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)

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

The third and the fourth fraction of the complement (C3 and C4), haptoglobin, fibrinogen, alpha 1-glycoprotein, alpha 2-macroglobulin and transferrin were examined in 692 patients with inflammatory joint disease--rheumatism, rheumatoid arthritis, ankylosing spondylarthritis, psoriatic arthritis, Reiter's syndrome, sacroiliitis [correction of sacroileitis], reactive arthritis, gout, osteoarthrosis and nosologically undefined arthritis in active or nonactive phase and in 60 healthy controls. The complement fractions studied show an increase of various degree and importance in almost all groups of patients in both phases studied. The relations between the complement fractions and the other acute phase indices show significant correlations between them and the other acute phase indices. C3 and to a certain degree C4 could be added to the acute phase reacting indices. Their place in the downgrade scale is as follows: fibrinogen, haptoglobin, alpha 1-glycoprotein, C3, C4, alpha 2-macroglobulin, transferrin.
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PMID:[A comparative study of serum complement (C3 and C4) in inflammatory joint diseases]. 170 1

It is reported on results of comparative biochemical examinations in asymptomatic hyperuricaemia and manifest gout. Restriction of the urate clearance of the kidney, which could be proved also in young patients with asymptomatic hyperuricaemia, and a disturbance of the lipid metabolism which appeared in most cases are discussed from the pathogenetic point of view, in which cases the hyperlipoproteinaemia is regarded as a possible partial pathogenetic factor. For the separation of serum and urine the polyacrylamide gel-pore gradient electrophoresis was used. Using a modifiable concentration gradient this method is superior to the usual disc electrophoresis. The distribution pattern of the types of haptoglobin established by serum separation showed clear deviations from the normal distribution in hyperuricaemia or manifest gout and may be explained as a reference to the influence of genetic factors. By parallel performed electrophoretic separation of serum and urine a microproteinuria could be established and differentiated between glomerular and tubular proteinuria which is regarded as an early symptom of renal changes and was already present in 9 of 20 young patients with asymptomatic hyperuricaemia. These findings emphasize the necessity of an early renal diagnostics.
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PMID:[Comparative biochemical studies in asymptomatic hyperuricemia and manifest gout with special reference to renal change]. 728 41

A 37-year-old male presented with severe anemia, mild jaundice, and hemoglobinuria during his second course of diclofenac for gout. The peripheral blood showed microspherocytes and nucleated red blood cells (RBCs). The reticulocyte count was 21 percent and haptoglobin was < 0.1 g/L. A presumptive diagnosis of diclofenac-induced immune hemolysis was made and blood, urine, and drug samples were referred for investigation. Direct antiglobulin testing showed the RBCs to be coated with IgG1, IgG4, and C3d, but an eluate only yielded weakly reacting IgG antibodies. In tests for drug-dependent antibodies, group O, R1R2 red cells were incubated with the patient's serum that had been mixed with either urine (which contained diclofenac metabolites) or diclofenac solution and then tested by an antiglobulin method. Strongly positive reactions with anti-IgG occurred in the tests using urine but only weak reactions in those tests employing diclofenac solution. All controls gave negative results. These findings support the role of diclofenac in causing hemolysis and the importance of employing urine as a source of drug metabolites. The findings also showed that an immune complex mechanism predominated and that the eluted IgG (detectable independently of the presence of the drug or its metabolites) confirmed a minor autoimmune component. Diclofenac was stopped and treatment with prednisolone and folic acid instituted; this resulted in complete recovery.
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PMID:Immune hemolytic anemia due to diclofenac. 1538 91