Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “GOUT”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 217 records · Page 12Linked to original sources
PubMed2003

[Tophaceous gout of the cervical spine, causing cord compression. Case report and review of the literature].

We present the case of a 74-year-old patient with long-standing gout who developed C4-C5 tophaceous gout causing cord compression. The patient had undergone 4 years earlier for a disco-osteophytic cord compression (anterior C4-C5 and C5-C6 discectomy). When admitted, the patient presented quadriparesia which had developed during the previous week in association with acute tophaceous gout on the knees, and the metarsophalangeal articulations, in the context of a bronchial infection. The diagnosis of spondylodiscitis was initially retained because of the clinical features of severe infection and the radiological data (C4-C5 cord compression, with anterior epidural lesions in MRI). The intervention allowed decompression and pathological diagnosis of tophaceous gout. Spinal gout is well-known, and very rarely responsible for cord compression: only 15 cases of cervical gout have been described in the literature. Radiological findings are not specific, and treatment is surgical in the event of medullar compression despite medical treatment.

Aged↗
PubMed2006

[Hyperuricemia and gout: diagnosis and therapy].

In our modern society hyperuricemia is one of the most frequent metabolism disturbances. So far, every fourth man and every tenth woman suffer from an asymptomatic or a symptomatic hyperuricemia named gout. Mostly, over nutrition and malnutrition as well as other secondary factors with a genetically determined renal secretion disturbance of uric acid lead to an increase of serum uric acid. By deposition of uric acid crystals in tissues with intermittent immunologic activation of inflammation cells a manifestation of gout can be seen. The clinical image of gout varies widely. It may manifest as acute or chronic arthritis, tophi on the skin, subcutaneous tissue and the skeletal system as well as urate nephropathy. To eliminate the consequences of hyperuricemia in the long term, apart from a thorough anamnesis of nutritional habits a general examination of metabolic parameters is necessary to exclude a metabolic syndrome and other causes for a secondarily caused hyperuricemia. As gout is very often primarily caused by a renal secretion disturbance of uric acid special diagnostics should be done. Basing on literature research and inclusion of experts opinions this article represents the therapeutically options in treatment of hyperuricemia and gout with their resulting side effects and contraindications.

Allopurinol↗
PubMed2006

Gout: can we create an evidence-based systematic approach to diagnosis and management?

The management of gout can be subdivided into four phases. Asymptomatic hyperuricaemia represents the basic underlying metabolic abnormality that can lead to gout. Studies are evaluating whether interventions may be indicated in some cases. Diagnostic criteria for gout and acute flares are still not well defined unless urate crystals are found. Acute attacks of gout are treated with anti-inflammatory measures and the agent of choice is often determined by attack stage, severity and comorbidities that may contra-indicate one or more agents. After attacks subside, there are asymptomatic periods during which decisions must be made about when and how to start urate-lowering measures. If hyperuricaemia persists, there is generally persistence of urate crystals in the joint. Anti-inflammatory prophylaxis is needed when urate-lowering therapy is started. Lifestyle measures should be addressed. If chronic tophaceous gout is diagnosed, urate lowering should be started without delay. New agents are under development that may help with difficult cases.

Acute Disease↗
PubMed1995

Granulomatous tophaceous gout mimicking tuberculous tenosynovitis: report of two cases.

Granulomatous inflammation in a tissue specimen raises concern about infection with Mycobacterium tuberculosis, atypical mycobacteria, certain fungi, Brucella species, and other infectious agents. Inflammatory disorders, such as sarcoidosis, crystal-associated arthritis, or foreign body reactions also are considered when granulomatous changes are seen on histological examination of a tissue specimen. We describe two cases of granulomatous tenosynovitis due to tophaceous deposits in patients with gout. In one case, tuberculous synovitis was considered the primary diagnosis until the diagnosis of gout was confirmed by examination of a tissue specimen with polarized light. In the second case, gout and tuberculosis were found in the patient's wrist joint. After antituberculous therapy was discontinued, he continued to have wrist synovitis and chronic drainage due to granulomatous tophaceous gout. The findings in this report suggest that gouty tenosynovitis can mimic tuberculous tenosynovitis and that gout should be considered in the differential diagnosis of granulomatous tenosynovitis, especially when acid-fast stains and cultures are negative for mycobacteria.

