of crystal arthritis are monosodium urate (gout), calcium pyrophosphate dihydrate, and calcium phosphate (usually hydroxyapatite). A clinical approach to diagnosis and management.
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PMID:Crystal arthritis: a clinician's view. 180 73

Problems of pathogenesis, diagnosis and therapy of gout and chondrocalcinosis in which deposits of uric acid salts and calcium are found in the articular tissue are of primary importance in modern rheumatology. The authors give observations of 10 out of 218 patients with primary gout in whom roentgenology had revealed signs of calcium salt deposits in the joints and periarticular tissue.
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PMID:[Chondrocalcinosis in gout]. 181 58

The effect of serum and synovial fluid obtained from six healthy subjects and from 12 patients with gout, six with rheumatoid arthritis and 18 with calcium pyrophosphate dihydrate arthropathy (CPPD) on the rate of in vitro urate crystal formation was measured. Gouty and normal serum produced similar results. Gouty synovial fluids promoted urate crystal formation significantly more than did rheumatoid or CPPD fluids. The promotion of urate crystal formation by gouty synovial fluid was not due to native urate crystals nor to an effect on the level of urate supersaturation. The development of gout in some, but not other, hyperuricaemic subjects may relate to the presence of promoters (or relative lack of inhibitors) of urate crystal formation in the group who develop gout.
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PMID:Evidence for a promoter of urate crystal formation in gouty synovial fluid. 188 97

Crystals of monosodium urate (MSU) provide a dose-dependent stimulus for the production by human blood monocytes of tumor necrosis factor (TNF), a cytokine with proinflammatory properties; TNF activity was inhibited selectively by monoclonal antibody to TNF alpha. Biologically active cell-associated TNF activity peaked at 3 h and was exceeded at 6 h by extracellular activity, which peaked at 12-18 h. Comparable kinetics were observed with immunoreactive TNF alpha. TNF alpha mRNA accumulation in monocytes stimulated with MSU crystals appeared as a single peak at 2-4 h, kinetics compatible with rapid production of a short half-life transcript. In contrast, crystals of calcium pyrophosphate or of hydroxyapatite did not stimulate significant production of TNF or of message. Fresh tophaceous material from a patient with gout contained significant levels of TNF alpha and cells cultured from the tophus produced TNF alpha in vitro. In rheumatoid synovial cells, spontaneous release of TNF alpha was increased by in vitro exposure to MSU crystals. Taken together with earlier work, these results support an expanded view of gouty inflammation in which the crystal-stimulated production of cytokines provides a crucial link between crystal deposition and many of the clinical and pathological facts of both acute and chronic gouty arthritis.
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PMID:Urate crystals stimulate production of tumor necrosis factor alpha from human blood monocytes and synovial cells. Cytokine mRNA and protein kinetics, and cellular distribution. 201 May 50

This review presents up-to-date information on many unusual causes of musculoskeletal disorders. These disorders are grouped together because in each there is abnormal accumulation of normal materials or accumulation of abnormal materials in cells or interstitial tissues. Most of these conditions or their associated musculoskeletal manifestations are rare. However, they may present to the adult or pediatric rheumatologist for diagnosis or therapy or both. Gout, because of its prevalence, has been excluded from this review, but it is included briefly in the discussion of the specific arthritides associated with hyperlipidemias. Disorders associated with abnormal lipid storage in which bone and joint pathology occur frequently include Gaucher's disease, histiocytosis-X, and multicentric reticulohistiocytosis. The rarer disorders of this type discussed are Fabry's disease, sea-blue histiocytosis, and Farber's disease. The abnormal accumulation of metal ions in hemochromatosis and in Wilson's disease are probably causative, either directly or indirectly, in the musculoskeletal features of these diseases, while in ochronosis, calcium crystal deposition accompanies the cartilage degradation characteristic of this disease.
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PMID:Hyperlipidemias, lipid storage disorders, metal storage disorders, and ochronosis. 204 43

The activation of leukocytes by particulates is a critical event in certain inflammatory syndromes, including acute gout associated with microcrystals of monosodium urate monohydrate. In this study we have evaluated mechanisms of human neutrophil activation by urate crystals. Both N-formyl-nor-leu-leu-phe-nor-leu-tyr-lys and uncoated urate crystals (0.5 to 5 mg/ml) but not urate crystals coated with human low density lipoprotein (which suppresses crystal-induced neutrophil responsiveness), stimulated pertussis toxin (PT)-sensitive GTPase activity in purified preparations of human neutrophil membranes. Hydroxyapatite crystals (up to 5 mg/ml) were inactive. Pretreatment of neutrophil membranes with cholera toxin also inhibited crystal-induced and formylated peptide-induced GTPase activity. Pretreatment of whole neutrophils with PT resulted in nearly complete inhibition of formylated peptide-induced cytosolic calcium mobilization, release of superoxide and release of the azurophil granule constituent alpha-mannosidase. In contrast, identical pretreatment of whole neutrophils with PT only partially suppressed urate crystal-induced alpha-mannosidase and superoxide release and failed to inhibit crystal phagocytosis and increases in cytosolic free calcium. Mechanisms of neutrophil activation by monosodium urate crystals appear to be heterogeneous in comparison with activation by formylated peptides and there is no absolute requirement for PT-sensitive membrane G proteins in neutrophil responsiveness to urate crystals.
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PMID:Neutrophil activation by inflammatory microcrystals of monosodium urate monohydrate utilizes pertussis toxin-insensitive and -sensitive pathways. 210 11

The authors have established that to higher calciuria in patients with calcium nephrolithiasis correspond higher vales of uric acid serum concentrations and urine excretion than in the controls. In the oral calcium tolerance test a significant correlation was found between the changes in the uric acid urine excretion and those in the diuresis. The following conclusions are put forward. I. In the patients with recurrent calcium nephrolithiasis and hypercalcinosis one should look for active impairment of uric acid metabolism which should be kept in mind when an antirecurrence treatment is planned. 2. The established parallel increase of uricosuria and calciuria in the oral calcium tolerance test means that to patients with recurrent calcium nephrolithiasis and gout a rich calcium diet should not be prescribed since it increases the risk of formation of calcium oxalate stones.
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PMID:[The effect of oral calcium loading on the serum concentrations and urinary excretion of uric acid in patients with recurrent calcium nephrolithiasis and hypercalciuria]. 228 2

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

The disease caused by the deposition of dehydrated calcium pyrophosphate crystals (chondrocalcinosis) is a metabolic joint disease poorly known outside rheumatologic media. It is estimated that about 5% of the adult population has deposits in the knees and that prevalence increases with age. The incidence of symptomatic disease is about the same as that of gout. The clinical presentation is variable, from pseudogouty forms, pseudorheumatoid arthritis or secondary degenerative joint disease, to 20% of asymptomatic cases. In the systematic evaluation family history should be sought, and metabolic diseases such as gout, diabetes, hemochromatosis, hyperparathyroidism and hypothyroidism should be ruled out. The condition is treated with nonsteroidal antiinflammatory drugs, and although the outcome is generally favorable, severe destructive joint disease may develop. In the present article we review this condition on the basis of the presentation forms of 10 of our patients.
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PMID:[Chondrocalcinosis: a diagnostic-therapeutic approach. Presentation of 10 clinical cases]. 251 33

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


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