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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, 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

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