Urate-lowering Treatment Research Articles

Association between serum urate, gout and comorbidities: a case-control study using data from the UK Biobank.

To examine the association between comorbidities and serum urate (SU), gout and comorbidities, and to determine whether the association between gout and comorbidities is independent of SU. We performed a case-control study using UK Biobank data. Two separate analyses were conducted: one excluding participants with gout to investigate the association between comorbidities and SU and the other with participants with gout as the index condition to examine the association between gout and comorbidities. SU was measured at the baseline visit. Self-reported physician-diagnosed illnesses were used to define gout and comorbidities, except for chronic kidney disease (CKD), which was defined using an estimated glomerular filtration rate cut-off. Participants prescribed urate-lowering treatment were also classified as gout. Logistic regression was used to examine associations. Odds ratios (ORs) and 95% CIs were calculated and adjusted for covariates including comorbidities and SU. Data for 458781 UK Biobank participants were used to examine the association between comorbidities and SU. There was an association between hypertension, ischaemic heart disease (IHD), congestive cardiac failure (CCF), hyperlipidaemia, CKD and SU with and adjusted OR (aOR) of 1.10-3.14 for each 1 mg/dl SU increase. A total of 10265 gout cases and 458781 controls were included in the analysis of association between gout and comorbidities. Gout associated independently with hypertension, IHD, CCF, hyperlipidaemia and diabetes, with aORs of 1.21-4.15 after adjusting for covariates including SU. Comorbidities associate with increasing SU. The association between gout and cardiometabolic comorbidities was independent of SU, suggesting separate SU-independent mechanisms such as inflammation driven by crystal deposition, pro-inflammatory genotype or non-purine dietary factors.

High Rate of Adherence to Urate-Lowering Treatment in Patients with Gout: Who's to Blame?

IntroductionGout is commonly associated with low adherence rates, thus limiting the effectiveness of treatment. Nevertheless, informed and empowered patients may be more likely to achieve high adherence. We intend to demonstrate that adherence in clinical practice may reach that achieved in clinical trials.MethodsThis was a transversal study within an inception cohort of patients with gout prospectively followed up. Patients were informed at entrance in the cohort of outcomes, targets, and means to implement for successful treatment. Adherence was evaluated through electronic medication possession ratio (MPR) for urate-lowering medication and oral medications for hypertension, diabetes, and hyperlipidemia for comparison. Factors associated with nonadherence, and the relation between nonadherence and serum urate levels while on treatment were analyzed.ResultsData were retrieved from 336 patients, who showed a mean MPR of 87.5%, with 82.1% of patients showing MPR ≥ 0.8. Rates of adherence for hypertension, hyperlipidemia, and diabetes were quite similar (88%, 87%, and 83%, respectively), although MPR > 0.8 was significantly lower for oral medications for diabetes. Adherence was lower, but nevertheless quite fair, during the first year of follow-up, and increasing over time. Active follow-up and comorbidity were associated with good adherence, and adherence and long-term follow-up were associated with higher rates of achieving serum urate within therapeutic target.ConclusionPatients with gout show high rates of adherence if empowered. Active follow-up and comorbidity are associated with high rates of adherence. Adherence is strongly associated with higher rates of achievement of therapeutic serum urate target.

Ultrasound shows rapid reduction of crystal depositions during a treat-to-target approach in gout patients: 12-month results from the NOR-Gout study

ObjectivesAs ultrasound is sensitive for detecting crystal depositions in patients with gout, our objectives were to explore the main locations for depositions and the extent of dissolution of depositions during...

