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 systematic examination of synovial fluid confirms the noninflammatory nature of degenerative joint disease, is diagnostic of gout, pseudogout, and septic arthritis, and will usually allow the identification of rheumatoid arthritis, systemic lupus erythematosus and Reiter's syndrome.
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PMID:Current concepts in synovial fluid analysis. 72 54

Synovial fluids from 106 patients with various types of arthritis were examined for the presence of conversion products of C3 by means of crossed antigen-antibody electrophoresis and for products of factor B by immunoelectrophoresis. C3 conversion was found in all 15 fluids from patients with seropositive rheumatoid arthritis, in 11 of 15 with seronegative rheumatoid arthritis, in the majority with probable and possible rheumatoid arthritis, juvenile rheumatoid arthritis, SLE, pseudogout, gout, Reiter's syndrome, and frequently in other arthritides studied, but in only one of 15 with degenerative arthritis. In 53 synovial fluids a single C3 conversion peak was seen in addition to the native protein and in 18 others two conversion peaks were present. In many synovial fluids showing conversion whole-complement titers and C3 protein concentrations were normal. In both rheumatoid arthritis and crystal synovitis the per cent of C3 conversion, as estimated by planimetry, correlated with synovial fluid leukocyte counts, Factor B conversion was found in 31 fluids and usually occurred in fluids also showing C3 conversion. The findings indicate that in vivo activation of components of the classical and alternative considered mediated by immune complexes. Activation is also commonly present in a wide variety of other inflammatory arthritides and ofter would not be recognized by measuring only concentrations of hemolytic whole complement or C3 by immunodiffusion. The positive association between C3 conversion and synovial fluid polymorphonuclear leukocytes suggests that chemotactic factors generated from complement may be responsible for the attraction of leukocytes into the synovial space in these diseases.
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PMID:Activation of complement components C3 and factor B in synovial fluids. 83 Jul 76

Lysozyme and lactoferrin levels were measured in 71 synovial fluids (SF) of patients with traumatic effusions, osteoarthritis, rheumatoid arthritis, pseudogout, septic arthritis, and gout, as well as in 91 synovial fluids graded according to their neutrophil count. Elevated lysozyme levels were found in all the inflammatory arthritides and also in osteoarthritis. Lactoferrin levels were not increased in osteoarthritis but displayed a close correlation to the extent of the inflammatory response as judged by SF neutrophilia. The ratio of lysozyme to lactoferrin decreased progressively with increasing SF neutrophilia. In vitro experiments showed that lactoferrin is released from neutrophils isochronously with lysozyme and beta-glucuronidase. Lactoferrin was not found in hyaline cartilage, a tissue known to contain lysozyme. These results are consistent with belief that SF lysozyme has a major derivation from both cartilage and neutrophils, and that lactoferrin arises only from neutrophils. These findings indicate that the simultaneous measurement of lysozyme and lactoferrin provides a potentially useful index of both joint inflammation and cartilage degradation.
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PMID:Lactoferrin and lysozyme levels in synovial fluid: differential indices of articular inflammation and degradation. 83 40

The American Rheumatism Association sub-committe on classification criteria for gout analyzed data from more than 700 patients with gout, pseudogout, rheumatoid arthritis, or septic arthritis. Criteria for classifying a patient as having gout were a) the presence of characteristic urate crystals in the joint fluid, and/or b) a topus proved to contain urate crystals by chemical or polarized light microscopic means, and/or c) the presence of six of the twelve clinical, laboratory, and X-ray phenomena listed in Table 5.
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PMID:Preliminary criteria for the classification of the acute arthritis of primary gout. 85 19

The diagnosis of gout and pseudogout has traditionally been established by the identification, in synovial fluid, of monosodium urate and calcium pyrophosphate dihydrate crystals with compensated polarizing light microscopy. In this paper the utility of electron microscopy in establishing these diagnosis in two cases, when the conventional means of synovial fluid analysis had failed to do so, is discussed. The application of ultrastructural analysis of synovial fluid increases diagnostic capability in the crystal deposition diseases, and it is recommended for those patients in whom the more usual studies have not established a diagnosis.
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PMID:Crystal deposition disease. Diagnosis by electron microscopy. 87 90

