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

40% of the male patients suffering from gouty arthritis treated in our rheumatological unit during a three years period showed a chronic polyarticular course. In polyarticular gout, acute gouty attacks affect above all the joints of the upper limbs. Gouty arthritis in these patients shows an ascending pattern. Therefore, in case of unawareness of the clinical symptoms, differential diagnosis can be difficult especially when laboratory findings including uric acid levels are in normal ranges and classical radiological findings are missing. It is important to notice that the atypical joint attack in gouty arthritis is typical for polyarticular gout. In case of unclear arthritis the polarized light microscopy of the synovial fluid should always be demanded.
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PMID:[Polyarticular gout--change in the clinical picture?]. 877 36

Therapy of hyperuricemia and gout has to depend on pathogenesis and stage of the disease. Dietary regimen are in the forefront in treatment of asymptomatic hyperuricemia. Uric acid lowering drugs can only be supported in repeated serum-measures from 9 mg/dl up. The therapy of an acute attack of gout primarily is done with non-steroidal antiinflammatory drugs, in rare cases with colchicine or corticoids. Gouty arthritis in intermission, independent of the extent of hyperuricemia, as well as chronic gout are indications for an uric acid lowering pharmacotherapy, usually for life. A special therapeutic challenge arises out of renal complications and the frequent association with the metabolic syndrome.
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PMID:[Therapy of hyperuricemia and gout]. 944 17

Gouty arthritis is the culmination of a number of physiologic mechanisms that ultimately result in deposition of uric acid within joints and soft tissues. Decreased uric acid clearance through the kidney is the most common cause of gout. Tophaceous gout occurs in less than 10% of patients. Acute episodes are treated with NSAIDs or colchicine. Low-dose therapy with these agents can also prevent recurrent attacks. Most patients with gout need long-term treatment with either uricosuric agents or xanthine oxidase inhibitors.
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PMID:A practical approach to gout. Current management of an 'old' disease. 1053 12

Gout is a common disease arising due to abnormal purin metabolism and excessive accumulation of uric acid in the blood (hyperuricemia) and manifesting with attacks of acute gouty arthritis. In long duration of gout uric acids accumulate in the bones and periarticular tissues as tophuses. Repeat attacks lead to development of chronic gouty arthritis. Purins restriction diet is an important component of gout treatment. Treatment of acute arthritis should be started early, in initial pains before the development of the attacks. Gouty arthritis in the presence of continuous hyperuricemia, tophyses and urolithiasis is treated with allopurinol. Its intake should be long and controlled by the blood level of uric acid. Balneotherapy is recommended for patients with chronic gouty arthritis associated with cardiovascular diseases, urolithiasis.
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PMID:[Gout: current views. Stage oriented treatment]. 1189 31

Gout is not a new disease for clinicians; nevertheless, there are still many secrets awaiting discovery for improving knowledge with respect to uric acid metabolism and monosodium urate crystal-induced inflammation. This review of the literature will focus on new insights on the pathogenesis of idiopathic hyperuricemia, and on secondary hyperuricemia and gout. There are also important advances on the pathophysiology of acute gout, especially as a self-limited process (switch from monocyte to macrophage, peroxisome proliferator activated receptor-gamma, and nitric oxide), but also of chronic gouty arthropathy. Armaments for treating hyperuricemia and gout may be already improved by losartan or fenofibrate and, in the future, by urate oxydase-polyethylene glycol 20 and renal handling regulatory molecules. Finally, control of hyperuricemia may also be considered in the prevention and treatment of cardiovascular disease.
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PMID:Hyperuricemia and gout. 1274 16

The negative association between gout and rheumatoid arthritis is widely accepted, and gout is also speculated to be rare in systemic lupus erythematosus (SLE), as only a few sporadic cases have been reported. From 1985 to 2001 we encountered 15 lupus patients at Chang-Gung Memorial Hospital, including two with lupus-scleroderma and one with lupus-scleroderma-polymyositis overlap syndrome coexisting with gout. This study retrospectively analyses the clinical and laboratory characteristics of these patients. A lower female predominance is found, and most patients developed gout after the onset of SLE, although gout preceded SLE in two cases. Measurement of serum uric acid and 24-h urine uric acid found all of the patients to be hyperuricaemic and underexcretors of uric acid. Furthermore, most of the patients (14/15) were receiving diuretics. Also, many had hypertension and serious cardiovascular diseases. Renal impairment during gouty attacks seemed to be a predisposing factor for developing end-stage renal disease. Gouty arthritis usually occurred during relative SLE inactivity, podagra was frequent, and tophi were found in a few patients. Compared with the unselected population of SLE patients, the cases studied here had a higher incidence of chronic arthritis, malar rash, haematologic disorder, photosensitivity, serositis and neurologic disorder. Renal disease in the patients sampled was frequently membranous nephropathy.
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PMID:Gout in systemic lupus erythematosus and overlap syndrome - a hospital-based study. 1457 59