Effects of Allopurinol on the Progression of Chronic Kidney Disease

BackgroundElevated serum urate levels are associated with progression of chronic kidney disease. Whether urate-lowering treatment with allopurinol can attenuate the decline of the estimated glomerular filtration rate (eGFR) in patients with chronic kidney disease who are at risk for progression is not known.MethodsIn this randomized, controlled trial, we randomly assigned adults with stage 3 or 4 chronic kidney disease and no history of gout who had a urinary albumin:creatinine ratio of 265 or higher (with albumin measured in milligrams and creatinine in grams) or an eGFR decrease of at least 3.0 ml per minute per 1.73 m2 of body-surface area in the preceding year to receive allopurinol (100 to 300 mg daily) or placebo. The primary outcome was the change in eGFR from randomization to week 104, calculated with the Chronic Kidney Disease Epidemiology Collaboration creatinine equation.ResultsEnrollment was stopped because of slow recruitment after 369 of 620 intended patients were randomly assigned to receive allopurinol (185 patients) or placebo (184 patients). Three patients per group withdrew immediately after randomization. The remaining 363 patients (mean eGFR, 31.7 ml per minute per 1.73 m2; median urine albumin:creatinine ratio, 716.9; mean serum urate level, 8.2 mg per deciliter) were included in the assessment of the primary outcome. The change in eGFR did not differ significantly between the allopurinol group and the placebo group (−3.33 ml per minute per 1.73 m2 per year [95% confidence interval {CI}, −4.11 to −2.55] and −3.23 ml per minute per 1.73 m2 per year [95% CI, −3.98 to −2.47], respectively; mean difference, −0.10 ml per minute per 1.73 m2 per year [95% CI, −1.18 to 0.97]; P=0.85). Serious adverse events were reported in 84 of 182 patients (46%) in the allopurinol group and in 79 of 181 patients (44%) in the placebo group.ConclusionsIn patients with chronic kidney disease and a high risk of progression, urate-lowering treatment with allopurinol did not slow the decline in eGFR as compared with placebo. (Funded by the National Health and Medical Research Council of Australia and the Health Research Council of New Zealand; CKD-FIX Australian New Zealand Clinical Trials Registry number, ACTRN12611000791932.)

A retrospective cross-sectional study of the associated factors of hyperuricemia in patients with chronic kidney disease

ObjectiveTo investigate the prevalence of hyperuricemia in patients at different stages of chronic kidney disease (CKD) and the association of serum uric acid (SUA) with several clinical factors in a retrospective cross-sectional study of non-dialysis CKD patients at two hospitals in Shanghai, China.MethodsThe prevalence of hyperuricemia in CKD patients and the association of SUA with other clinical factors were examined using analysis of variance, chi-squared test, multivariate analysis, and other statistical methods.ResultsA total of 663 CKD patients were enrolled, of which approximately 52% had hyperuricemia. CKD patients with hyperuricemia had lower hemoglobin and estimated glomerular filtration rate (eGFR) levels but higher blood urea nitrogen, serum creatinine, and serum phosphate levels than those without hyperuricemia. Serum uric acid level was positively associated with age, blood urea nitrogen , serum creatinine, cystatin C, and serum phosphate and negatively associated with hemoglobin and eGFR. In addition, CKD patients with anemia and hyperphosphatemia had a higher prevalence of hyperuricemia than those without anemia or hyperphosphatemia.ConclusionsThe prevalence of hyperuricemia increased with CKD progression supporting the use of urate-lowering treatment for patients with CKD stage 1 to 4.

Combined Use of Febuxostat and Colchicine Does Not Increase Acute Hepatotoxicity in Patients with Gout: A Retrospective Study.

Colchicine has been effectively used to prevent acute flares in patients with gout, but drug-related adverse events have frequently occurred. We investigated whether colchicine therapy with febuxostat is associated with hepatotoxicity in gout patients. Gout patients treated with (n = 121) or without (n = 57) colchicine were enrolled upon initiating febuxostat as a urate-lowering treatment, and clinical and laboratory data at diagnosis were compared. Logistic regression analysis was performed to evaluate the risk factors related to hepatotoxicity. Median age of the with-colchicine and without-colchicine groups was 51.0 (37.0–62.0) and 56.0 (43.5–68.5) years, respectively. During the three months of febuxostat prescription, the prevalence of hepatotoxicity was 13/121 (10.9%) in the with-colchicine group and 4/57 (7.0%) in the without-colchicine group, without statistical significance. The rate of colchicine use was not different between the study subjects with or without hepatotoxicity (76.5% vs. 67.1%, p = 0.587). Pre-existing liver disease was significantly associated with increased risk of hepatotoxicity after febuxostat treatment (odds ratio, 4.083; 95% confidence interval, 1.326–12.577; p = 0.014). Colchicine may be safely used as a prophylactic agent for gout patients with febuxostat. However, upon initiating febuxostat, it is recommended to monitor the development of acute liver injury in gout patients with underlying liver disease.

Evaluation of febuxostat initiation during an acute gout attack: A prospective, randomized clinical trial.

