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

Analysis of clinical-roentgen-laboratory features of the course of hereditarily determined gout in 74 patients is represented. It is exhibited that hereditarily induced gout begins at the young age and is accompanied by the acute disturbance of purine exchange resulting in serious relapsing course of the articular (with availability of radiological attributes of osteal destruction) and the renal syndromes (urate nephrolithiasis, immune complex glomerulonephritis, tubulointerstitional nephritis) as well as in the early occurrence and rapidly progressing chronic renal insufficiency. The disease is accompanied by high frequency of the cardiovascular pathologies negatively influencing the mean lifetime of patients.
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PMID:[Genetically determined gout: characteristics of the course]. 1693 56

Gout is a chronic metabolic disease caused by a disorder of the purine metabolism leading to hyperuricaemia. It is determined by the deposition of monosodium urate crystals in joints and other tissues which causes an acute inflammatory response and can induce a permanent tissue damage which defines the urate chronic joint disease which is characterised by the appearance of ulceration of the joint cartilage, marginal osteophytosis, geodic and erosive lesions and chronic inflammation of synovial membrane. Gout and hyperuricaemia usually occur after the age of 30 years and more frequently in men. Hyperuricaemia is the result of an increased production of uric acid or its hypoexcretion by the kidneys, or both. In the pathogenesis of gout and hyperuricaemia are involved genetic and environmental factors; further, different pathologic condition such as glycogenosis, renal insufficiency, use of some drugs, are associated with gout. Treatment of acute gout includes colchicine, nonsteroidal anti-inflammatory drugs and glucocorticoids, whereas in the intercritical periods colchicine is effective for preventive purposes. Urate-lowering therapy with xanthine-oxidase inhibitors or uricosuric agents is indicate only in patients with more than two gout crisis per year, tophaceous deposits, uric acid nephrolithiasis, and interstitial renal disease, as asymptomatic hyperuricaemia does not requires any treatment but can be controlled with preventive dietetic measures and changes in lifestyle.
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PMID:Pathogenesis, clinical findings and management of acute and chronic gout. 1721 86

Gout is the most common inflammatory arthropathy for men. Asymptomatic hyperuricemia, which should lead to diet, but not to medication, is much more common still. Increased uric acid levels mostly result from diminished renal excretion, which is more commonly familiar than secondary (renal failure, diuretics). With the first episode of often typical (red, hot, exquisitely painful first MTP joint) acute arthritis or with urate nephrolithiasis, increased uric acid turns pathological. Attacks are treated with NSAIDs or corticosteroids. More common attacks, chronic gout, or urate nephropathy are definite indications for long-term (at least 5 years) therapy with allopurinol or febuxostat. Additional anti-inflammatory medication will be necessary during the first months. Calcium pyrophosphate deposition arthropathy, the second common crystal-induced arthritis, is diagnosed by synovial fluid analysis or for chondrocalcinosis. Treatment for attacks resembles therapy of acute gout; causal therapy is possible in case of secondary forms (e.g. hypothyroidism. hyperparathyroidism, hemochromatosis).
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PMID:[Crystal-induced arthritis--old but important]. 1756 56

Patients with gout frequently have low urinary pH, though the underlying mechanism has not been identified. Recently, nephrolithiasis has been reported to be involved with renal manifestation of metabolic syndrome. The present study was conducted to clarify the mechanism of low urinary pH in gout patients. The relationships between urine pH and factors contributing to metabolic syndrome were investigated. In addition, the effects of PPAR alpha agonists on urine pH were examined. Patients with 24-hour urine samples below a level of pH 5.5 showed higher values for factors constituting metabolic syndrome, compared with those with 24-hour urine pH equal to or greater than 5.5. Multiple regression analysis demonstrated that HOMA index was the only contributing factor to low urinary pH in gout patients, except for serum uric acid. Administrations of PPAR alpha agonists significantly raised 24-hour urine pH levels in gout patients in accordance with a reduction in serum triglyceride concentration, probably through their activities to improve insulin resistance. Our results suggest that insulin resistance plays an important role in the development of low urinary pH in patients with gout and that PPAR alpha agonist is preferable for raising urinary pH of the gout patients with hypertriglyceridemia.
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PMID:Relationship between insulin resistance and low urinary pH in patients with gout, and effects of PPARalpha agonists on urine pH. 1761 4

