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.
Minerva Med 1979 Sep 19
PMID:[Value and significance of the immunologic determination of various serum sialoglycoproteins in rheumatic diseases of inflammatory nature]. 11 11

A 25-year-old white man with gout and nephropathy and with a previous reaction to allopurinol was given a trial dose of oxypurinol. He developed malaise, a generalized erythematous reaction with edema, pruritus, and emesis; this was clinically identical to the reaction he experienced with allopurinol. When the patient's lymphocytes were exposed in vitro to oxypurinol and allopurinol, increased DNA synthesis was observed, suggesting an immunologic basis for the reaction. This patient indicates that clinical cross reactivity to allopurinol and oxypurinol does occur and may be of an immunologic basis. There is a need for additional xanthine oxidase inhibitors for such patients.
Ann Intern Med 1976 Sep
PMID:Allergic reaction to allopurinol with cross-reactivity to oxypurinol. 13 55

Articular chondrocalcinosis results from the deposits of calcium pyrophosphate microcrystals in the articular hyalin and fibrocartilages, the synovium and at times the tendons. In our area it is seen most frequently as isolated cases in the elderly and may be asymptomatic. When the affected joints present clinical manifestations, they vary from acute to subacute or chronic recurrent arthritis. A marked articular destruction can be observed in some cases. There is a classical radiological picture: linear opacities are most frequently seen localized in the mid-zone layer of the hyalin cartilage running parallel to but at a certain distance from the bone cortex. A part of our research has shown that in contrast to urate gout, articular chondrocalcinosis results from a metabolic disturbance of the calcium pyrophosphate localized almost exclusively in the same articular structures. Precise information is lacking at the present time to explain why calcium pyrophosphate mycrocrystals accumulate in the cartilage, the synovium and at times at the tendons; nor do we understand the precise role played by the pyrophosphate in bone and cartilage destruction.
Bull Schweiz Akad Med Wiss 1979 Sep
PMID:[Arthropathies due to calcium pyrophosphates]. 23 70

The condition of generalized periarthritis calcarea (hydroxyapatite deposition disease) is characterised by multiple periarticular calcification which can be localised around practically any joint and also in proximity to the spine. This calcification consists of hydroxyapatite crystals which are responsible for the episodes of acute, subacute or chronic periarticular or articular inflammation so typical of the condition. Because of this one can classify periarthritis calcarea along with gout and chondrocalcinosis in the group of crystal deposition diseases. The actual cause of the calcification remains unknown but it is probable that, along with hereditary factors, disturbances in metabolism play an important role. The diagnosis of generalised periarthritis is made from the characteristic X-ray picture in conjunction with the clinical findings and, on occasion, the demonstration of hydroxyapatite crystals in the affected tissues. In the differential diagnosis gout, chondrocalcinosis, various inflammatory rheumatic conditions and septic arthritis must be excluded and various calcification processes, particularly interstitial calcinosis and lipocal cinogranulomatosis, must also be considered. Since the etiology of the calcification remains unknown to specific treatment is available. Symptomatic treatment with colchicine is mostly inadequate which is why one often has recourse to the use of non-steroid anti-inflammatory drugs and corticosteroids.
Bull Schweiz Akad Med Wiss 1979 Sep
PMID:[Generalized periarthritis calcarea (generalized hydroxyapatite disease)]. 39 90

A patient with intractable tophaceous gout and advanced renal failure responded favorably to treatment by long-term hemodialysis and administration of allopurinol. Plasma uric acid levels returned to normal, tophi decreased in size, and the frequency of attacks of gout decreased markedly and permitted the patient to return to full-time employment.
Mayo Clin Proc 1979 Sep
PMID:Chronic gouty nephropathy treated by long-term hemodialysis and allopurinol. 47 Apr 61

