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)

The sequence of events that may initiate the inflammatory reaction in acute gout has been investigated with specific reference to phagocytosis of urate crystals by polymorphonuclear leucocytes and the results have shown (1) that neutrophil leucocytes avidly ingest microcrystals of sodium monourate, (2) that this causes the rapid degranulation and disintegration of the leucocytes, (3) that fresh leucocytes ingest the debris and crystals liberated by the dead cells, and in their turn degranulate and die, thus possibly establishing a vicious circle in the system.
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PMID:Observations on phagocytosis of urate crystals by polymorphonuclear leucocytes. 4 39

Examination of synovial fluid should be performed in a systematic manner so as to derive the maximum of information. Synovial fluids should be divided into (1) non-inflammatory, (2) inflammatory, (3) purulent and (4) hemorrhagic types. In addition to general description, analysis should include mucin clot test, fibrin clog formation, microscopic examination for cell count and differential cell count, microscopic examination for crystals of gout and pseudogout and microgiological examination. Chemical examination should include estimation of glucose and uric acid. Immunochemical examination may include determination of immunoglobulins, antinuclear factor and LE factor.
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PMID:Clinical pathology of synovial fluid. 5 6

Microsomal and thyroglobulin autoantibody activity has been detected in synovial fluid from 34 of 50 patients with various arthritides (rheumatoid arthritis, ankylosing spondylitis, osteoarthrosis, and gout). Serum from only 4 of these patients showed thyroid-autoantibody activity, and the serum titres were considerably lower than the synovial-fluid titres. This suggests that thyroid autoantibody is produced locally in the joints of these patients.
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PMID:Antithyroid-antibody activity in the snyovial fluid of patients with various arthritides. 8 33

Synovial fluid C3 was measured by electroimmunoassay. When C3 was expressed as mg/ml, the amounts found in Reiter's disease, psoriatic arthritis, gout, and systemic lupus erythematosus were significantly different from degenerative arthritis. When C3 was corrected for total protein, the levels for rheumatoid arthritis, Reiter's disease, psoriatic arthritis, and systemic lupus were significantly different from degenerative arthritis. When C3 was corrected for synovial fluid globulin, only rheumatoid arthritis and systemic lupus were significantly different from degenerative arthritis. Correction of C3 for globulin increases the difference between rheumatoid arthritis and degenerative arthritis. A proportion of gouty fluids with a relative decrease in C3 is demonstrated. It is argued that correction of C3 for globulin is more meaningful than correction for total protein. While many nonrheumatoid inflammatory effusions demonstrate split products of C3, the majority of fluids from patients with systemic lupus have none.
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PMID:Immunoelectrophoretic assay for synovial fluid C3 with correction for synovial fluid globulin. 10 40

Articular manifestations may be the onset of genetic alpha galactosidase deficiency (Fabry's disease). Ultrastructural study shows typical osmiophilic lamellar inclusions of trihexosylceramides in synoviocytes, capillaries and adipocytes. Furthermore microcrystals identical to those seen in Gaucher's disease and type II hyperlipoproteinemia were observed in mitochondria and free in cytoplasm. These data suggest a microcrystalline pathogenesis of these arthropathies, as in gout and chondrocalcinosis, and what we have generally called crystallopathic arthropathies.
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PMID:[Lipid thesaurismosis rheumatism. Arthropathies in alpha galactosidase A deficiency (Fabry's disease). Ultrastructural study of the synovial membrane demonstrating microcrystals in the mitochondria of synoviocytes]. 10 31

A mutant hypoxanthine-phosphoribosyltransferase (EC 2.4.2.8.) from a patient with gout is examined. The activity of the erythrocyte enzyme is about 5% of normal in this case. Immunoprecipitation studies using antiserum against highly purified human hypoxanthine-phosphoribosyltransferase reveal that the patient's erythrocytes contain a normal amount of cross-reacting material. The mutant enzyme has an altered net charge as shown by preparative isoelectric focusing (pI values of 5.75 and 4.55). The influence of chemical modification on enzymic activity was studied using a number of different reagents directed against sulfhydryl-, amino-, and guanidino-groups. Compared with normal hypoxanthine-phosphoribosyltransferase the mutant enzyme shows a generally lowered susceptibility to active site-directed inhibition. It is concluded that the patient's enzyme is the product of a structural mutation.
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PMID:Partial deficiency of hypoxanthine-phosphoribosyltransferase:evidence for a structural mutation in a patient with gout. 11 May 99

For 13 years polyarthritis with specific synovial involvement was observed in a case of type II hyperlipoproteinemia. Microcrystals similar to those described in Gaucher's and Fabry's disease were seen in synovial cytoplasm and mitochondria. These data suggest a microcrystalline pathogenesis for type II hyperlipoproteinemia arthritis as in gout and chondrocalcinosis.
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PMID:[Rheumatism caused by lipid thesaurismosis. Articular involvement in hyperlipoproteinemia type II : presence of microcrystals in the mitochondria of synoviocytes]. 11 27

The enzyme guanine aminohydrolase (guanase) is inhibited by low levels of Pb2+. The inhibition is noncompetitive and the Ki is 3.0 X 10(-6) M. The only other heavy metals that are inhibitory at low concentrations are Ag+, which is 36% more, and Hg2+, which is about 50% less inhibitory than Pb2+. The inhibition of guanase by Pb2+ and Hg2+ is synergistic and the inhibition of the enzyme was readily reversed by EDTA. The relationship of these studies with guanase and to the etiology and treatment of saturnine gout, which appears in humans suffering from lead poisoning, is discussed.
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PMID:Effects of plumbous ion on guanine metabolism. 11 6

A statistical method was used in the evaluation of alpha-1-antitrypsin, acid alpha-1-glycoprotein, and haptoglobin in patients with rheumatic fever, rheumatoid arthritis, gout, periarthritis, arthrosis with inflammation, and primary arthrosis. A highly significant increase was noted in rheumatic fever and rheumatoid arthritis, less so in arthrosis with inflammation and acute gout, while increases were poorly significant for periarthritis and not significant for primary arthrosis. It can be concluded that the determination of these serum sialoglycoproteins serves to distinguish inflammatory and degenerative rheumatism. Haptoglobin proved the most sensitive of the three. Moreover, there was a distinct correlation between ESR and the three indices. It is felt that sialoglycoproteins act as an indirect pointer to acute inflammation, since their degree of increase is related to the formation of inflammatory proteases.
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PMID:[Value and significance of the immunologic determination of various serum sialoglycoproteins in rheumatic diseases of inflammatory nature]. 11 11

Colchicine suppresses the development of carrageenan-induced edema in the rat with a minimum effective oral dose of 6.0 mg/kg. The slope of the dose-response regression line for colchicine differs significantly from that of indomethacin and phenylbutazone. Based on the dosages required to achieve a 50% suppression of this inflammation, colchicine is 0.6 and 1.5 times as potent as indomethacin and phenylbutazone, respectively. In the reversed passive Arthus reaction in the rat, the suppressive activity of colchicine is at least 50 times that of indomethacin and 100 times that of phenylbutazone. The possible significance of these results with regard to the unique effectiveness of colchicine in the treatment of gout is discussed.
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PMID:Mechanism of action of colchicine. III. Antiinflammatory effects of colchicine compared with phenylbutazone and indomethacin. 12 87


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