Urate-lowering treatment (ULT) is recommended in gout management. However, initiation of ULT during an acute gout flare is still inconclusive. This study aimed to evaluate the efficacy and safety of the ULT febuxostat administered at initiation of an acute gout attack. A prospective randomized controlled clinical trial was conducted for 12 weeks in primary gout patients who were admitted with acute gout attacks. Subjects were randomly assigned to the febuxostat group in which febuxostat, 40mg daily, was administered in the primary care setting for attacks, or to the control group in which febuxostat, 40mg daily, was administered after the attacks. All patients received adequate anti-inflammatory and analgesic therapies. Serum urate (SU) levels were monitored throughout the study. Pain, measured using a visual analogue scale (VAS), and gout recurrence rate were used as primary outcomes. Flare-related inflammation biomarkers were selected as secondary outcomes. Fifty-two patients completed the study (febuxostat group: n=28; control group: n=24). No significant differences were detected in VAS scores between the two groups over the first 14-day observation period (P>0.05). Administration of febuxostat decreased SU levels significantly during the first 2-week period. However, the gout recurrent rate or gout flare-related inflammation indicators did not change in the febuxostat or control groups. Treatment-related adverse events were mild and similar between groups. Initiation of the urate-lowering drug febuxostat during an acute gout attack caused no significant difference in daily pain, recurrent flares, or adverse effects. The treatment significantly decreased SU levels in the early stage and might have potential long-term benefits in these patients.

Changes in Urinary Microalbumin Levels after Correction of Hyperuricemia in Patients with Gout: An Observational Cohort Study.

Background Gout is commonly associated with metabolic syndrome. Strong association between the serum uric acid level and microalbuminuria has also been observed in various studies. Aim To observe the change in urinary microalbumin after urate-lowering treatment in patients with gout and microalbuminuria. Methodology. A prospective, observational study was conducted at a tertiary-level rheumatic center (NCRD) in Kathmandu, Nepal. Adults diagnosed with gout using the 2015 ACR/EULAR criteria and microalbuminuria were enrolled in the study after obtaining informed consent. Sociodemographic profile and clinical history were recorded at baseline. Serum uric acid levels, spot urinary microalbumin (MAU) excretion, blood sugar, lipid profile, and blood pressure were measured at baseline, 3-month follow-up, and 6-month follow-up. A paired t-test was used to compare the change in mean MAU after treatment. Results A total of 778 patients diagnosed with gout were screened for microalbuminuria. Among them, 114 (14.6%) had urinary microalbumin levels of >30.0 mg/L during presentation. Mean MAU level among those with microalbuminuria was 132.4 ± 124.6 mg/L. Thirty-five patients had concomitant HTN and were put on ARBs (20 mg of telmisartan). All received 40 mg of febuxostat. In patients with ARBs, MAU reduced significantly after 3 months of treatment with ARBs. Reduction in MAU in those without ARBs was seen after the 6-month follow-up, and the change was statistically significant. Conclusions There is significant reduction in MAU after the use of urate-lowering drugs in patients with gout.

Debates in gout management.

This review discusses the findings of recently published translational research studies that have the potential to directly impact on the management of gout patients. Recent research suggests that treat-to-target urate-lowering treatment (ULT) alongside individualized education about gout, and shared decision making results in excellent adherence with ULT and prevents gout flares in the long term. Such interventions should preferentially be delivered face-to-face rather than remotely. The recently published CARES study raises the possibility that febuxostat increases the risk of death in people with preexisting major cardiovascular diseases, and, allopurinol should remain the first-choice ULT. There is paucity of data on the dosing of ULT for managing hyperuricaemia in gout patients with chronic kidney disease. However, recent research suggests that the dose of allopurinol can be gradually increased to above the conventional renal dose in people with chronic kidney disease without allopurinol hypersensitivity syndrome. However, additional larger studies are needed in this field. In summary, long-term treat-to-target ULT prevents gout flares and improves quality of life. Given the recent safety concerns, gradually up-titrated allopurinol remains the first-line urate-lowering drug.

