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World J Rheumatol. Nov 12, 2014; 4(3): 62-71
Published online Nov 12, 2014. doi: 10.5499/wjr.v4.i3.62
Gout: A clinical overview and its association with cardiovascular diseases
Laura BE Kienhorst, Hein JEM Janssens, Matthijs Janssen
Laura BE Kienhorst, Matthijs Janssen, Department of Rheumatology, Rijnstate Hospital, 6880 TA Arnhem, The Netherlands
Hein JEM Janssens, Department of Primary and Community Care, Radboud University Medical Centre, 6525 GA Nijmegen, The Netherlands
Hein JEM Janssens, Department of Clinical Research, Rijnstate Hospital, 6880 TA Arnhem, The Netherlands
Author contributions: All authors contributed to this paper.
Correspondence to: Laura BE Kienhorst, MD, LLM, Department of Rheumatology, Rijnstate Hospital, PO Box 9555, 6880 TA Arnhem, The Netherlands. lkienhorst@rijnstate.nl
Telephone: +31-88-0055400 Fax: +31-88-0056612
Received: June 29, 2014
Revised: August 8, 2014
Accepted: September 4, 2014
Published online: November 12, 2014

Abstract

Gout is a common disease caused by the deposition of monosodium urate (MSU) crystals in patients with hyperuricemia, and characterized by very painful recurrent acute attacks of arthritis. The gold standard for diagnosing gout is the identification of MSU crystals in synovial fluid by polarization light microscopy. Arthritis attacks can be treated with anti-inflammatory medications, such as non-steroidal anti-inflammatory drugs, colchicine, oral prednisone, or intra-articular or intramuscular glucocorticoids. To prevent gout uric acid lowering therapy with for example allopurinol can be prescribed. When gout is adequately treated, the prognosis is good. Unfortunately, the management of gout patients is often insufficient. Gout is associated with dietary factors, the use of diuretics, and several genetic factors. Comorbidities as hypertension, chronic kidney disease, cardiovascular diseases, the metabolic syndrome, diabetes, obesity, hyperlipidemia, and early menopause are associated with a higher prevalence of gout. Xanthine oxidase and chronic systemic inflammation seem to play an important role in the pathophysiology of the association between gout and cardiovascular diseases. To prevent cardiovascular diseases gout patients must be early screened for cardiovascular risk factors.

Key Words: Gout, Review, Clinical, Cardiovascular diseases

Core tip: Gout is a common disease caused by the deposition of monosodium urate (MSU) crystals in patients with hyperuricemia, and characterized by very painful recurrent acute attacks of arthritis. The gold standard for diagnosing gout is the identification of MSU crystals in synovial fluid. Arthritis attacks are treated with anti-inflammatory medications, to prevent gout uric acid lowering therapy can be prescribed. When gout is adequately treated, the prognosis is good. Comorbidities as chronic kidney disease, cardiovascular diseases, and the metabolic syndrome are associated with gout. Gout patients must be early screened for cardiovascular risk factors.



INTRODUCTION

Gout is a common disease caused by the deposition of monosodium urate (MSU) crystals in patients with hyperuricemia, and characterized by very painful recurrent acute attacks of arthritis. Gout has been recognized as a clinical entity for a long period of time. Acute gout occurring in the first metatarsophalangeal (MTP-1) joint, first identified by the Egyptians in 2640 BC, was later recognized by Hippocrates in the 5th century BC, who referred to it as “the unwalkable disease”[1]. The first person to use the word gout (gutta quam podagram vel artiticam vocant - the gout that is called podagra or arthritis) was the Dominican monk Randolphus of Bocking, domestic chaplain to the Bishop of Chichester (1197-1258)[2]. Through the ages gout was known as “the king of diseases and the disease of kings”, because of its association with alcohol consumption, purine-rich diet and obesity[3].

This review starts with a clinical overview on the epidemiology, pathogenesis, clinical presentation, risk factors, diagnosis, treatment, and prognosis of gout. Hereafter, the review discusses the association between gout and cardiovascular diseases.

CLINICAL OVERVIEW OF GOUT
Epidemiology

Gout is one of the most common rheumatic diseases with a prevalence of 1%-2% in the adult population in developed countries[4]. The prevalence of gout is higher in men, and rises with age[5]. Gout occurs four to ten times more often in men than in women among patients under the age of 65[5]. In the elderly, gout has a somewhat more equal sex distribution[5], possibly due to the fall of uricosuric estrogen in women after the menopause[6,7]. Accumulating evidence suggests an increase in the prevalence of gout in the last decades, which might be caused by an increased longevity and an increased prevalence of factors that promote hyperuricemia such as obesity, the metabolic syndrome, chronic kidney disease, and dietary changes[5,8-11].

Pathogenesis

Gout is caused by a disorder of the purine metabolism and results from MSU crystal deposition in and around the joints which is associated with hyperuricemia. The serum uric acid concentration is determined by the endogenous production of uric acid by synthesis and cell turnover, the exogenous supply via dietary intake, and renal (two-third) and intestinal (one-third) excretion[12]. Hyperuricemia is the result of uric acid overproduction, uric acid underexcretion, or a combination of the two[12]. Hyperuricemia is defined as a serum uric acid concentration that exceeds the solubility at physiologic temperature and pH (0.38-0.40 mmol/L)[3,13]. Although hyperuricemia is necessary to develop gout, it is not sufficient to cause gout. Only one cohort study from 1987 investigated the association between the level of serum uric acid and the cumulative incidence of gout. Gout occurred in just 22% of the patients with a baseline serum uric acid of more than 0.54 mmol/L over a 5-year period[14].

Necessary for the occurrence of gout arthritis is the formation of MSU crystals when hyperuricemia is present. The formation of MSU crystals depends on the solubility of uric acid in joint fluid. The solubility is influenced by factors such as temperature, pH, level of articular dehydration, concentration of cations, and the presence of nucleating agents (collagen, chondroitin sulfate, and nonaggregating proteoglycans)[12]. Variation in these factors might explain partly the preference of gout attacks in the MTP-1 joint (the relatively low temperature of this peripheral joint)[15] and in osteoarthritic joints (degeneration with decreased collagen and proteoglycans)[16], and the nocturnal onset of the attack (articular dehydration)[12,13]. However, these factors do not explain for example why gout does rarely occur in the MTP-5 joint which has probably a lower temperature than the MTP-1 joint, and gout is also rarely seen in often osteoarthritic hip joints.

MSU crystal formation leads to MSU crystal deposition in synovial fluids. MSU crystals are pro-inflammatory stimuli. MSU crystals are phagocytosed as particles by monocytes and cause an inflammatory response with the release of pro-inflammatory mediators as tumor necrosis factor (TNF)-α, interleukin (IL)-1b, and IL-6[12,13]. Mechanisms by which MSU crystals activate cells in the joint and the role of these pro-inflammatory mediators are not yet fully explained. The generally accepted hypothesis is that MSU crystals activate monocytes via the inflammasome leading to IL-1b production[17-21]. IL-1b can induce recruitment of other inflammatory cells within the joint to produce cytokines and chemotactic factors. This results in neutrophil influx to the joint, which is the hallmark of gouty arthritis.

Clinical presentation

Typically, a patient with a gout attack has an acute painful and swollen joint, which is often red and warm. The onset of the arthritis is abrupt. A gout attack usually affects one joint in the lower limbs. Most often, in 57% of the primary care patients[22], the MTP-1 joint was involved[23]. In 86% of primary care patients with gouty arthritis the lower leg was affected[22]. Next most frequent locations are the mid-foot, the ankle and the knee[16]. Gout attacks are self-limiting and resolve within 7-10 d. However, the arthritis attacks are often recurrent.

Recurrent gout attacks can lead to permanent joint damage and tophi depositions. Tophi can be found in or close to joints, in bursas, tendon sheaths, and in articular cartilage[24]. Clinical experience shows that in some patients later in the course of the disease the gout attacks can occur more often, and it takes more days before the attack is resolved. Then the arthritis is more frequently polyarticular and spreads to the upper limbs[16,23].

Risk factors

Many factors have been described as risk factors for the development of gout. However, the associations between these “risk” factors and gout are almost exclusively based on epidemiological studies, which of course cannot proof causal relations between these factors and gout. Epidemiological studies show that several dietary factors might increase the risk of gout, such as alcohol consumption[25,26], purine-rich meat and seafood intake[26-28], and consumption of fructose-sweetened soft drinks[26,29]. The consumption of dairy products[28], skim milk powder[30], folate, vegetables, and coffee are associated with a decreased prevalence of gout[26]. According to epidemiological studies the use of thiazide and loop diuretics, but not aldosteron antagonists, are associated with the risk of gout[26,31,32]. However, these results might be confounded by cardiovascular indications[33].