Adult↗
PubMed2003

Fenofibrate enhances urate reduction in men treated with allopurinol for hyperuricaemia and gout.

OBJECTIVE: To assess the short-term urate-lowering effect of fenofibrate in men on long-term allopurinol therapy for hyperuricaemia and gout. METHODS: Ten male patients (38-74 yr) with a history of chronic tophaceous or recurrent acute gout with hyperuricaemia and on established allopurinol at 300-900 mg/day for > or =3 months were studied in an open-crossover study of fenofibrate therapy. Allopurinol at the established dose was continued throughout the study. Clinical and biochemical assessments (serum urate and creatinine, 24-h urinary excretion of urate and creatinine, liver function tests, creatine kinase and fasting serum lipids) were undertaken at: (i) baseline, (ii) after 3 weeks of once-daily therapy with micronized fenofibrate (Lipantil Micro) at 200 mg and (iii) 3 weeks after fenofibrate was withdrawn. RESULTS: Fenofibrate was associated with a 19% reduction in serum urate after 3 weeks of treatment (mean+/-S.E. 0.37+/-0.04 vs 0.30+/-0.02 mM/l; P=0.004). The effect was reversed after a 3-week fenofibrate withdrawal period (0.30+/-0.02 vs 0.38+/-0.03 mM/l). There was a rise in uric acid clearance with fenofibrate treatment of 36% (7.2+/-0.9 vs 11.4+/-1.6 ml/min, normal range 6-11; P=0.006) without a significant change in creatinine clearance. Both total cholesterol and serum triglycerides were also reduced. No patient developed acute gout whilst taking fenofibrate. CONCLUSIONS: Fenofibrate has a rapid and reversible urate-lowering effect in patients with hyperuricaemia and gout on established allopurinol prophylaxis. Fenofibrate may be a potential new treatment for hyperuricaemia and the prevention of gout, particularly in patients with coexisting hyperlipidaemia or those resistant to conventional therapy for hyperuricaemia.

Acute Disease↗
PubMed2006

EULAR evidence based recommendations for gout. Part II: Management. Report of a task force of the EULAR Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT).

OBJECTIVE: To develop evidence based recommendations for the management of gout. METHODS: The multidisciplinary guideline development group comprised 19 rheumatologists and one evidence based medicine expert representing 13 European countries. Key propositions on management were generated using a Delphi consensus approach. Research evidence was searched systematically for each proposition. Where possible, effect size (ES), number needed to treat, relative risk, odds ratio, and incremental cost-effectiveness ratio were calculated. The quality of evidence was categorised according to the level of evidence. The strength of recommendation (SOR) was assessed using the EULAR visual analogue and ordinal scales. RESULTS: 12 key propositions were generated after three Delphi rounds. Propositions included both non-pharmacological and pharmacological treatments and addressed symptomatic control of acute gout, urate lowering therapy (ULT), and prophylaxis of acute attacks. The importance of patient education, modification of adverse lifestyle (weight loss if obese; reduced alcohol consumption; low animal purine diet) and treatment of associated comorbidity and risk factors were emphasised. Recommended drugs for acute attacks were oral non-steroidal anti-inflammatory drugs (NSAIDs), oral colchicine (ES = 0.87 (95% confidence interval, 0.25 to 1.50)), or joint aspiration and injection of corticosteroid. ULT is indicated in patients with recurrent acute attacks, arthropathy, tophi, or radiographic changes of gout. Allopurinol was confirmed as effective long term ULT (ES = 1.39 (0.78 to 2.01)). If allopurinol toxicity occurs, options include other xanthine oxidase inhibitors, allopurinol desensitisation, or a uricosuric. The uricosuric benzbromarone is more effective than allopurinol (ES = 1.50 (0.76 to 2.24)) and can be used in patients with mild to moderate renal insufficiency but may be hepatotoxic. When gout is associated with the use of diuretics, the diuretic should be stopped if possible. For prophylaxis against acute attacks, either colchicine 0.5-1 mg daily or an NSAID (with gastroprotection if indicated) are recommended. CONCLUSIONS: 12 key recommendations for management of gout were developed, using a combination of research based evidence and expert consensus. The evidence was evaluated and the SOR provided for each proposition.

Acute Disease↗
PubMed2007

Time required for disappearance of urate crystals from synovial fluid after successful hypouricaemic treatment relates to the duration of gout.