Ten patients with inflammatory disease (rheumatoid arthritis, ankylosing spondylitis, Reiter's disease) or metabolic disease (gout, pseudogout, tendinous xanthomatosis) affecting the Achilles tendons are presented and discussed. Radiological lateral views of heel were obtained with xeroradiographic techniques, which permitted the recording on the same image of details of both bone and soft tissue and the evaluation and quantification of the changes in the Achilles tendons. Xeroradiography seems to be a very suitable radiological technique for routine use in the evaluation and follow up of rheumatic diseases of the foot.
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PMID:Xeroradiographic techniques applied to assessment of Achilles tendon in inflammatory or metabolic diseases. 122 36

Acute carpal tunnel syndrome caused by pseudogout occurred in a Chinese patient. The radiological findings mimicked those of synovial chondromatosis. Such radiological findings were very unusual. Diagnosis of such conditions may be difficult, since the clinical features may be confused with those of gout and infection. Surgical release is the treatment of choice.
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PMID:Acute carpal tunnel syndrome caused by pseudogout. 156 78

We suggest that crystals, when introduced into an organism, may behave as conventional antigens, mediating the production of specific antibodies. These antibodies would bear an imprint of the crystal surface and may consequently behave as a nucleating matrix in a new crystallization event. Thus, they would behave as catalytic antibodies. We show that IgG antibodies isolated from patients suffering from gout, a joint disease caused by crystals of monosodium urate monohydrate (MSUM), accelerate the appearance of new crystals of MSUM from a supersaturated solution of the salt in vitro. The same effect is not observed for IgG antibodies isolated from the joint fluids of patients with other joint diseases, such as pseudogout, rheumatoid arthritis, or osteoarthritis. Furthermore, IgG antibodies obtained from rabbits injected subcutaneously with crystals of MSUM, were also nucleating towards MSUM crystals.
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PMID:Antibodies against crystals. 159 11

We measured 5'-nucleotidase (5NT) activity in synovial fluid from 159 patients with various diagnoses. The activity of 5NT was compared with activities of nucleotide pyrophosphohydrolase, alkaline and neutral phosphatases, and adenosine deaminase, in the same samples. Higher levels of 5NT activity occurred in synovial fluid from osteoarthritic joints than from joints of patients with gout, pseudogout, or rheumatoid arthritis. The highest levels of 5NT activity were found in synovial fluid from patients with Milwaukee shoulder syndrome and from osteoarthritis patients in whom deposition of calcium-containing crystals was also present.
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PMID:Synovial fluid 5'-nucleotidase activity. Relationship to other purine catabolic enzymes and to arthropathies associated with calcium crystal deposition. 165 Feb 20

To determine whether complement turnover in synovial fluids of patients with rheumatoid arthritis (RA) reflects activation by the classical or alternative pathway, we used novel immunoassays to measure products of complement activation (the membrane attack complex SC5b-9 and the cleavage fragments Bb and C4d). Mean synovial fluid levels of SC5b-9 were more than 8 times higher in RA than in crystal-induced arthritis (gout and pseudogout) and over 16 times higher than in degenerative joint disease (DJD). Similarly, Bb levels were more than 3 times higher in RA synovial fluids than in crystal-induced arthritis and over 7 times higher than in DJD. Levels of C4d did not differ among the groups. SC5b-9 levels correlated with synovial fluid C3 anaphylatoxin (C3a), Bb, and C4d levels (r = 0.81, 0.62, and 0.51, respectively). In patients with RA, synovial fluid SC5b-9 levels correlated with C3a and Bb (r = 0.6 and 0.56, respectively) but not with C4d. Therefore, novel assays for complement activation indicate that both classical and alternative pathways are involved in complement turnover and that the alternative pathway contributes more to complement activation in RA than in DJD or crystal-induced arthritis.
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PMID:Synovial fluid levels of complement SC5b-9 and fragment Bb are elevated in patients with rheumatoid arthritis. 174 38


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