Other factors can cause the development of gout. Genetics (sex[5], some genes such as SLC2A9, ABCG2, SLC17A3, and SLC22A12[3,13] and Asian descent[34,35]), age[5], and constitutional influences (body composition) are risk factors, and these cannot be influenced. Comorbidities as hypertension[36], chronic kidney disease, cardiovascular diseases[37-41], the metabolic syndrome[36,42], diabetes[42,43], obesity[36], hyperlipidemia[36], and early menopause[6] are associated with a higher prevalence of gout[26]. Nowadays, especially the association between gout and cardiovascular diseases is a large research field[37-41,44,45], but the exact mechanism of why these diseases are associated is not fully understood.

Diagnosis

The gold standard for diagnosing gout is the identification of MSU crystals in synovial fluid or in a tophus by polarization light microscopy[46]. The accuracy of the gold standard has been tested in only a few studies. The sensitivity of detection of MSU crystals was shown to be 69% with a specificity of 97%[47]. After training the sensitivity of the detection of MSU crystals can become 95% with a specificity of 97%[48]. In clinical practice most synovial fluid is aspirated from the affected joint during a gout attack. A longstanding opinion is that synovial fluid should be analyzed with a polarization microscope rapidly after aspiration, because the formation and solubility of MSU crystals might be affected by pH and temperature[49]. A recent systematic review has shown that MSU crystals can also be detected in synovial fluid which has been stored for a maximum of 8 wk[49].

Although there is a gold standard, in primary care synovial fluid analysis is often not possible or not available. Polarization light microscopes are expensive and almost only available at rheumatology departments. But approximately 90% of the gout patients are diagnosed and treated by primary care physicians[50]. Primary care physicians diagnose gout without the gold standard, based on clinical signs and symptoms, which has demonstrated to have a limited predictive value[22]. In patients with MTP-1 arthritis the diagnosis gout was right in only 77%, while primary care physicians supposed gout to be the diagnosis in 98% of the patients[51]. Even in rheumatology departments the gold standard is not always used for diagnosing gout[52,53].

Several criteria sets were developed to improve the validity of the clinical diagnosis, such as the American College of Rheumatology criteria[54], which showed a limited sensitivity (90%; 79%) and specificity (64%; 70%) in primary[55] and secondary care[56] in MSU crystal-proven gout patients, respectively. A diagnostic rule to diagnose gout without joint fluid analysis developed in a primary care population of MSU crystal-proven gout patients had better results[22], but the validity of this rule is unknown in secondary care.

Nowadays imaging techniques are increasingly used for diagnosing gout patients. Ultrasonography and dual-energy computed tomography (DECT) are promising but expensive methods for diagnosis and monitoring gout, but with yet an unknown validity in medical practice[57-62]. Compared to the gold standard of synovial fluid aspiration the main advantage of these techniques is that they are non-invasive. A disadvantage of DECT is its high exposure to radiation.

Treatment

Standard treatment consists of anti-inflammatory drugs for gout attacks, sometimes followed by long-term preventive urate lowering therapy. Acute gout attacks are treated with non-steroidal anti-inflammatory drugs (NSAIDs), colchicine, oral prednisone, or intra-articular or intramuscular glucocorticoids. Unfortunately, there are only a few trials which compare the efficacy and safety of these therapeutics in gout patients. NSAIDs and prednisone have a comparable therapeutic effect during a gout attack[63-65]. Low-dose colchicine has the same therapeutic effect after 24 h as high-dose colchicine, but with less adverse effects[66]. Because of the lack of trials, the choice which anti-inflammatory therapy is prescribed is mainly based on comorbidity and comedications. In case of no restrictions by comorbidity and comedications, the cost of the therapy can be taken into account. In the United States, the cost of colchicine have risen after the rebranding of this therapeutic. IL-1b blockers such as canakinumab[67], anakinra[68-70], and rilonacept[71-75] are new therapeutic opportunities in patients with gouty arthritis, but their efficacy and safety should be further tested. However, these new therapeutics are expensive, and should only be prescribed in patients with frequent gout attacks who failed or have contra-indications for the traditional anti-inflammatory drugs. Trials concerning the efficacy of non-pharmacological interventions for gout attacks are even more rare, probably due to ethical and practical difficulties to set up these type of trials[76]. Only one trial was performed which shows that local ice therapy can be useful during gout attacks[77].

Preventive uric acid lowering therapy is indicated in patients with two or more gout attacks per year, tophaceous gout, or a history of uric acid urolithiasis[78,79]. The decision whether to start preventive uric acid lowering therapy or to accept frequent gout attacks and/or tophi should always be made in accordance with the patient. The aim of the uric acid lowering therapy is to decrease the frequency of gout attacks[80,81] and/or to reduce tophi[82] by sufficiently reducing the serum uric acid level. The target serum uric acid level should be at least below 0.36 mmol/L[79]. A lower target serum uric acid of 0.30 mmol/L can be aimed for in case of severe gout (for instance tophaceous gout)[78,83]. Based on evidence and experience the first choice uric acid lowering agent is the xanthine oxidase inhibitor allopurinol[78,79]. The uricosuricum benzbromarone 100-200 mg per day and allopurinol 300-600 mg per day have comparable efficacy and safety profiles[82,84]. Probenecid, an old uricosuricum, has moderate efficacy as uric acid lowering therapeutic in patients with lack of effectiveness of or intolerance to allopurinol[85]. A trial has shown similar effects of allopurinol 200-300 mg per day and febuxostat, a new xanthine oxidase inhibitor, 80-120 mg per day[86], but in clinical practice the dose of allopurinol can be further enhanced until 600 mg. At this moment, because of high costs and little clinical experience, febuxostat should only be used when the target serum uric acid level cannot be reached by an appropriate dose of allopurinol, or when the patient is intolerant to allopurinol. In both cases benzbromarone is also a good and less expensive alternative. The uricase derivative rasburicase is now only registered for tumor lysis syndrome, but might be beneficial as uric acid lowering therapy in gout patients[87-90]. A new uricase derivative pegloticase is proven to be useful in patients who are refractory to or intolerant for conventional therapy[91-95]. Uricases should be administered intravenously with a risk of infusion reactions, and there always remains a risk for antibody formation due to the conjugation to proteins. The latter might impede the efficacy of uricases. The selective uric acid reabsorption inhibitor lesinurad might be another future treatment option[96].

Only a few studies have compared the efficacy and safety of uric acid lowering monotherapy, and solely one study looked at combination therapy of two uric acid lowering therapeutics. The combination of lesinurad and febuxostat was well tolerated, and the target serum uric acid level was achieved in all patients[97]. Based on clinical experience benzbromarone can be added to allopurinol when the target serum uric acid cannot be reached by allopurinol monotherapy. The dose of the uric acid lowering medications should be carefully increased to reduce adverse effects, and should be titrated based on serum uric acid levels[78,79]. It is generally accepted that uric acid lowering therapy should be started under several months of prophylactic anti-inflammatory medications (colchicine or NSAIDs) to prevent paradoxal gout attacks at the start, although there are no studies to prove this[78,79]. The uric acid lowering therapy should be continued lifelong.

In addition to the uric acid lowering therapy some other pharmacological measures can be helpful to reduce serum uric acid. When a gout patient is also diagnosed with hypertension, losartan could be considered as antihypertensive treatment, because of its small uric acid lowering effect[98]. Vitamin C, a safe supplement, might have a very small uric acid lowering effect[99,100], although a small randomized controlled trial in gout patients could not confirm this[101].

Additional non-pharmacological measures, like dietary advices, to reduce serum uric acid may be useful, but their uric acid lowering effects are small (10%-18%) and therapeutically insufficient (i.e., no reduce of the frequency of gout flares) in most patients[26]. Observational studies showed that the intake of purine-rich meat and seafood, fructose-rich soft drinks, and alcohol should be reduced, and dairy intake and the consumption of vegetables should be encouraged[26,78,79,102]. Trials concerning the efficacy of non-pharmacological interventions to lower serum uric acid are also lacking. The only trial of dietary intervention in gout patients suggested that skim milk powder enriched with glycomacropeptide and G600 milk fat extract might reduce the frequency of gout flares[30].

Prognosis

Gout is a potentially curable disease. Unfortunately, the management of gout patients is often insufficient[5,103-107]. An important reason is the limited use of uric acid lowering therapy. Only 30%-60% of the patients are still prescribed allopurinol one year after the start of the therapy[4], and only 17% of the gout patients might be fully adherent to allopurinol therapy[108]. The poor adherence is often, unfairly, blamed on gout patients unwilling to take uric acid lowering therapy. Lack of appropriate information from their doctor is an important factor which plays a role in the poor adherence. An observational study showed that patient education, individual lifestyle advice and slow upward titration of uric acid lowering therapy according to serum uric acid levels can improve the adherence to uric acid lowering therapy[109].