The present paper adopts a definite attitude to the differentiated therapy of the disturbances of the uric acid metabolism. This demands an exacter subdivision of the kind of the metabolic disturbance (types Ia, Ib, IIa, IIb, and III). On the basis of this classification in types an individually adapted therapy is possible. It might form the prerequisite of a still more effective meeting of the nephrogenic complications of the gout and of the reduction of the side effects of the necessary permanent therapy.
Z Gesamte Inn Med 1979 Sep 15
PMID:[Modern differential-therapeutic aspects of the drug therapy of chronic gout]. 58 91

Gout is rarely noted as a clinical problem in secondary polycythemia-- even if profound polycythemia exists, as in cyanotic congenital heart disease. A retrospective study of 81 patients with congenital heart disease was done to assess the incidence of hyperuricemia. Twenty of 46 patients with cyanotic congenital heart disease had serum levels of uric acid greater than 8 mg/dl. Thirteen of 16 (81%) cyanotic male patients more than 15 years old had serum levels greater than 8 mg/dl. For cyanotic patients, serum levels of uric acid were related directly to the degree of polycythemia (r = .44; P less than .02). Impaired renal function or drug therapy did not seem to account for the hyperuricemia. Because levels of uric acid greater than 10 mg/dl probably are nephropathic, many of these patients may be incurring subclinical uric acid nephropathy.
Am J Dis Child 1978 Sep
PMID:Hyperuricemia in congenital heart disease. 68 9

The effect of feeding on plasma-uric acid concentrations of the snake was studied. The values were monitored in 2 gopher snakes and 2 black rat snakes which were fed mice. Plasma uric acid values in snakes increased after eating and gradually returned to base line with the digestion of the mice. Uric acid concentrations were greater in snakes eating 2 mice than in those eating only 1 mouse. The base-line plasma uric acid concentration in snakes was approximately 2 to 5 mg/dl. Plasma uric acid concentrations may be useful in making a diagnosis of gout. Presence of gout is usually indicated by increased uric acid concentrations; however, interpretation of these concentrations should be based on information about the feeding schedule.
Am J Vet Res 1978 Sep
PMID:Effect of feeding on plasma uric acid levels in snakes. 69 68

A study of the distribution of the various risk factors for coronary artery disease as a function of the age and sex of a homogenous population of 316 patients has brought to light the following findings: -- These was found to be a greater incidence (statistically significant) of hypertension disorders of glucose metabolism obesity and hypercholesterolaemia in the females, and of tobacco consumption (cigarettes) and, to a lesser extent, of hypertriglyceridaemia and of gout in the males; -- The females who 'tot up' risk factors have their myocardial infarction at a greater age than the males -- The risk factor which separates the two sexes in the consumption of cigarette tobacco. These findings agree with those already in the literature.
Arch Mal Coeur Vaiss 1976 Sep
PMID:[Myocardial infarction: comparative study of principal risk factors in the two sexes]. 82 69

De novo purine biosynthesis has been investigated in circulating blood lymphocytes in vitro. N-formyl-glycinamide ribonucleotide (FGAR) has been mesured using 14C-formate incorporation in the presence of azaserine, a metabolic inhibitor blocking the metabolical pathway at the level of FGAR synthesis. Such a synthesis was measured in 20 healthy controls, 24 patients with primary gout (11 on allopurinol therapy) and 26 patients with chronic renal failure and secondary hyperuricemia (8 on allopurinol therapy). Among gouty patients without allopurinol therapy, FGAR synthesis was normal in 5 and increased in the others. FGAR synthesis was decreased in patients with renal failure whatever the therapy. However, FGAR synthesis remained increased in patients with a primary gout complicated with renal insufficiency. The test we propose for de novo purine biosynthesis measurement is simple and of value to analyse the patho-physiology of hyperuricemia and its therapy. The test allows an acurate discrimination between primary and secondary hyperuricemia in the presence of renal insufficiency.
Nouv Presse Med 1977 Sep 10
PMID:[De novo purine biosynthesis. In vitro measurement in hyperuricemia (author's transl)]. 90 38


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