The purpose of the present study was to compare the clinical characteristics of "pure" uric acid (UA) stone formers with that of "pure" calcium oxalate (CaOx) stone formers and to determine whether renal handling of UA, urinary pH, and urinary excretion of promoters and inhibitors of stone formation were different between the two groups. Study subjects comprised 59 patients identified by records of stone analysis: 30 of them had "pure" UA stones and 29 had "pure" CaOx nephrolithiasis. Both groups underwent full outpatient evaluation of stone risk analysis that included renal handling of UA and urinary pH. Compared to CaOx stone formers, UA stone formers were older (53.3 +/- 11.8 years vs. 44.5 +/- 10.0 years; P = 0.003); they had higher mean weight (88.6 +/- 12.5 kg vs. 78.0 +/- 11.0 kg; P = 0.001) and body mass index (29.5 +/- 4.2 kg/m(2) vs. 26.3 +/- 3.5 kg/m(2); P = 0.002) with a greater proportion of obese subjects (43.3% vs. 16.1%; P = 0.01). Patients with "pure" UA lithiasis had significantly lower UA clearance, UA fractional excretion, and UA/creatinine ratio, with significantly higher serum UA. The mean urinary pH was significantly lower in UA stone formers compared to CaOx stone formers (5.17 +/- 0.20 vs. 5.93 +/- 0.42; P < 0.0001). Patients with CaOx stones were a decade younger, having higher 24-h urinary calcium excretion (218.5 +/- 56.3 mg/24 h vs. 181.3 +/- 57.1 mg/24 h; P = 0.01) and a higher activity product index for CaOx [AP (CaOx) index]. Overweight/obesity and older age associated with low urine pH were the principal characteristic of "pure" UA stone formers. Impairment in urate excretion associated with increased serum UA was also another characteristic of UA stone formers that resembles patients with primary gout. Patients with pure CaOx stones were younger; they had a low proportion of obese subjects, a higher urinary calcium excretion, and a higher AP index for CaOx.
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PMID:Clinical and biochemical profile of patients with "pure" uric acid nephrolithiasis compared with "pure" calcium oxalate stone formers. 1778 20

Arthritis caused by gout (i.e., gouty arthritis) accounts for millions of outpatient visits annually, and the prevalence is increasing. Gout is caused by monosodium urate crystal deposition in tissues leading to arthritis, soft tissue masses (i.e., tophi), nephrolithiasis, and urate nephropathy. The biologic precursor to gout is elevated serum uric acid levels (i.e., hyperuricemia). Asymptomatic hyperuricemia is common and usually does not progress to clinical gout. Acute gout most often presents as attacks of pain, erythema, and swelling of one or a few joints in the lower extremities. The diagnosis is confirmed if monosodium urate crystals are present in synovial fluid. First-line therapy for acute gout is nonsteroidal anti-inflammatory drugs or corticosteroids, depending on comorbidities; colchicine is second-line therapy. After the first gout attack, modifiable risk factors (e.g., high-purine diet, alcohol use, obesity, diuretic therapy) should be addressed. Urate-lowering therapy for gout is initiated after multiple attacks or after the development of tophi or urate nephrolithiasis. Allopurinol is the most common therapy for chronic gout. Uricosuric agents are alternative therapies in patients with preserved renal function and no history of nephrolithiasis. During urate-lowering therapy, the dose should be titrated upward until the serum uric acid level is less than 6 mg per dL (355 micromol per L). When initiating urate-lowering therapy, concurrent prophylactic therapy with low-dose colchicine for three to six months may reduce flare-ups.
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PMID:Gout: an update. 1869