Acute gout attacks and the presence of tophi account for a major component of the reported decreased health-related quality of life in gout patients, and are associated with decreased work productivity which leads to an economic burden for the society[110-112]. This emphasizes the importance of the effective management of gout. Urate lowering therapy is cost-effective when patients have two or more recurrent attacks per year[113].

THE ASSOCIATION BETWEEN GOUT AND CARDIOVASCULAR DISEASES

Nowadays, an important study field within gout research is the association between gout and cardiovascular diseases. The increasing interest in this association is probably due to its great clinical importance, because of the high prevalence of gout and cardiovascular diseases. This part of the review elaborates more on the association between gout and cardiovascular diseases.

The association of gout with cardiovascular diseases

Most studies looked at the association between hyperuricemia and cardiovascular diseases. Two systematic reviews of prospective cohort studies show that, after correction for traditional risk factors for cardiovascular diseases, patients with hyperuricemia have a significant higher risk for cardiac diseases[45], cardiac mortality[38], stroke[37], and stroke-related mortality[37]. The mean association of the risk for cardiac mortality was 12% per increase of the serum uric acid of 0.059 mmol/L[38]. In women there was a stronger association between hyperuricemia and cardiovascular diseases and mortality than in men[37,38]. Higher levels of hyperuricemia are stronger risk factors for cardiovascular diseases and mortality than lower levels of hyperuricemia[114]. Interestingly, several studies observed a J-curve relationship between serum uric acid level and cardiovascular disease or all-cause mortality[115,116]. A low serum uric acid level might be associated with a higher mortality, because uric acid can play a protective antioxidant role[117]. It should be noticed that the definition of hyperuricemia differed between several studies and it was not always corrected for sex. Also, patients with hyperuricemia could be symptomatic (i.e., gout) or asymptomatic. However, it is likely that the conclusions from studies about patients with hyperuricemia are also valid in patients with gout.

Some studies investigated the association between gout and cardiovascular diseases. Gout was shown to be associated with an increased risk for heart failure[39] and myocardial infarction[45]. Several prospective cohort studies showed that gout was also associated with cardiovascular mortality[40,41,44,118] and with overall mortality[39-41,44,118]. Gout is a stronger risk factor for cardiovascular diseases and mortality than hyperuricemia[40,41]. Tophaceous gout was a very strong risk factor for cardiovascular mortality[114]. Unfortunately, the diagnosis of gout was often not based on identification of MSU crystals, but on self-report. In MSU crystal-proven gout the association might be stronger than in gout otherwise diagnosed, and therefore the association of gout and cardiovascular diseases can be underestimated.

The pathophysiology of the association of gout with cardiovascular diseases

The pathophysiological pathways that link gout with cardiovascular diseases are not fully clear. Gout might lead to cardiovascular diseases through endothelial dysfunction caused by oxidative stress through xanthine oxidase activation. Another pathway is based on chronic systemic inflammation in patients with gout, also in asymptomatic periods, which might lead to cardiovascular diseases. Both pathways are now discussed in more detail.

Accumulating evidence shows that xanthine oxidase plays a central role in the association of hyperuricemia and gout with cardiovascular diseases. Upregulation of xanthine oxidase activity rather than decreased renal excretion of uric acid is an important factor underlying the increased serum uric acid levels in heart failure patients[119]. Endothelial dysfunction might be caused by accelerated inactivation of nitric oxide by reactive oxygen species, and xanthine oxidase is a source of reactive oxygen species production[120].

Several studies suggest that allopurinol, a xanthine oxidase inhibitor, has cardioprotective effects. Most studies looked at indicators for higher cardiovascular risk. Allopurinol improved the endothelial function[121] and resulted in an improved vasodilated capacity and peripheral blood flow in patients with heart failure[122]. Allopurinol gave a significant blood pressure reduction in patients with hyperuricemia[123-126]. In patients with chronic stable angina allopurinol increased the time to chest pain and the total exercise time[127,128]. Allopurinol inhibits the oxidation of low-density lipoprotein, which plays an important role in the development of atherosclerosis[129]. These mechanisms might contribute to a favorable effect of allopurinol on the cardiovascular risk in gout patients. The effect of allopurinol on mortality was the topic of several studies. These studies showed that allopurinol reduced the mortality in heart failure patients[130-133]. One recent study investigated the effect of allopurinol on cardiovascular outcome. Allopurinol was associated with a reduced risk of myocardial infarction[134]. On contrary, benzbromarone, an uricosuricum, did not have beneficial cardioprotective effects[129,135].

A different pathway which might link gout to cardiovascular diseases is based on chronic systemic inflammation. Low-grade chronic systemic inflammation can contribute to the development of cardiovascular diseases. Some evidence is found that in patients with hyperuricemia or gout low-grade chronic systemic inflammation is present. Serum uric acid levels were associated with C-reactive protein levels, TNF-α levels and IL-6 levels[136]. Typical gout signs seen with ultrasonography are present in asymptomatic joints of patients with hyperuricemia or gout[137]. This might imply that also in between gout attacks low-grade inflammation is present. Also in tophaceous gout, a severe form of gout with widespread urate deposition, more low-grade inflammation might be present compared to non-tophaceous gout. Tophaceous gout was shown to be stronger risk factor for cardiovascular diseases and mortality than non-tophaceous gout[114].

CONCLUSION

Gout is no longer ‘the king of diseases and the disease of kings’, but a very common disease which is associated with cardiovascular diseases. Not only the gout attacks should be treated, but gout patients should also be screened and treated for cardiovascular risk factors.

Footnotes

P- Reviewer: Baran DA, Beltowski J S- Editor: Ji FF L- Editor: A E- Editor: Wu HL