OBJECTIVES: To determine whether hypouricaemic treatment results in the disappearance of urate crystals from gouty joints and to define the time required. METHODS: In 18 patients with monosodium urate (MSU) crystal proven gout, and after the initiation of successful serum uric acid (SUA)-lowering treatment, an arthrocentesis of the asymptomatic signal joint (11 knees, 7 first metatarsophalangeal joints) was performed every 3 months to obtain a synovial fluid (SF) sample. The sample was then analysed for the presence of MSU crystals, and the number of crystals/400x field was noted. SUA levels and the duration of gout were also noted. RESULTS: MSU crystals disappeared from the SF of all 18 joints after reduction of SUA to normal levels. The time required for disappearance ranged from 3 to 33 months; disappearance time correlated with the duration of gout (r(s) = 0.71; p<0.01). The median number of MSU crystals in the SF samples before urate-lowering treatment was 7.5 (2.5-11) crystals/400x field, reducing to 3 (1-6.5) crystals/400x field (p<0.05) at 3 months. Crystal counts continued to decrease after 3 months. CONCLUSIONS: In gout, reduction of SUA to normal levels results in disappearance of urate crystals from SF, requiring a longer time in those patients with gout of longer duration. This indicates that urate crystal deposition in joints is reversible. Normalisation of SUA levels results in a decrease in the concentration of MSU crystals in SF in the asymptomatic gouty joints. This may partially explain the reduced frequency of gouty attacks when a patient has been treated with SUA-lowering drugs.

Adult↗
PubMed2000

Improvement of renal function in patients with chronic gout after proper control of hyperuricemia and gouty bouts.

AIM: To evaluate the effect of nonsteroidal anti-inflammatory drug (NSAID) withdrawal on renal function in patients with chronic gout after proper control of hyperuricemia and gouty symptoms. METHODS: Patients with chronic gout, who regularly used NSAIDs to control gouty symptoms prior to urate-lowering therapy, were prospectively followed up in an observational study. Risk factors for renal function impairment were recorded, and the clearance of creatinine (Ccr) was initially measured while on colchinine therapy to prevent gouty bouts. Therapy with urate-lowering drugs was started in order to keep serum urate levels under 6.0 mg/dl (275 micromol/l), and the Ccr was monitored during the follow-up period. Final assessment of the renal function was made after 1 year free from gouty bouts and without NSAID therapy during this period. RESULTS: 87 patients completed a 1-year period of NSAID withdrawal. Low initial Ccr was related to age, hypertension, hypertriglyceridemia and the presence of previous renal diseases. After proper control of gout and NSAID withdrawal during 1 year, the mean Ccr significantly raised from 94 to 104 ml/min. The improvement was especially significant in patients whose initial Ccr was under 80 ml/min. Their mean Ccr rose from 60 to 78 ml/min, and 12 of 29 patients achieved normal Ccr at the end of the study. No risk factor correlated with improvement of the renal function. CONCLUSIONS: Renal function impairment in patients with chronic gout is mainly related to vascular risk factors, but improvement of the renal function was observed after proper control of hyperuricemia and NSAID withdrawal. Optimal control of hyperuricemia and, therefore, of symptoms of gout should be especially considered in patients with vascular risk factors in order to avoid renal function loss due to NSAID use.

Adult↗
PubMed2004

Treating gout in kidney transplant recipients.

OBJECTIVE: To review the etiology, treatment, and preventive strategies of hyperuricemia and gout in kidney transplant recipients. DATA SOURCES: Primary literature was obtained via Medline (1966-June 2003). STUDY SELECTION AND DATA EXTRACTION: Studies evaluating treatment and prevention of hyperuricemia and gout in kidney transplantation were considered for evaluation. English-language studies were selected for inclusion. DATA SYNTHESIS: Approximately 14,000 kidney transplantations were performed in the United States in 2003, and of those transplant recipients, nearly 13% will experience a new onset of gout. The prevalence of hyperuricemia is even greater. There are several mechanisms by which hyperuricemia and gout develop in kidney transplant recipients. Medication-induced hyperuricemia and renal dysfunction are 2 of the more common mechanisms. Prophylactic and treatment options include allopurinol, colchicine, corticosteroids, and, if absolutely necessary, nonsteroidal antiinflammatory drugs. CONCLUSION: It is generally recommended to decide whether the risks of prophylactic therapy and treatment outweigh the benefits. Often, the risk of adverse events associated with agents to treat these ailments tends to outweigh the benefits; therefore, treatment is usually reserved for symptomatic episodes of acute gout. Practitioners must also decide if changes in immunosuppressive regimens may be of benefit on a patient-by-patient basis.