Analysis of risk factors for susceptibility of frequent gout attacks: A case-control study of 579 patients with primary gout

Objective To analyze the risk factors of frequent gout flare, and to evaluate its susceptibility to identify patients with≥2 acute attacks per year. Methods A total of 579 of cases gout patients with no history of taking urate lowering treatment (ULT) in recent 12 months were enrolled. The patients were divided into frequent group (gout episodes≥twice per year) and non-frequent group(gout attacks<twice per year). The clinical information was collected and relevant biochemical indices were detected. Results There were significant differences in involvement of upper limb joints, tophi, combining hypertension and renal stone between two groups. The two groups had no statistical differences in family history, gender, history of smoking and drinking, ratios of regular exercise, and combining diabetes, hepatic insufficiency, hypertriglyceridemia, hypercholesterolemia, and overweight/obesity. There was significant differences in the number of joints involved, the history of disease duration, the level of SUA and TG[(4.66±2.54) vs (2.77±1.64), (6.68±5.11) vs (5.14±3.89) years, (525.82±132.11) vs (489.33±139.81) μmol/L, (2.51±1.94) vs (2.05±1.22) mmol/L, P 2, and the sensitivity, specificity, positive predictive value and negative predictive value were 77.8%, 43.3%, 85.6%, and 56.6%, respectively, and the difference was significant. Conclusion Higher SUA and a larger number of joints involved associate independently with frequent gout attacks. The number of joints involved at initial diagnosis>2, which can predict the frequent flare, and start ULT as earlier as possible. Patients with joints involved at initial diagnosis>2 are at greater risk of frequent gout flare. Key words: Gout; Flare; Frequency; Risk factors; ROC curve

Uric acid in CKD: has the jury come to the verdict?

Epidemiological studies show that hyperuricemia independently predicts the development of chronic kidney disease (CKD) in individuals with normal kidney function both in the general population and in subjects with diabetes. As a matter of fact, an unfavorable role of uric acid may somewhat be harder to identify in the context of multiple risk factors and pathogenetic mechanisms typical of overt CKD such as proteinuria and high blood pressure. Although the discrepancy in clinical results could mean that urate lowering treatment does not provide a constant benefit in all patients with hyperuricemia and CKD, we believe that the inconsistency in the results from available meta-analysis is mainly due to inadequate sample size, short follow-up times and heterogeneity in study design characterizing the randomized controlled trials included in the analyses. Therefore, available data support the view that hyperuricemia has a damaging impact on kidney function, while preliminary evidence suggests that treatment of so-called asymptomatic hyperuricemia may be helpful to slow or delay the progression of chronic kidney.

Asymptomatic hyperuricemia: is it really asymptomatic?

Hyperuricemia is highly prevalent, affecting approximately 38 million individuals in the United States. However, the significance of asymptomatic hyperuricemia - hyperuricemia in the absence of gout - continues to be debated. Asymptomatic hyperuricemia results in monosodium urate crystal deposition in tissues, which may promote chronic inflammation. Intracellularly, hyperuricemia inhibits the master regulator adenosine monophosphate (AMP)-associated protein kinase and may condition innate immune responses through durable epigenetic modifications. At the population level, asymptomatic hyperuricemia is associated with multiple comorbidities, including hypertension, chronic kidney disease, coronary artery disease, and diabetes; limitations of these studies include that most are retrospective and some do not rigorously distinguish between asymptomatic hyperuricemia and gout. Treatment studies suggest that urate lowering may reduce the risk of incidence or progression of some of these comorbidities; unfortunately, many of these treatment studies are small or flawed, and not all study results are consistent. Accumulating evidence suggests that asymptomatic hyperuricemia contributes to the comorbidities with which it associates and that proper asymptomatic hyperuricemia treatment may reduce future risk. Additional prospective trials are needed to definitely establish causality and support decision-making as to whether, and which patients with asymptomatic hyperuricemia would warrant urate-lowering treatment.

Gout is not a life sentence: be informed.

“I knew as much about gout as you could fit on a postage stamp. I had a vision of a cartoon Lord-of-the-manor image, drinking with a large bandage around his foot.” Malcolm is not alone in his thinking, nor is he alone in receiving sub-optimal gout treatment. He articulates the impact gout has had on his mind, body, and quality of life: “I know pain, I've had broken bones, I've been shot, even a knee replacement, but nothing compares to a gout attack—it takes over completely; I can't function, can't move, nothing relieves it.” By the time his flare-ups had escalated from two per year to an overall 50% occurrence, the anxiety and depression caused by more than 4 years of progressive and sustained attacks led him to thoughts of suicide. Efficacy and cost-effectiveness of nurse-led care involving education and engagement of patients and a treat-to-target urate-lowering strategy versus usual care for gout: a randomised controlled trialNurse-led gout care is efficacious and cost-effective compared with usual care. Our findings illustrate the benefits of educating and engaging patients in gout management and reaffirm the importance of a treat-to-target urate-lowering treatment strategy to improve patient-centred outcomes. Full-Text PDF Open Access

Nurse-led care is preferred over GP-led care of gout and improves gout outcomes: results of Nottingham Gout Treatment Trial follow-up study.