References
1.  Nuki G, Simkin PA. A concise history of gout and hyperuricemia and their treatment. Arthritis Res Ther. 2006;8 Suppl 1:S1.  [PubMed]  [DOI]  [Cited in This Article: ]
2.  Copeman WSC. A short history of gout and the rheumatic disease. Med Hist. 1964;8:394–395.  [PubMed]  [DOI]  [Cited in This Article: ]
3.  Richette P, Bardin T. Gout. Lancet. 2010;375:318-328.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 587]  [Cited by in F6Publishing: 80]  [Article Influence: 48.9]  [Reference Citation Analysis (0)]
4.  Annemans L, Spaepen E, Gaskin M, Bonnemaire M, Malier V, Gilbert T, Nuki G. Gout in the UK and Germany: prevalence, comorbidities and management in general practice 2000-2005. Ann Rheum Dis. 2008;67:960-966.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 324]  [Cited by in F6Publishing: 111]  [Article Influence: 23.1]  [Reference Citation Analysis (0)]
5.  Kuo CF, Grainge MJ, Mallen C, Zhang W, Doherty M. Rising burden of gout in the UK but continuing suboptimal management: a nationwide population study. Ann Rheum Dis. 2014;Jan 15; Epub ahead of print.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 295]  [Cited by in F6Publishing: 74]  [Article Influence: 42.1]  [Reference Citation Analysis (0)]
6.  Hak AE, Curhan GC, Grodstein F, Choi HK. Menopause, postmenopausal hormone use and risk of incident gout. Ann Rheum Dis. 2010;69:1305-1309.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 75]  [Cited by in F6Publishing: 24]  [Article Influence: 6.3]  [Reference Citation Analysis (0)]
7.  Puig JG, Michán AD, Jiménez ML, Pérez de Ayala C, Mateos FA, Capitán CF, de Miguel E, Gijón JB. Female gout. Clinical spectrum and uric acid metabolism. Arch Intern Med. 1991;151:726-732.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 84]  [Cited by in F6Publishing: 21]  [Article Influence: 2.8]  [Reference Citation Analysis (0)]
8.  Roddy E, Doherty M. Epidemiology of gout. Arthritis Res Ther. 2010;12:223.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 223]  [Cited by in F6Publishing: 65]  [Article Influence: 20.3]  [Reference Citation Analysis (0)]
9.  Saag KG, Choi H. Epidemiology, risk factors, and lifestyle modifications for gout. Arthritis Res Ther. 2006;8 Suppl 1:S2.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 157]  [Cited by in F6Publishing: 52]  [Article Influence: 10.5]  [Reference Citation Analysis (0)]
10.  Wallace KL, Riedel AA, Joseph-Ridge N, Wortmann R. Increasing prevalence of gout and hyperuricemia over 10 years among older adults in a managed care population. J Rheumatol. 2004;31:1582-1587.  [PubMed]  [DOI]  [Cited in This Article: ]
11.  Bhole V, de Vera M, Rahman MM, Krishnan E, Choi H. Epidemiology of gout in women: Fifty-two-year followup of a prospective cohort. Arthritis Rheum. 2010;62:1069-1076.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 136]  [Cited by in F6Publishing: 41]  [Article Influence: 12.4]  [Reference Citation Analysis (0)]
12.  Choi HK, Mount DB, Reginato AM. Pathogenesis of gout. Ann Intern Med. 2005;143:499-516.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 589]  [Cited by in F6Publishing: 206]  [Article Influence: 36.8]  [Reference Citation Analysis (0)]
13.  Neogi T. Clinical practice. Gout. N Engl J Med. 2011;364:443-452.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 311]  [Cited by in F6Publishing: 51]  [Article Influence: 31.1]  [Reference Citation Analysis (0)]
14.  Campion EW, Glynn RJ, DeLabry LO. Asymptomatic hyperuricemia. Risks and consequences in the Normative Aging Study. Am J Med. 1987;82:421-426.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 507]  [Cited by in F6Publishing: 203]  [Article Influence: 14.9]  [Reference Citation Analysis (0)]
15.  Roddy E. Revisiting the pathogenesis of podagra: why does gout target the foot? J Foot Ankle Res. 2011;4:13.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 43]  [Cited by in F6Publishing: 14]  [Article Influence: 4.3]  [Reference Citation Analysis (0)]
16.  Roddy E, Zhang W, Doherty M. Are joints affected by gout also affected by osteoarthritis? Ann Rheum Dis. 2007;66:1374-1377.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 99]  [Cited by in F6Publishing: 28]  [Article Influence: 7.1]  [Reference Citation Analysis (0)]
17.  Chen CJ, Shi Y, Hearn A, Fitzgerald K, Golenbock D, Reed G, Akira S, Rock KL. MyD88-dependent IL-1 receptor signaling is essential for gouty inflammation stimulated by monosodium urate crystals. J Clin Invest. 2006;116:2262-2271.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 317]  [Cited by in F6Publishing: 119]  [Article Influence: 21.1]  [Reference Citation Analysis (0)]
18.  Martinon F, Pétrilli V, Mayor A, Tardivel A, Tschopp J. Gout-associated uric acid crystals activate the NALP3 inflammasome. Nature. 2006;440:237-241.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 3160]  [Cited by in F6Publishing: 1982]  [Article Influence: 210.7]  [Reference Citation Analysis (0)]
19.  Joosten LA, Netea MG, Mylona E, Koenders MI, Malireddi RK, Oosting M, Stienstra R, van de Veerdonk FL, Stalenhoef AF, Giamarellos-Bourboulis EJ. Engagement of fatty acids with Toll-like receptor 2 drives interleukin-1β production via the ASC/caspase 1 pathway in monosodium urate monohydrate crystal-induced gouty arthritis. Arthritis Rheum. 2010;62:3237-3248.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 198]  [Cited by in F6Publishing: 118]  [Article Influence: 18.0]  [Reference Citation Analysis (0)]
20.  Cronstein BN, Terkeltaub R. The inflammatory process of gout and its treatment. Arthritis Res Ther. 2006;8 Suppl 1:S3.  [PubMed]  [DOI]  [Cited in This Article: ]
21.  Pope RM, Tschopp J. The role of interleukin-1 and the inflammasome in gout: implications for therapy. Arthritis Rheum. 2007;56:3183-3188.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 123]  [Cited by in F6Publishing: 57]  [Article Influence: 8.8]  [Reference Citation Analysis (0)]
22.  Janssens HJ, Fransen J, van de Lisdonk EH, van Riel PL, van Weel C, Janssen M. A diagnostic rule for acute gouty arthritis in primary care without joint fluid analysis. Arch Intern Med. 2010;170:1120-1126.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 123]  [Cited by in F6Publishing: 31]  [Article Influence: 11.2]  [Reference Citation Analysis (0)]
23.  Grahame R, Scott JT. Clinical survey of 354 patients with gout. Ann Rheum Dis. 1970;29:461-468.  [PubMed]  [DOI]  [Cited in This Article: ]
24.  Forbess LJ, Fields TR. The broad spectrum of urate crystal deposition: unusual presentations of gouty tophi. Semin Arthritis Rheum. 2012;42:146-154.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 58]  [Cited by in F6Publishing: 15]  [Article Influence: 6.4]  [Reference Citation Analysis (0)]
25.  Choi HK, Atkinson K, Karlson EW, Willett W, Curhan G. Alcohol intake and risk of incident gout in men: a prospective study. Lancet. 2004;363:1277-1281.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 412]  [Cited by in F6Publishing: 66]  [Article Influence: 24.2]  [Reference Citation Analysis (0)]
26.  Singh JA, Reddy SG, Kundukulam J. Risk factors for gout and prevention: a systematic review of the literature. Curr Opin Rheumatol. 2011;23:192-202.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 45]  [Cited by in F6Publishing: 19]  [Article Influence: 4.5]  [Reference Citation Analysis (0)]
27.  Zhang Y, Chen C, Choi H, Chaisson C, Hunter D, Niu J, Neogi T. Purine-rich foods intake and recurrent gout attacks. Ann Rheum Dis. 2012;71:1448-1453.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 97]  [Cited by in F6Publishing: 36]  [Article Influence: 10.8]  [Reference Citation Analysis (0)]
28.  Choi HK, Atkinson K, Karlson EW, Willett W, Curhan G. Purine-rich foods, dairy and protein intake, and the risk of gout in men. N Engl J Med. 2004;350:1093-1103.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 597]  [Cited by in F6Publishing: 100]  [Article Influence: 35.1]  [Reference Citation Analysis (0)]
29.  Choi HK, Curhan G. Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study. BMJ. 2008;336:309-312.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 331]  [Cited by in F6Publishing: 66]  [Article Influence: 25.5]  [Reference Citation Analysis (0)]
30.  Dalbeth N, Ames R, Gamble GD, Horne A, Wong S, Kuhn-Sherlock B, MacGibbon A, McQueen FM, Reid IR, Palmano K. Effects of skim milk powder enriched with glycomacropeptide and G600 milk fat extract on frequency of gout flares: a proof-of-concept randomised controlled trial. Ann Rheum Dis. 2012;71:929-934.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 59]  [Cited by in F6Publishing: 19]  [Article Influence: 6.6]  [Reference Citation Analysis (0)]
31.  Bruderer S, Bodmer M, Jick SS, Meier CR. Use of diuretics and risk of incident gout: a population-based case-control study. Arthritis Rheumatol. 2014;66:185-196.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 48]  [Cited by in F6Publishing: 9]  [Article Influence: 6.9]  [Reference Citation Analysis (0)]