Acute Disease↗
PubMed1963

BLOOD COAGULATION AND PLATELET ECONOMY IN SUBJECTS WITH PRIMARY GOUT.

Previous studies have suggested that there is an increased incidence of degenerative vascular disease in patients with gout and an increased rate of turnover of blood platelets in patients and animals with atherosclerosis. A disturbed uric acid metabolism and "secondary" gout have long been known to occur with bone marrow diseases. A study of platelet economy and blood clotting factors in subjects with primary gout was therefore undertaken.Twenty-two male subjects with gout but with no clinical evidence of vascular disease were studied. Half of these had a negative family history for vascular disease and half had less fortunate ancestors. The most striking differences were found when gouty patients with a negative family history for vascular disease were compared with similar control subjects. The mean platelet half-life was 2.85 days in the gouty subjects and 3.74 days in the controls. The mean platelet turnover (number/c.mm./day) was 58,750 in gouty subjects, 42,370 in controls. Platelet adhesiveness and plasma thromboplastic activity were correspondingly increased in the gouty subjects. Control subjects with a positive family history all showed relatively active clotting system and platelet turnover, similar to the values found in atherosclerotic subjects. The data indicated that there is increased platelet destruction and production in some patients with primary gout. The relation between this anomaly and the vascular disease, and disturbed urate metabolism in gouty subjects, remains to be investigated.

Arteriosclerosis↗
PubMed2004

Gout: a review of its aetiology and treatment.

OBJECTIVE: To review the current understanding of the causes and the management of gout. DATA SOURCES: Publications on all peer-review literature from MEDLINE from 1965 to January 2004. STUDY SELECTION: Selected and evaluated by the author. DATA EXTRACTION: Extracted and evaluated by the author. DATA SYNTHESIS: The underlying metabolic disorder in gout is hyperuricaemia. Most patients with hyperuricaemia remain asymptomatic throughout their lifetime. The phase of asymptomatic hyperuricaemia ends with the first attack of gouty arthritis or urolithiasis. The risk of gout and stone formation is increased with the degree and duration of hyperuricaemia. Drugs available for the treatment of acute gouty arthritis, such as non-steroidal anti-inflammatory drugs, selective cyclo-oxygenase 2 inhibitors, systemic corticosteroids, or colchicine, are effective. For periods between attacks, prophylactic therapy, such as low-dose colchicine, is effective. In those with recurrent attacks of more than two to three times yearly, a uric acid-lowering agent as a long-term therapy should be considered to avoid recurrence and the development of tophaceous gout. CONCLUSIONS: Effective management of gout can be achieved through better understanding of the causes of the condition, preventive measures as well as drug treatment.

Adrenal Cortex Hormones↗
PubMed2005

Female gout: clinical and laboratory features.

OBJECTIVE: To evaluate and compare clinical and laboratory features of gout in men and women. METHODS: Twenty-seven women and 31 men with gout underwent clinical and laboratory evaluation and review of medical records. RESULTS: Disease onset in women was a mean of 7 years later than in men. There were no differences between women and men regarding systemic hypertension, diabetes mellitus, hyperlipidemia, chronic renal failure, renal stones, ischemic heart disease, or heavy alcohol consumption. Tophaceous gout was similar in both groups, although female gender seemed to be protective against risk of developing tophi (odds ratio: 0.449; 95% confidence interval: 0.151-1.330). Podagra was more common in men, and women showed a higher frequency of upper limb joint involvement. Most patients had low urate excretion rates. Achieving disease control was similar in women and men. Of the 8 women who were premenopausal at disease onset, 7 had secondary causes for gout; 5 of the 8 had high serum urate despite treatment. CONCLUSION: Gout in women had a later onset and higher frequency of upper limb joint involvement in comparison to men. Those with premenopausal onset tended to be refractory to standard therapy.

Age of Onset↗
PubMed2005

Frequency and predictors of inappropriate management of recurrent gout attacks in a longitudinal study.