To explore patient satisfaction, gout knowledge, medication adherence and flares among participants receiving nurse-led or general practitioner (GP)-led care of gout in the Nottingham Gout Treatment Trial phase-II (NGTT-II). A total of 438 participants of NGTT-II were sent a questionnaire enquiring about gout knowledge, satisfaction with health-care practitioner, urate-lowering treatment being undertaken, and gout flares ⩾1 year after their final visit. Nurse-led care participants were asked about their preference for receiving gout treatment from either a GP or a nurse. Completed questionnaires were returned by 82% of participants. Participants previously receiving nurse-led care reported greater satisfaction with health-care practitioner (P < 0.001), had better gout knowledge (P = 0.02), were more likely to be taking urate-lowering treatment [adjusted relative risk (95% CI) 1.19 (1.09, 1.30)], and self-reported fewer flares in the previous 12 months [median (inter-quartile range) 0 (0-0) vs 1 (0-3), P < 0.001] than those receiving GP-led care. Of participants receiving nurse-led care, 41-63% indicated preference for receiving gout treatment from a nurse, while only 5-20% indicated preference for receiving treatment from GPs. The results of this study favour nurse-led care, involving individualized patient education and engagement and a treat-to-target strategy, in terms of patient acceptability, long-term adherence, and flares. Further research is required to evaluate the feasibility of implementing such a model of care in clinical practice.

Cardiovascular Safety of Urate Lowering Therapies.

The effect of urate lowering treatment (ULT) on cardiovascular (CV) risk and mortality in gout has been a topic of interest. This review discusses the CV effect of ULT and comparative CV safety among ULT agents. The mechanism linking gout with CV risk is not fully understood but seems multifactorial involving hyperuricemia, xanthine oxidase (XO), oxidative stress, and chronic inflammation. Conflicting data exist regarding CV benefits of ULT in adults with and without hyperuricemia. Although meta-analyses on randomized controlled trials (RCTs) suggest CV benefits with allopurinol, few high-quality RCTs have examined the CV effect of ULT among patients with hyperuricemia or gout. The recent CARES trial adds new information on comparative CV safety between two XO inhibitors (XOIs), febuxostat and allopurinol, in patients with gout. It remains unclear whether ULT reduces CV risk in patients with gout or hyperuricemia. Comparative CV safety studies of XOIs suggest that additional mechanisms beyond urate-lowering effect or XO inhibition are likely involved in CV risk modification in patients with gout. Ongoing RCTs of ULT may be able to further determine the effect of ULT on CV risk.

Hyperuricaemia and vascular risk: the debate continues.

To update the evidence about the role of elevated levels of uric acid as a risk factor for cardiovascular disease. The review includes the most recent epidemiological evidence as well as the possible mechanisms supporting the interaction between uric acid and cardiovascular, metabolic and renal disease. The confirmed role of uric acid as involved in the onset and progression of cardiovascular and metabolic diseases. In particular, the review will focus on the possible mechanism of action of uric acid and the level of involvement of xanthine-oxidase as a mechanism responsible for both hyperuricaemia and oxidative stress. The review also briefly summarizes the most recent findings of the studies carried out with xanthine-oxidase inhibitors in patients at risk of cardiovascular disease by focusing on the possible benefits. Elevated levels of serum uric acid have been demonstrated to be closely related to the development of cardiovascular, metabolic and renal disease. The mechanism responsible for such interaction directly or indirectly involves xanthine-oxidase activation and the inflammatory system leading to structural and functional abnormalities. Preliminary results from different trials have demonstrated the favourable effects of urate-lowering treatment in the prevention of cardiovascular disease beyond the treatment of gout.

Urate-lowering therapy alleviates atherosclerosis inflammatory response factors and neointimal lesions in a mouse model of induced carotid atherosclerosis.