32.  Hueskes BA, Roovers EA, Mantel-Teeuwisse AK, Janssens HJ, van de Lisdonk EH, Janssen M. Use of diuretics and the risk of gouty arthritis: a systematic review. Semin Arthritis Rheum. 2012;41:879-889.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 21]  [Cited by in F6Publishing: 6]  [Article Influence: 2.3]  [Reference Citation Analysis (0)]
33.  Janssens HJ, van de Lisdonk EH, Janssen M, van den Hoogen HJ, Verbeek AL. Gout, not induced by diuretics? A case-control study from primary care. Ann Rheum Dis. 2006;65:1080-1083.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 38]  [Cited by in F6Publishing: 15]  [Article Influence: 2.4]  [Reference Citation Analysis (0)]
34.  Kuo CF, Grainge MJ, See LC, Yu KH, Luo SF, Valdes AM, Zhang W, Doherty M. Familial aggregation of gout and relative genetic and environmental contributions: a nationwide population study in Taiwan. Ann Rheum Dis. 2013;Epub ahead of print.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 39]  [Cited by in F6Publishing: 12]  [Article Influence: 4.9]  [Reference Citation Analysis (0)]
35.  Lin KC, Lin HY, Chou P. Community based epidemiological study on hyperuricemia and gout in Kin-Hu, Kinmen. J Rheumatol. 2000;27:1045-1050.  [PubMed]  [DOI]  [Cited in This Article: ]
36.  Choi HK, Ford ES, Li C, Curhan G. Prevalence of the metabolic syndrome in patients with gout: the Third National Health and Nutrition Examination Survey. Arthritis Rheum. 2007;57:109-115.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 280]  [Cited by in F6Publishing: 105]  [Article Influence: 20.0]  [Reference Citation Analysis (0)]
37.  Kim SY, Guevara JP, Kim KM, Choi HK, Heitjan DF, Albert DA. Hyperuricemia and risk of stroke: a systematic review and meta-analysis. Arthritis Rheum. 2009;61:885-892.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 271]  [Cited by in F6Publishing: 114]  [Article Influence: 22.6]  [Reference Citation Analysis (0)]
38.  Kim SY, Guevara JP, Kim KM, Choi HK, Heitjan DF, Albert DA. Hyperuricemia and coronary heart disease: a systematic review and meta-analysis. Arthritis Care Res (Hoboken). 2010;62:170-180.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 48]  [Cited by in F6Publishing: 12]  [Article Influence: 4.4]  [Reference Citation Analysis (0)]
39.  Krishnan E. Gout and the risk for incident heart failure and systolic dysfunction. BMJ Open. 2012;2:e000282.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 55]  [Cited by in F6Publishing: 24]  [Article Influence: 6.1]  [Reference Citation Analysis (0)]
40.  Krishnan E, Svendsen K, Neaton JD, Grandits G, Kuller LH. Long-term cardiovascular mortality among middle-aged men with gout. Arch Intern Med. 2008;168:1104-1110.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 233]  [Cited by in F6Publishing: 110]  [Article Influence: 17.9]  [Reference Citation Analysis (0)]
41.  Kuo CF, See LC, Luo SF, Ko YS, Lin YS, Hwang JS, Lin CM, Chen HW, Yu KH. Gout: an independent risk factor for all-cause and cardiovascular mortality. Rheumatology (Oxford). 2010;49:141-146.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 145]  [Cited by in F6Publishing: 57]  [Article Influence: 12.1]  [Reference Citation Analysis (0)]
42.  Li C, Hsieh MC, Chang SJ. Metabolic syndrome, diabetes, and hyperuricemia. Curr Opin Rheumatol. 2013;25:210-216.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 164]  [Cited by in F6Publishing: 26]  [Article Influence: 20.5]  [Reference Citation Analysis (0)]
43.  Lai HM, Chen CJ, Su BY, Chen YC, Yu SF, Yen JH, Hsieh MC, Cheng TT, Chang SJ. Gout and type 2 diabetes have a mutual inter-dependent effect on genetic risk factors and higher incidences. Rheumatology (Oxford). 2012;51:715-720.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 31]  [Cited by in F6Publishing: 11]  [Article Influence: 3.1]  [Reference Citation Analysis (0)]
44.  Choi HK, Curhan G. Independent impact of gout on mortality and risk for coronary heart disease. Circulation. 2007;116:894-900.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 389]  [Cited by in F6Publishing: 79]  [Article Influence: 27.8]  [Reference Citation Analysis (0)]
45.  Kuo CF, Yu KH, See LC, Chou IJ, Ko YS, Chang HC, Chiou MJ, Luo SF. Risk of myocardial infarction among patients with gout: a nationwide population-based study. Rheumatology (Oxford). 2013;52:111-117.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 67]  [Cited by in F6Publishing: 31]  [Article Influence: 7.4]  [Reference Citation Analysis (0)]
46.  Zhang W, Doherty M, Pascual E, Bardin T, Barskova V, Conaghan P, Gerster J, Jacobs J, Leeb B, Lioté F. EULAR evidence based recommendations for gout. Part I: Diagnosis. Report of a task force of the Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis. 2006;65:1301-1311.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 446]  [Cited by in F6Publishing: 128]  [Article Influence: 29.7]  [Reference Citation Analysis (0)]
47.  Gordon C, Swan A, Dieppe P. Detection of crystals in synovial fluids by light microscopy: sensitivity and reliability. Ann Rheum Dis. 1989;48:737-742.  [PubMed]  [DOI]  [Cited in This Article: ]
48.  Lumbreras B, Pascual E, Frasquet J, González-Salinas J, Rodríguez E, Hernández-Aguado I. Analysis for crystals in synovial fluid: training of the analysts results in high consistency. Ann Rheum Dis. 2005;64:612-615.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 77]  [Cited by in F6Publishing: 19]  [Article Influence: 4.8]  [Reference Citation Analysis (0)]
49.  Graf SW, Buchbinder R, Zochling J, Whittle SL. The accuracy of methods for urate crystal detection in synovial fluid and the effect of sample handling: a systematic review. Clin Rheumatol. 2013;32:225-232.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 25]  [Cited by in F6Publishing: 6]  [Article Influence: 2.8]  [Reference Citation Analysis (0)]
50.  Owens D, Whelan B, McCarthy G. A survey of the management of gout in primary care. Ir Med J. 2008;101:147-149.  [PubMed]  [DOI]  [Cited in This Article: ]
51.  Kienhorst LB, Janssens HJ, Fransen J, van de Lisdonk EH, Janssen M. Arthritis of the first metatarsophalangeal joint is not always gout: a prospective cohort study in primary care patients. Joint Bone Spine. 2014;81:342-346.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 17]  [Cited by in F6Publishing: 3]  [Article Influence: 2.4]  [Reference Citation Analysis (0)]
52.  Pascual E, Sivera F. Why is gout so poorly managed? Ann Rheum Dis. 2007;66:1269-1270.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 59]  [Cited by in F6Publishing: 17]  [Article Influence: 4.2]  [Reference Citation Analysis (0)]
53.  Pascual E, Sivera F, Andrés M. Synovial fluid analysis for crystals. Curr Opin Rheumatol. 2011;23:161-169.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 19]  [Cited by in F6Publishing: 5]  [Article Influence: 1.9]  [Reference Citation Analysis (0)]
54.  Wallace SL, Robinson H, Masi AT, Decker JL, McCarty DJ, Yü TF. Preliminary criteria for the classification of the acute arthritis of primary gout. Arthritis Rheum. 1977;20:895-900.  [PubMed]  [DOI]  [Cited in This Article: ]
55.  Janssens HJ, Janssen M, van de Lisdonk EH, Fransen J, van Riel PL, van Weel C. Limited validity of the American College of Rheumatology criteria for classifying patients with gout in primary care. Ann Rheum Dis. 2010;69:1255-1256.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 44]  [Cited by in F6Publishing: 18]  [Article Influence: 3.7]  [Reference Citation Analysis (0)]
56.  Malik A, Schumacher HR, Dinnella JE, Clayburne GM. Clinical diagnostic criteria for gout: comparison with the gold standard of synovial fluid crystal analysis. J Clin Rheumatol. 2009;15:22-24.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 113]  [Cited by in F6Publishing: 17]  [Article Influence: 9.4]  [Reference Citation Analysis (0)]
57.  Rettenbacher T, Ennemoser S, Weirich H, Ulmer H, Hartig F, Klotz W, Herold M. Diagnostic imaging of gout: comparison of high-resolution US versus conventional X-ray. Eur Radiol. 2008;18:621-630.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 91]  [Cited by in F6Publishing: 33]  [Article Influence: 6.5]  [Reference Citation Analysis (0)]
58.  Thiele RG, Schlesinger N. Diagnosis of gout by ultrasound. Rheumatology (Oxford). 2007;46:1116-1121.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 250]  [Cited by in F6Publishing: 67]  [Article Influence: 17.9]  [Reference Citation Analysis (0)]
59.  Dalbeth N, Doyle AJ. Imaging of gout: an overview. Best Pract Res Clin Rheumatol. 2012;26:823-838.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 26]  [Cited by in F6Publishing: 4]  [Article Influence: 3.3]  [Reference Citation Analysis (0)]
60.  Glazebrook KN, Guimarães LS, Murthy NS, Black DF, Bongartz T, Manek NJ, Leng S, Fletcher JG, McCollough CH. Identification of intraarticular and periarticular uric acid crystals with dual-energy CT: initial evaluation. Radiology. 2011;261:516-524.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 157]  [Cited by in F6Publishing: 56]  [Article Influence: 15.7]  [Reference Citation Analysis (0)]