OBJECTIVE: To evaluate the patterns and determinants of medication use during recurrent gout attacks. METHODS: We followed participants with documented gout in an online prospective case-crossover study. During an attack, subjects were asked if they had consulted a physician for the attack and what medications they were using. Definitely inappropriate therapy was defined as use of allopurinol or a uricosuric agent acutely without having used it as a prophylactic. Potentially inappropriate therapy was defined as use of analgesics alone, alternative remedies, or no medications. We estimated the risk of having >or= 1 attack in 1 year using life table methods. We examined the relation of various risk factors to the risk of inappropriate therapy using Poisson regression. RESULTS: Among 232 participants (mean age 52 yrs, 81% male) with documented gout, the risk of having >or= 1 attack in a year was 69%. One hundred ten participants consulted a physician for each attack, 49 did so for only some attacks, while 43 never consulted a physician for any attack. Fifty-three participants had definitely (n = 10) or potentially (n = 43) inappropriate therapy for their recurrent attacks. Physician consultation for an attack was associated with increased risk of inappropriate therapy (risk ratio, RR, 2.5, p = 0.006), whereas an increasing number of gout attacks was associated with lower risk of inappropriate therapy (RR 0.8, p = 0.01). CONCLUSION: Given the high risk of recurrent attacks and the substantial number of persons whose attacks are not appropriately managed, further education about management of gout attacks for both patients and physicians may be warranted.

Adult↗
PubMed2005

Understanding treatments for gout.

Gout is one of the most readily manageable of the rheumatic diseases. This article reviews basic pathways in purine metabolism, uric acid handling, and the pathogenic mechanism of clinical gout, as well as the areas in those pathways amenable to intervention. Attention is also given to associated comorbidities, such as hyperuricemia and obesity, hypertension, hyperinsulinemia, and coronary artery disease. The significance of lifestyle modifications, such as weight loss and alcohol reduction, is discussed as an important adjunct to pharmacotherapy in gout. Current and investigational agents used in gout management are also reviewed. Finally, treatment recommendations for acute and chronic gout are suggested.

Acute Disease↗
PubMed2006

[Decision-making about gout by physicians of China and influencing factors thereof].

OBJECTIVE: To investigate the decision-making about gout by physicians of China and influencing factors thereof. METHODS: A questionnaire survey, including 13 multiple choice questions, was divided into 2 stages. The first/stage questionnaire survey was conducted among 121 physicians of the departments of internal medicine and rheumatology respectively during the grand ward rounds, and the second-stage questionnaire survey was conducted among 75 physicians attending a national continuous medical education (CME) workshop of rheumatology. The data thus collected were pooled and analyzed by logistic regression models. RESULTS: 62 effective questionnaires were collected in the first/stage survey, and 38 effective questionnaires were collected in the second-stage survey, both with a missing rate < 10%. 78.3% of the respondents considered aspiration of the joint fluid as critical for the definitive diagnosis of gout, but only 2.4% of the respondents did so frequently. When treating acute gout in otherwise healthy patients, 69.2% of the respondents preferred oral colchicine, and while treating the patients with renal dysfunction, 41.7% of the respondents used corticosteroids or corticotrophin as the first choice. For long-term uric acid-lowering therapy, 99 of them (82.5%) described a variety of incorrect indications, 107 of them (89.2%) initiated the treatment too early (< or = 2 weeks after the remission), and 92 of them (76.7%) failed to sustain the treatment for at least 5 years. Only 17 physicians (14.2%) used prophylaxis while initiating the uric acid-lowering treatment and only 7 of them (5.8%) selected a prophylaxis time of 7 approximately 12 months. Multiple logistic regression analysis showed that only CMD on gout was associated with correct diagnosis strategy (OR 7.1, 95% CI 2.1 approximately 23.7). CONCLUSION: The management of gout by the physicians in China is often not consistent with that generally accepted internationally. High quality CME may improve the decision-making ability of physicians.

Decision Making↗
PubMed2004

Complex segregation and linkage analysis of familial gout in Taiwanese aborigines.