Gouty arthritis, a common source of pain and disability, is the most common form of inflammatory arthritis affecting older people. The authors review the epidemiology and pathogenesis of hyperuricemia and gout, as well as the clinical forms of gouty arthritis. Gout is part of a clinical spectrum of conditions (obesity, diabetes mellitus, hyperlipidemia, coronary artery disease) and need for better patient education on management of these associated conditions is emphasized. The general algorithm of gout management is presented. Clinical particularities of gout presentation in older patients (increased incidence in women, polyarticular onset with hand involvement, earlier development of tophi, association with use of diuretics) are reviewed. Barriers against an optimal control of gout include lack of patient education, presence of comorbid conditions, particularly renal impairment, use of multiple drugs such as diuretics, and cognitive decline. Gout management in older adults remains unsatisfactory.
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PMID:Gouty arthritis. A primer on late-onset gout. 1602 79

Gouty arthritis is a characteristically intense acute inflammatory reaction that erupts in response to articular deposits of monosodium urate (MSU) crystals. Important recent molecular biologic advances in this field have given us a clear picture of the mechanistic basis of gouty inflammation. The innate immune inflammatory response is critically involved in the pathology of gout. Specifically, MSU crystals promote inflammation directly by stimulating cells via Toll-like receptor signaling and by providing a surface for cleavage of C5 and formation of complement membrane attack complex (C5b-9), culminating in secretion of cytokines, chemokines, and other inflammatory mediators with a dramatic influx of neutrophils into the joint. Despite the detailed mechanistic picture for gouty inflammation, there are no placebo-controlled, randomized clinical studies for any of the therapies commonly used, although comparative studies have demonstrated that many nonsteroidal anti-inflammatory drugs are equivalent to indomethacin with respect to controlling acute gouty attacks. In general, the first line of anti-inflammatory therapy for acute gout is nonsteroidal anti-inflammatory drugs, and the selective cyclo-oxygenase-2 inhibitor celecoxib can be used where appropriate. The second line of treatment is glucocorticosteroids, given systemically (oral, intravenous, or intramuscular) or intra-articularly. Alternatively, synthetic adrenocorticotropic hormone is effective, partly via induction of adrenal glucocorticosteroids and partly via rapid peripheral suppression of leukocyte activation by melatonin receptor 3 signaling. The third line of treatment is oral colchicine, which is highly effective when given early in an acute gouty attack, but it is poorly tolerated because of predictable gastrointestinal side effects.
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PMID:The inflammatory process of gout and its treatment. 1700 28

Juvenile chronic gout in its polyarticular deformative form has rarely been described in medical literature. We report a rare case of destructive polyarticular tophaceous gout in a 31-year-old Senegalese man. He consulted for bilateral asymmetric polyarthritis with deformities of the hands and feet that had been ongoing in recurrent episodes since the age of 18 years in association with tophus. He had received no previous medication. All laboratory investigations were normal except hyperuricemia 104 mg/l. Radiographs of affected joints demonstrated evidence of destructive polyarthritis, i.e., articular narrowing and osteo-condensation of the left great toe. The patient responded favourably to colchicine, allopurinol and diet. Gouty arthropathy must be differentiated from rheumatoid arthritis, psoriasic arthritis and distal chronic osteoarthrosis. In our case, definitive diagnosis of gouty arthropathy was based on chronic polyarthritis associated with tophus, hyperuricemia and therapeutic response to colchicine. Polyarticular gout can be suspected in case of chronic seronegative polyarthritis and diagnosis can be confirmed on the basis of plain radiographs and laboratory investigations showing uricemia. Treatment is effective, well tolerated and inexpensive.
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PMID:[Polyarticular gout in young adults: a curable rheumatic disease]. 1692 21

Gout refers to heterogeneous group of metabolic diseases characterized by production of deposits of sodium urate crystals in tissues. Gout manifests as acute gouty arthritis with classic clinical picture, or as chronic gouty arthropathy with periarticular and subcutaneous deposits of sodium urate crystals, i.e. tophi. As for kidney, gout is manifested as acute or chronic gouty nephropathy and urolithiasis. These manifestations occur separately or they are combined. Hyperuricemia of primary gout is caused rather by impaired renal secretion than overproduction of uric acid. Secondary hyperuricemia is associated with many pathological conditions; it is also connected with the use of various medicaments. Pathogenesis of gouty arthritis is critically influenced by sodium urate crystals and inflammatory processes they induce. Hyperuricemia is part of metabolic syndrome X which is associated with unanswered question of the relationship between uric acid and atherosclerosis. Although gouty arthritis is the most frequent inflammatory disease of joints in men over 50 years of age, it is often diagnosed and treated inadequately. On that account, the indication of long-term hypouricemic therapy should be always based on the following criteria: secondary causes of hyperuricemia have to be excluded first; frequency of gout attacks and the risk of their recurrence should be taken into consideration; then it is necessary to search for renal manifestations of gout; and last but not least, we should check whether there are any associated diseases classified in metabolic syndrome X.
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PMID:[Pathogenesis, diagnostics and therapy of gout]. 1696 17


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