61.  Manger B, Lell M, Wacker J, Schett G, Rech J. Detection of periarticular urate deposits with dual energy CT in patients with acute gouty arthritis. Ann Rheum Dis. 2012;71:470-472.  [PubMed]  [DOI]  [Cited in This Article: ]
62.  Huppertz A, Hermann KG, Diekhoff T, Wagner M, Hamm B, Schmidt WA. Systemic staging for urate crystal deposits with dual-energy CT and ultrasound in patients with suspected gout. Rheumatol Int. 2014;34:763-771.  [PubMed]  [DOI]  [Cited in This Article: ]
63.  Janssens HJ, Janssen M, van de Lisdonk EH, van Riel PL, van Weel C. Use of oral prednisolone or naproxen for the treatment of gout arthritis: a double-blind, randomised equivalence trial. Lancet. 2008;371:1854-1860.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 188]  [Cited by in F6Publishing: 16]  [Article Influence: 14.5]  [Reference Citation Analysis (0)]
64.  Man CY, Cheung IT, Cameron PA, Rainer TH. Comparison of oral prednisolone/paracetamol and oral indomethacin/paracetamol combination therapy in the treatment of acute goutlike arthritis: a double-blind, randomized, controlled trial. Ann Emerg Med. 2007;49:670-677.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 104]  [Cited by in F6Publishing: 34]  [Article Influence: 7.4]  [Reference Citation Analysis (0)]
65.  Underwood M. Gout. Clin Evid (Online). 2011;2011:1120.  [PubMed]  [DOI]  [Cited in This Article: ]
66.  Terkeltaub RA, Furst DE, Bennett K, Kook KA, Crockett RS, Davis MW. High versus low dosing of oral colchicine for early acute gout flare: Twenty-four-hour outcome of the first multicenter, randomized, double-blind, placebo-controlled, parallel-group, dose-comparison colchicine study. Arthritis Rheum. 2010;62:1060-1068.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 289]  [Cited by in F6Publishing: 65]  [Article Influence: 26.3]  [Reference Citation Analysis (0)]
67.  Schlesinger N, Alten RE, Bardin T, Schumacher HR, Bloch M, Gimona A, Krammer G, Murphy V, Richard D, So AK. Canakinumab for acute gouty arthritis in patients with limited treatment options: results from two randomised, multicentre, active-controlled, double-blind trials and their initial extensions. Ann Rheum Dis. 2012;71:1839-1848.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 223]  [Cited by in F6Publishing: 77]  [Article Influence: 24.8]  [Reference Citation Analysis (0)]
68.  So A, De Smedt T, Revaz S, Tschopp J. A pilot study of IL-1 inhibition by anakinra in acute gout. Arthritis Res Ther. 2007;9:R28.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 512]  [Cited by in F6Publishing: 280]  [Article Influence: 36.6]  [Reference Citation Analysis (0)]
69.  Chen K, Fields T, Mancuso CA, Bass AR, Vasanth L. Anakinra’s efficacy is variable in refractory gout: report of ten cases. Semin Arthritis Rheum. 2010;40:210-214.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 70]  [Cited by in F6Publishing: 26]  [Article Influence: 6.4]  [Reference Citation Analysis (0)]
70.  Ottaviani S, Moltó A, Ea HK, Neveu S, Gill G, Brunier L, Palazzo E, Meyer O, Richette P, Bardin T. Efficacy of anakinra in gouty arthritis: a retrospective study of 40 cases. Arthritis Res Ther. 2013;15:R123.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 81]  [Cited by in F6Publishing: 31]  [Article Influence: 11.6]  [Reference Citation Analysis (0)]
71.  Terkeltaub R, Sundy JS, Schumacher HR, Murphy F, Bookbinder S, Biedermann S, Wu R, Mellis S, Radin A. The interleukin 1 inhibitor rilonacept in treatment of chronic gouty arthritis: results of a placebo-controlled, monosequence crossover, non-randomised, single-blind pilot study. Ann Rheum Dis. 2009;68:1613-1617.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 215]  [Cited by in F6Publishing: 118]  [Article Influence: 17.9]  [Reference Citation Analysis (0)]
72.  Schumacher HR, Sundy JS, Terkeltaub R, Knapp HR, Mellis SJ, Stahl N, Yancopoulos GD, Soo Y, King-Davis S, Weinstein SP. Rilonacept (interleukin-1 trap) in the prevention of acute gout flares during initiation of urate-lowering therapy: results of a phase II randomized, double-blind, placebo-controlled trial. Arthritis Rheum. 2012;64:876-884.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 71]  [Cited by in F6Publishing: 33]  [Article Influence: 7.9]  [Reference Citation Analysis (0)]
73.  Schumacher HR, Evans RR, Saag KG, Clower J, Jennings W, Weinstein SP, Yancopoulos GD, Wang J, Terkeltaub R. Rilonacept (interleukin-1 trap) for prevention of gout flares during initiation of uric acid-lowering therapy: results from a phase III randomized, double-blind, placebo-controlled, confirmatory efficacy study. Arthritis Care Res (Hoboken). 2012;64:1462-1470.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 75]  [Cited by in F6Publishing: 38]  [Article Influence: 9.4]  [Reference Citation Analysis (0)]
74.  Terkeltaub RA, Schumacher HR, Carter JD, Baraf HS, Evans RR, Wang J, King-Davis S, Weinstein SP Rilonacept in the treatment of acute gouty arthritis: a randomized, controlled clinical trial using indomethacin as the active comparator Arthritis Res Ther. 2013;15:R25.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 81]  [Cited by in F6Publishing: 30]  [Article Influence: 10.1]  [Reference Citation Analysis (0)]
75.  Mitha E, Schumacher HR, Fouche L, Luo SF, Weinstein SP, Yancopoulos GD, Wang J, King-Davis S, Evans RR. Rilonacept for gout flare prevention during initiation of uric acid-lowering therapy: results from the PRESURGE-2 international, phase 3, randomized, placebo-controlled trial. Rheumatology (Oxford). 2013;52:1285-1292.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 61]  [Cited by in F6Publishing: 24]  [Article Influence: 7.6]  [Reference Citation Analysis (0)]
76.  Moi JH, Sriranganathan MK, Edwards CJ, Buchbinder R. Lifestyle interventions for acute gout. Cochrane Database Syst Rev. 2013;11:CD010519.  [PubMed]  [DOI]  [Cited in This Article: ]
77.  Schlesinger N, Detry MA, Holland BK, Baker DG, Beutler AM, Rull M, Hoffman BI, Schumacher HR. Local ice therapy during bouts of acute gouty arthritis. J Rheumatol. 2002;29:331-334.  [PubMed]  [DOI]  [Cited in This Article: ]
78.  Khanna D, Fitzgerald JD, Khanna PP, Bae S, Singh MK, Neogi T, Pillinger MH, Merill J, Lee S, Prakash S. 2012 American College of Rheumatology guidelines for management of gout. Part 1: systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia. Arthritis Care Res (Hoboken). 2012;64:1431-1446.  [PubMed]  [DOI]  [Cited in This Article: ]
79.  Zhang W, Doherty M, Bardin T, Pascual E, Barskova V, Conaghan P, Gerster J, Jacobs J, Leeb B, Lioté F. 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). Ann Rheum Dis. 2006;65:1312-1324.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 791]  [Cited by in F6Publishing: 240]  [Article Influence: 52.7]  [Reference Citation Analysis (0)]
80.  Perez-Ruiz F. Treating to target: a strategy to cure gout. Rheumatology (Oxford). 2009;48 Suppl 2:ii9-ii14.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 80]  [Cited by in F6Publishing: 29]  [Article Influence: 7.3]  [Reference Citation Analysis (0)]
81.  Shoji A, Yamanaka H, Kamatani N. A retrospective study of the relationship between serum urate level and recurrent attacks of gouty arthritis: evidence for reduction of recurrent gouty arthritis with antihyperuricemic therapy. Arthritis Rheum. 2004;51:321-325.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 274]  [Cited by in F6Publishing: 99]  [Article Influence: 16.1]  [Reference Citation Analysis (0)]
82.  Perez-Ruiz F, Calabozo M, Pijoan JI, Herrero-Beites AM, Ruibal A. Effect of urate-lowering therapy on the velocity of size reduction of tophi in chronic gout. Arthritis Rheum. 2002;47:356-360.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 295]  [Cited by in F6Publishing: 102]  [Article Influence: 15.5]  [Reference Citation Analysis (0)]
83.  Perez-Ruiz F, Herrero-Beites AM, Carmona L. A two-stage approach to the treatment of hyperuricemia in gout: the “dirty dish” hypothesis. Arthritis Rheum. 2011;63:4002-4006.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 50]  [Cited by in F6Publishing: 14]  [Article Influence: 5.6]  [Reference Citation Analysis (0)]
84.  Reinders MK, van Roon EN, Jansen TL, Delsing J, Griep EN, Hoekstra M, van de Laar MA, Brouwers JR. Efficacy and tolerability of urate-lowering drugs in gout: a randomised controlled trial of benzbromarone versus probenecid after failure of allopurinol. Ann Rheum Dis. 2009;68:51-56.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 99]  [Cited by in F6Publishing: 33]  [Article Influence: 7.6]  [Reference Citation Analysis (0)]