OBJECTIVE: The prevalence of gout and hyperuricemia in Taiwanese aborigines is remarkably high. Although previous studies have failed to find evidence of a major gene responsible for gout, the disease is thought to involve genetic predisposition. We sought to determine whether genetic factors for familial gout exist among Taiwanese aborigines, and, if so, their chromosomal location. METHODS: We first performed complex segregation analysis. The study sample comprised 945 relatives distributed in 64 pedigrees; among them, 261 affected members (including probands) were found. In all of the aboriginal probands with gout, the disease was diagnosed and confirmed by rheumatologists. Blood specimens were then collected from 127 individuals living in one community that was used in the segregation analysis (from 25 pedigrees, 36 nuclear families, and 112 full sibpairs), and sibpair linkage analysis and a combined transmission disequilibrium test (TDT) method were used to test the genetic components. RESULTS: In segregation analysis, after adjusting for sex and age, an autosomal-arbitrary major gene model was found to fit the data best, with disease allelic frequency of 0.31 and susceptibility of 0.92. In sibpair analysis, there was a clustering of many flanking markers showing significant linkage, including D1S498 (regression coefficient -0.52), D1S2635 (regression coefficient -0.47), and D1S196 (regression coefficient -0.51), in the 1q21 region of chromosome 1 (all P < 0.005). Results of the combined TDT showed that the marker D1S484 was significantly associated (had linkage) with allele 1 and was transmitted more frequently than other markers to the affected offspring (P < 0.005). CONCLUSION: Results of this study provide evidence of a genetic basis for familial gout in the aboriginal Taiwanese population and suggest that a susceptibility locus may be located in the 1q21 region of chromosome 1.

Adult↗
PubMed1982

Aspiration of the asymptomatic metatarsophalangeal joint in gout patients and hyperuricemic controls.

Asymptomatic metatarsophalangeal joints were aspirated in a group of patients with gout, in 2 control groups with hyperuricemia, and in 1 normouricemic control group. Extracellular urate crystals were present in 70% of gout patients, in 1 of 19 patients with asymptomatic hyperuricemia, and in 2 of 9 patients with renal failure and hyperuricemia but no history of joint disease. Crystals were not found in the 10 normouricemic patients who had other types of arthritis. The presence of crystals in the subjects with gout was not correlated with a history of podagra, duration of gout, presence of tophi, or degree of control of hyperuricemia. Though crystals were found on rare occasions in joint fluid of asymptomatic hyperuricemic subjects, the presence of these crystals in asymptomatic joints was more common in subjects with gout.

Arthritis↗
PubMed2005

Febuxostat, a novel nonpurine selective inhibitor of xanthine oxidase: a twenty-eight-day, multicenter, phase II, randomized, double-blind, placebo-controlled, dose-response clinical trial examining safety and efficacy in patients with gout.

OBJECTIVE: Gout affects approximately 1-2% of the American population. Current options for treating hyperuricemia in chronic gout are limited. The purpose of this study was to assess the safety and efficacy of febuxostat, a nonpurine selective inhibitor of xanthine oxidase, in establishing normal serum urate (sUA) concentrations in gout patients with hyperuricemia (>or=8.0 mg/dl). METHODS: We conducted a phase II, randomized, double-blind, placebo-controlled trial in 153 patients (ages 23-80 years). Subjects received febuxostat (40 mg, 80 mg, 120 mg) or placebo once daily for 28 days and colchicine prophylaxis for 14 days prior to and 14 days after randomization. The primary end point was the proportion of subjects with sUA levels <6.0 mg/dl on day 28. RESULTS: Greater proportions of febuxostat-treated patients than placebo-treated patients achieved an sUA level <6.0 mg/dl at each visit (P < 0.001 for each comparison). The targeted sUA level was attained on day 28 in 0% of those taking placebo and in 56% of those taking 40 mg, 76% taking 80 mg, and 94% taking 120 mg of febuxostat. The mean sUA reduction from baseline to day 28 was 2% in the placebo group and 37% in the 40-mg, 44% in the 80-mg, and 59% in the 120-mg febuxostat groups. Gout flares occurred with similar frequency in the placebo (37%) and 40-mg febuxostat (35%) groups and with increased frequency in the higher dosage febuxostat groups (43% taking 80 mg; 55% taking 120 mg). During colchicine prophylaxis, gout flares occurred less frequently (8-13%). Incidences of treatment-related adverse events were similar in the febuxostat and placebo groups. CONCLUSION: Treatment with febuxostat resulted in a significant reduction of sUA levels at all dosages. Febuxostat therapy was safe and well tolerated.

Adult↗