One of the earliest described conditions, gout continues to plague humanity. It is characterised by the deposition of monosodium urate crystals in the joints and soft tissue. The main clinical features of gout are hyperuricaemia, acute monoarticular arthritis, tophi and chronic arthritis, along with nephrolithiasis. Gout typically occurs in middle age and more commonly in men. Asymptomatic hyperuricaemia does not require treatment. The initial attack of acute gout usually affects a single joint, often the first metatarsal phalangeal joint. Definitive diagnosis requires demonstration of urate crystals in the joint fluid. Treatment of acute gout includes nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine and corticosteroids. The most important factor in success of treatment is how quickly therapy is begun after onset of symptoms. Drug treatment of hyperuricaemia includes allopurinol, sulfinpyrazone, probenecid and benzbromarone and should be used in patients with frequent gout attacks, tophi or urate nephropathy.
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PMID:Practical steps in the diagnosis and management of gout. 1803 62

The overall incidence of nephrolithiasis-related acute and chronic renal failure is poorly known and surely underestimated. However, obstructive nephropathy represents a potentially curable form of kidney disease that often requires for managing an instrumentation of urinary tract. Rasburicase is an enzyme that transforms uric acid to allantoin, a compound more water soluble that will be excreted by the kidney more easily. Rasburicase has been proven to be an effective therapy for prevention of tumour lysis syndrome. But it also represents an interesting new option in managing hyperuricemia in patients with severe tophaceous gout. We administered rasburicase intravenously (0.20 mg/kg/day, for 2 days) in 2 adults with acute obstructive nephropathy from renal calculi, which was receiving temporary haemodialysis. Rasburicase produced a sharp polyuria 12-18 hours after its administration accompanied with a fast reduction of serum creatinine levels, that returned to normal range without further dialysis. If we suppose that rasburicase can pass through glomerular filter by its relatively low molecular weight, it could dissolve tubular uric acid crystals in acute renal failure associated to tumour lysis syndrome, providing the restoration of renal function. But we also could postulate that rasburicase can act in urinary tract, fragmentating renal calculi, promoting relief of obstructive uropathy and the resolution of renal failure. We suggest rasburicase should be tried in this new indication to prove its potential efficacy.
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PMID:[Efficacy of rasburicase therapy in obstructive renal failure secondary to urolithiasis: a novel therapeutic option]. 1833 40

Urate lowering treatment is indicated in patients with recurrent acute attacks, tophi, gouty arthropathy, radiographic changes of gout, multiple joint involvement, or associated uric acid nephrolithiasis. Uricosuric agents like benzbromarone and probenecid are very useful to treat hyperuricemia as well as allopurinol (xanthine oxidase inhibitor). Uricosuric agents act the urate lowering effect through blocking the URAT1, an urate transporter, in brush border of renal proximal tubular cells. In order to avoid the nephrotoxicity and urolithiasis due to increasing of urinary urate excretion by using uricosuric agents, the proper urinary tract management (enough urine volume and correction of aciduria) should be performed.
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PMID:[Uricosuric agent]. 1840 25

Female carriers of hypoxanthine-guanine phosphoribosyltransferase (HPRT) deficiency have somatic cell mosaicism of HPRT activity and are healthy. We report a 50-year-old woman without gout or nephrolithiasis. She was never on allopurinol. Normal serum uric acid concentrations, increased plasma hypoxanthine, and xanthine were found. HPRT activity in erythrocytes was surprisingly low: at 8.6 nmol h(-1) mg (-1) haemoglobin. Mutation analysis revealed a heterozygous HPRT gene mutation, c.215A > G (p.Tyr72Cys). Assessment of X-inactivation ratio has shown that > 75% of the active X-chromosome bears the mutant allele and could explain these unusual, previously undescribed findings.
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PMID:Unusual presentation of Kelley-Seegmiller syndrome. 1860 May 21


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