85.  Pui K, Gow PJ, Dalbeth N. Efficacy and tolerability of probenecid as urate-lowering therapy in gout; clinical experience in high-prevalence population. J Rheumatol. 2013;40:872-876.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 37]  [Cited by in F6Publishing: 15]  [Article Influence: 4.6]  [Reference Citation Analysis (0)]
86.  Tayar JH, Lopez-Olivo MA, Suarez-Almazor ME. Febuxostat for treating chronic gout. Cochrane Database Syst Rev. 2012;11:CD008653.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 12]  [Cited by in F6Publishing: 3]  [Article Influence: 1.3]  [Reference Citation Analysis (0)]
87.  Moolenburgh JD, Reinders MK, Jansen TL. Rasburicase treatment in severe tophaceous gout: a novel therapeutic option. Clin Rheumatol. 2006;25:749-752.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 35]  [Cited by in F6Publishing: 7]  [Article Influence: 2.2]  [Reference Citation Analysis (0)]
88.  Richette P, Bardin T. Successful treatment with rasburicase of a tophaceous gout in a patient allergic to allopurinol. Nat Clin Pract Rheumatol. 2006;2:338-342; quiz 343.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 31]  [Cited by in F6Publishing: 6]  [Article Influence: 2.1]  [Reference Citation Analysis (0)]
89.  Richette P, Viguier M, Bachelez H, Bardin T. Psoriasis induced by anti-tumor necrosis factor therapy: a class effect? J Rheumatol. 2007;34:438-439.  [PubMed]  [DOI]  [Cited in This Article: ]
90.  De Angelis S, Noce A, Di Renzo L, Cianci R, Naticchia A, Giarrizzo GF, Giordano F, Tozzo C, Splendiani G, De Lorenzo A. Is rasburicase an effective alternative to allopurinol for management of hyperuricemia in renal failure patients? A double blind-randomized study. Eur Rev Med Pharmacol Sci. 2007;11:179-184.  [PubMed]  [DOI]  [Cited in This Article: ]
91.  Sundy JS, Becker MA, Baraf HS, Barkhuizen A, Moreland LW, Huang W, Waltrip RW, Maroli AN, Horowitz Z. Reduction of plasma urate levels following treatment with multiple doses of pegloticase (polyethylene glycol-conjugated uricase) in patients with treatment-failure gout: results of a phase II randomized study. Arthritis Rheum. 2008;58:2882-2891.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 122]  [Cited by in F6Publishing: 38]  [Article Influence: 11.1]  [Reference Citation Analysis (0)]
92.  Anderson A, Singh JA. Pegloticase for chronic gout. Cochrane Database Syst Rev. 2010;CD008335.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 9]  [Cited by in F6Publishing: 3]  [Article Influence: 0.8]  [Reference Citation Analysis (0)]
93.  Sundy JS, Baraf HS, Yood RA, Edwards NL, Gutierrez-Urena SR, Treadwell EL, Vázquez-Mellado J, White WB, Lipsky PE, Horowitz Z. Efficacy and tolerability of pegloticase for the treatment of chronic gout in patients refractory to conventional treatment: two randomized controlled trials. JAMA. 2011;306:711-720.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 245]  [Cited by in F6Publishing: 81]  [Article Influence: 24.5]  [Reference Citation Analysis (0)]
94.  Becker MA, Baraf HS, Yood RA, Dillon A, Vázquez-Mellado J, Ottery FD, Khanna D, Sundy JS. Long-term safety of pegloticase in chronic gout refractory to conventional treatment. Ann Rheum Dis. 2013;72:1469-1474.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 59]  [Cited by in F6Publishing: 14]  [Article Influence: 6.6]  [Reference Citation Analysis (0)]
95.  Baraf HS, Becker MA, Gutierrez-Urena SR, Treadwell EL, Vazquez-Mellado J, Rehrig CD, Ottery FD, Sundy JS, Yood RA. Tophus burden reduction with pegloticase: results from phase 3 randomized trials and open-label extension in patients with chronic gout refractory to conventional therapy. Arthritis Res Ther. 2013;15:R137.  [PubMed]  [DOI]  [Cited in This Article: ]
96.  Crittenden DB, Pillinger MH. New therapies for gout. Annu Rev Med. 2013;64:325-337.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 44]  [Cited by in F6Publishing: 15]  [Article Influence: 5.5]  [Reference Citation Analysis (0)]
97.  Fleischmann R, Kerr B, Yeh LT, Suster M, Shen Z, Polvent E, Hingorani V, Quart B, Manhard K, Miner JN, Baumgartner S; on behalf of the RDEA594-111 Study Group. Pharmacodynamic, pharmacokinetic and tolerability evaluation of concomitant administration of lesinurad and febuxostat in gout patients with hyperuricaemia. Rheumatology (Oxford). 2014;Feb 8; Epub ahead of print.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 67]  [Cited by in F6Publishing: 13]  [Article Influence: 9.6]  [Reference Citation Analysis (0)]
98.  Würzner G, Gerster JC, Chiolero A, Maillard M, Fallab-Stubi CL, Brunner HR, Burnier M. Comparative effects of losartan and irbesartan on serum uric acid in hypertensive patients with hyperuricaemia and gout. J Hypertens. 2001;19:1855-1860.  [PubMed]  [DOI]  [Cited in This Article: ]
99.  Huang HY, Appel LJ, Choi MJ, Gelber AC, Charleston J, Norkus EP, Miller ER. The effects of vitamin C supplementation on serum concentrations of uric acid: results of a randomized controlled trial. Arthritis Rheum. 2005;52:1843-1847.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 115]  [Cited by in F6Publishing: 43]  [Article Influence: 7.2]  [Reference Citation Analysis (0)]
100.  Juraschek SP, Miller ER, Gelber AC. Effect of oral vitamin C supplementation on serum uric acid: a meta-analysis of randomized controlled trials. Arthritis Care Res (Hoboken). 2011;63:1295-1306.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 79]  [Cited by in F6Publishing: 28]  [Article Influence: 7.9]  [Reference Citation Analysis (0)]
101.  Stamp LK, O’Donnell JL, Frampton C, Drake JM, Zhang M, Chapman PT. Clinically insignificant effect of supplemental vitamin C on serum urate in patients with gout: a pilot randomized controlled trial. Arthritis Rheum. 2013;65:1636-1642.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 52]  [Cited by in F6Publishing: 15]  [Article Influence: 6.5]  [Reference Citation Analysis (0)]
102.  Nederlandse Vereniging voor Reumatologie (Richtlijn Jicht. 2013).  Available from: http://www.nvr.nl/richtlijnen/richtlijnen2.  [PubMed]  [DOI]  [Cited in This Article: ]
103.  Neogi T, Hunter DJ, Chaisson CE, Allensworth-Davies D, Zhang Y. Frequency and predictors of inappropriate management of recurrent gout attacks in a longitudinal study. J Rheumatol. 2006;33:104-109.  [PubMed]  [DOI]  [Cited in This Article: ]
104.  Roddy E, Zhang W, Doherty M. Concordance of the management of chronic gout in a UK primary-care population with the EULAR gout recommendations. Ann Rheum Dis. 2007;66:1311-1315.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 147]  [Cited by in F6Publishing: 43]  [Article Influence: 10.5]  [Reference Citation Analysis (0)]
105.  Mikuls TR, Farrar JT, Bilker WB, Fernandes S, Saag KG. Suboptimal physician adherence to quality indicators for the management of gout and asymptomatic hyperuricaemia: results from the UK General Practice Research Database (GPRD). Rheumatology (Oxford). 2005;44:1038-1042.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 109]  [Cited by in F6Publishing: 37]  [Article Influence: 6.8]  [Reference Citation Analysis (0)]
106.  Doherty M, Jansen TL, Nuki G, Pascual E, Perez-Ruiz F, Punzi L, So AK, Bardin T. Gout: why is this curable disease so seldom cured? Ann Rheum Dis. 2012;71:1765-1770.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 175]  [Cited by in F6Publishing: 38]  [Article Influence: 19.4]  [Reference Citation Analysis (0)]
107.  De Vera MA, Marcotte G, Rai S, Galo JS, Bhole V. Medication adherence in gout: a systematic review. Arthritis Care Res (Hoboken). 2014;66:1551-1559.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 98]  [Cited by in F6Publishing: 19]  [Article Influence: 16.3]  [Reference Citation Analysis (0)]
108.  Zandman-Goddard G, Amital H, Shamrayevsky N, Raz R, Shalev V, Chodick G. Rates of adherence and persistence with allopurinol therapy among gout patients in Israel. Rheumatology (Oxford). 2013;52:1126-1131.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 42]  [Cited by in F6Publishing: 8]  [Article Influence: 5.3]  [Reference Citation Analysis (0)]
109.  Rees F, Jenkins W, Doherty M. Patients with gout adhere to curative treatment if informed appropriately: proof-of-concept observational study. Ann Rheum Dis. 2013;72:826-830.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 185]  [Cited by in F6Publishing: 40]  [Article Influence: 20.6]  [Reference Citation Analysis (0)]
110.  Brook RA, Forsythe A, Smeeding JE, Lawrence Edwards N. Chronic gout: epidemiology, disease progression, treatment and disease burden. Curr Med Res Opin. 2010;26:2813-2821.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 66]  [Cited by in F6Publishing: 16]  [Article Influence: 6.0]  [Reference Citation Analysis (0)]
111.  Edwards NL, Sundy JS, Forsythe A, Blume S, Pan F, Becker MA. Work productivity loss due to flares in patients with chronic gout refractory to conventional therapy. J Med Econ. 2011;14:10-15.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 53]  [Cited by in F6Publishing: 14]  [Article Influence: 4.8]  [Reference Citation Analysis (0)]
112.  Khanna PP, Nuki G, Bardin T, Tausche AK, Forsythe A, Goren A, Vietri J, Khanna D. Tophi and frequent gout flares are associated with impairments to quality of life, productivity, and increased healthcare resource use: Results from a cross-sectional survey. Health Qual Life Outcomes. 2012;10:117.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 105]  [Cited by in F6Publishing: 20]  [Article Influence: 11.7]  [Reference Citation Analysis (0)]
113.  Ferraz MB, O’Brien B. A cost effectiveness analysis of urate lowering drugs in nontophaceous recurrent gouty arthritis. J Rheumatol. 1995;22:908-914.  [PubMed]  [DOI]  [Cited in This Article: ]
114.  Perez-Ruiz F, Martínez-Indart L, Carmona L, Herrero-Beites AM, Pijoan JI, Krishnan E. Tophaceous gout and high level of hyperuricaemia are both associated with increased risk of mortality in patients with gout. Ann Rheum Dis. 2014;73:177-182.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 111]  [Cited by in F6Publishing: 27]  [Article Influence: 13.9]  [Reference Citation Analysis (0)]
115.  Culleton BF, Larson MG, Kannel WB, Levy D. Serum uric acid and risk for cardiovascular disease and death: the Framingham Heart Study. Ann Intern Med. 1999;131:7-13.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 778]  [Cited by in F6Publishing: 344]  [Article Influence: 35.4]  [Reference Citation Analysis (0)]
116.  Fang J, Alderman MH. Serum uric acid and cardiovascular mortality the NHANES I epidemiologic follow-up study, 1971-1992. National Health and Nutrition Examination Survey. JAMA. 2000;283:2404-2410.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 992]  [Cited by in F6Publishing: 442]  [Article Influence: 47.2]  [Reference Citation Analysis (0)]
117.  Johnson RJ, Kang DH, Feig D, Kivlighn S, Kanellis J, Watanabe S, Tuttle KR, Rodriguez-Iturbe B, Herrera-Acosta J, Mazzali M. Is there a pathogenetic role for uric acid in hypertension and cardiovascular and renal disease? Hypertension. 2003;41:1183-1190.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 788]  [Cited by in F6Publishing: 152]  [Article Influence: 43.8]  [Reference Citation Analysis (0)]
118.  Teng GG, Ang LW, Saag KG, Yu MC, Yuan JM, Koh WP. Mortality due to coronary heart disease and kidney disease among middle-aged and elderly men and women with gout in the Singapore Chinese Health Study. Ann Rheum Dis. 2012;71:924-928.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 44]  [Cited by in F6Publishing: 15]  [Article Influence: 4.4]  [Reference Citation Analysis (0)]
119.  Landmesser U, Spiekermann S, Dikalov S, Tatge H, Wilke R, Kohler C, Harrison DG, Hornig B, Drexler H. Vascular oxidative stress and endothelial dysfunction in patients with chronic heart failure: role of xanthine-oxidase and extracellular superoxide dismutase. Circulation. 2002;106:3073-3078.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 357]  [Cited by in F6Publishing: 70]  [Article Influence: 18.8]  [Reference Citation Analysis (0)]
120.  Cai H, Harrison DG. Endothelial dysfunction in cardiovascular diseases: the role of oxidant stress. Circ Res. 2000;87:840-844.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 2366]  [Cited by in F6Publishing: 430]  [Article Influence: 112.7]  [Reference Citation Analysis (0)]
121.  Dawson J, Quinn T, Walters M. Uric acid reduction: a new paradigm in the management of cardiovascular risk? Curr Med Chem. 2007;14:1879-1886.  [PubMed]  [DOI]  [Cited in This Article: ]
122.  Doehner W, Schoene N, Rauchhaus M, Leyva-Leon F, Pavitt DV, Reaveley DA, Schuler G, Coats AJ, Anker SD, Hambrecht R. Effects of xanthine oxidase inhibition with allopurinol on endothelial function and peripheral blood flow in hyperuricemic patients with chronic heart failure: results from 2 placebo-controlled studies. Circulation. 2002;105:2619-2624.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 389]  [Cited by in F6Publishing: 93]  [Article Influence: 20.5]  [Reference Citation Analysis (0)]
123.  Feig DI, Soletsky B, Johnson RJ. Effect of allopurinol on blood pressure of adolescents with newly diagnosed essential hypertension: a randomized trial. JAMA. 2008;300:924-932.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 610]  [Cited by in F6Publishing: 272]  [Article Influence: 46.9]  [Reference Citation Analysis (0)]
124.  Kanbay M, Ozkara A, Selcoki Y, Isik B, Turgut F, Bavbek N, Uz E, Akcay A, Yigitoglu R, Covic A. Effect of treatment of hyperuricemia with allopurinol on blood pressure, creatinine clearence, and proteinuria in patients with normal renal functions. Int Urol Nephrol. 2007;39:1227-1233.  [PubMed]  [DOI]  [Cited in This Article: ]
125.  Gois PH, Souza ER. Pharmacotherapy for hyperuricemia in hypertensive patients. Cochrane Database Syst Rev. 2013;1:CD008652.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 8]  [Cited by in F6Publishing: 8]  [Article Influence: 1.0]  [Reference Citation Analysis (0)]
126.  Agarwal V, Messerli F. Effect of allopurinol on blood pressure (author response to Allopurinol on hypertension: insufficient evidence to recommend). J Clin Hypertens (Greenwich). 2013;15:701.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 3]  [Cited by in F6Publishing: 2]  [Article Influence: 0.4]  [Reference Citation Analysis (0)]
127.  Noman A, Ang DS, Ogston S, Lang CC, Struthers AD. Effect of high-dose allopurinol on exercise in patients with chronic stable angina: a randomised, placebo controlled crossover trial. Lancet. 2010;375:2161-2167.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 236]  [Cited by in F6Publishing: 42]  [Article Influence: 21.5]  [Reference Citation Analysis (0)]
128.  Struthers A, Shearer F. Allopurinol: novel indications in cardiovascular disease. Heart. 2012;98:1543-1545.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 23]  [Cited by in F6Publishing: 8]  [Article Influence: 2.6]  [Reference Citation Analysis (0)]
129.  Tsutsumi Z, Moriwaki Y, Takahashi S, Ka T, Yamamoto T. Oxidized low-density lipoprotein autoantibodies in patients with primary gout: effect of urate-lowering therapy. Clin Chim Acta. 2004;339:117-122.  [PubMed]  [DOI]  [Cited in This Article: ]
130.  Luk AJ, Levin GP, Moore EE, Zhou XH, Kestenbaum BR, Choi HK. Allopurinol and mortality in hyperuricaemic patients. Rheumatology (Oxford). 2009;48:804-806.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 64]  [Cited by in F6Publishing: 33]  [Article Influence: 5.3]  [Reference Citation Analysis (0)]
131.  Wei L, Mackenzie IS, Chen Y, Struthers AD, MacDonald TM. Impact of allopurinol use on urate concentration and cardiovascular outcome. Br J Clin Pharmacol. 2011;71:600-607.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 63]  [Cited by in F6Publishing: 18]  [Article Influence: 6.3]  [Reference Citation Analysis (0)]
132.  Struthers AD, Donnan PT, Lindsay P, McNaughton D, Broomhall J, MacDonald TM. Effect of allopurinol on mortality and hospitalisations in chronic heart failure: a retrospective cohort study. Heart. 2002;87:229-234.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 88]  [Cited by in F6Publishing: 42]  [Article Influence: 4.6]  [Reference Citation Analysis (0)]
133.  Wei L, Fahey T, Struthers AD, MacDonald TM. Association between allopurinol and mortality in heart failure patients: a long-term follow-up study. Int J Clin Pract. 2009;63:1327-1333.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 34]  [Cited by in F6Publishing: 19]  [Article Influence: 3.1]  [Reference Citation Analysis (0)]
134.  Grimaldi-Bensouda L, Alpérovitch A, Aubrun E, Danchin N, Rossignol M, Abenhaim L, Richette P; the PGRx MI Group. Impact of allopurinol on risk of myocardial infarction. Ann Rheum Dis. 2014;Jan 6; Epub ahead of print.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 61]  [Cited by in F6Publishing: 25]  [Article Influence: 8.7]  [Reference Citation Analysis (0)]
135.  Ogino K, Kato M, Furuse Y, Kinugasa Y, Ishida K, Osaki S, Kinugawa T, Igawa O, Hisatome I, Shigemasa C. Uric acid-lowering treatment with benzbromarone in patients with heart failure: a double-blind placebo-controlled crossover preliminary study. Circ Heart Fail. 2010;3:73-81.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 122]  [Cited by in F6Publishing: 28]  [Article Influence: 10.2]  [Reference Citation Analysis (0)]
136.  Lyngdoh T, Marques-Vidal P, Paccaud F, Preisig M, Waeber G, Bochud M, Vollenweider P. Elevated serum uric acid is associated with high circulating inflammatory cytokines in the population-based Colaus study. PLoS One. 2011;6:e19901.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 111]  [Cited by in F6Publishing: 38]  [Article Influence: 11.1]  [Reference Citation Analysis (0)]
137.  Chowalloor PV, Keen HI. A systematic review of ultrasonography in gout and asymptomatic hyperuricaemia. Ann Rheum Dis. 2013;72:638-645.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 75]  [Cited by in F6Publishing: 20]  [Article Influence: 9.4]  [Reference Citation Analysis (0)]