Hyperuricemia (HU) is a cause of gout. Clinical studies show a link between HU and cardiovascular disease. However, the role of soluble serum urate (SU) on atherosclerosis development remains elusive. We aimed to use a new HU mouse model [Uricase/Uox knockout (KO)] to further investigate the relationship between HU and atherosclerosis. A mouse model by perivascular collar placement of induced carotid atherosclerosis was established in male Uox‐ KO mice. The Uox‐ KO mice had elevated SU levels and enhanced levels of atherosclerosis inflammatory response proteins. In contrast, Uox‐ KO mice with carotid atherosclerosis showed severe neointimal changes in histology staining consistent with increases in intimal area and increases in proliferating cell nuclear antigen (PCNA)‐ and F4/80‐positive cells. Allopurinol reduced neointimal areas induced by the perivascular collar in hyperuricemic mice, accompanied by decreased expression of PCNA‐ and F4/80‐positive cells. Urate‐lowering treatment alleviated atherosclerosis inflammatory response factors and reactive oxygen species (ROS) intensities in both collar placement Uox‐ KO mice and urate‐stimulated human umbilical vein endothelial cells (HUVECs). In vitro results using HUVECs showed ROS was induced by urate and ROS induction was abrogated using antioxidants. These data demonstrate that urate per se does not trigger atherosclerosis intima lesions in male mice. Urate worsens carotid neointimal lesions induced by the perivascular collar and urate‐lowering therapy partially abrogates the effects. The current study warrants clinical studies on the possible benefits of urate‐lowering therapy in atherosclerosis patients with HU.

Facilitating equitable prevention and management of gout for Māori in Northland, New Zealand, through a collaborative primary care approach.

INTRODUCTION The Gout Stop Programme was developed for primary care in Northland, New Zealand, to address inequitable health outcomes for Māori and Pacific people with gout. AIM The aim of the programme was to make it easier for clinicians to prescribe urate-lowering treatment, facilitate patient adherence through education and support, and reduce barriers to gout prevention and long-term management. METHODS From 2015 to 2017, patients with acute gout who met inclusion criteria were prescribed treatment according to a 'Gout Stop Pack' option, based on renal function and diabetes status. Patients were monitored by community pharmacists. Gout educators and a Gout Kaiāwhina (community support worker) provided education and support to patients and whānau (families). Patient completion of the programme and outcomes, according to target serum urate level, were recorded. Patient experience was documented using a questionnaire and rating scale. RESULTS In total, 160 clinicians prescribed therapy at 887 patient presentations; 71% were Māori and Pacific patients. The completion rate was 55% in this group and 84% for the non-Māori and non-Pacific group. In the Māori and Pacific group, 40% reached the target serum urate level (≤0.36 mmol L-1) in 91 days, and 26% required further titration. In the non-Māori/non-Pacific group, these rates were 51% and 19% respectively. Following programme completion, 68% of Māori and Pacific patients and 65% of non-Māori and non-Pacific patients continued to take allopurinol. The 21 patients interviewed rated the programme as excellent or very good. DISCUSSION Culturally appropriate education and support for patients and the primary care team was essential. Collaboration between prescribers, community pharmacists and support workers reduced barriers to initiating prevention and long-term urate-lowering treatment and urate testing in this high-needs gout population.

Increasing trend of asymptomatic hyperuricemia under treatment with urate-lowering drugs in Japan

Objectives: To describe recent trends in the prevalence of gout and asymptomatic hyperuricemia regarding urate-lowering treatment (ULT) in Japan.Methods: A database of health insurance claims managed by the Japan Medical Data Center was used to estimate the annual prevalence of gout and asymptomatic hyperuricemia during 2010–2014. ULT was evaluated for status of the two diseases during the same period. The significance of time trends was evaluated by Cochrane–Armitage trend test.Results: The prevalence of physician-diagnosed gout in men aged 20–64 years was 1.54% (95% CI: 1.49%–1.58%) in 2010, with a slight but significant (p < 0.001) annual increase, up to 1.66% (95% CI: 1.62%–1.71%) in 2014. In women, gout prevalence was somewhat constant about 0.09% during 2010–2014. Among male patients with gout, 78% received ULT. The prevalence of male patients with asymptomatic hyperuricemia in the same age range, who received ULT, increased significantly from 1.77% (95% CI: 1.72%–1.81%) to 2.14% (95% CI: 2.09%–2.19%) during 2010–2014 (p < 0.001).Conclusion: Gout prevalence in adult men in Japan has increased significantly in recent years. The prevalence of asymptomatic hyperuricemia under ULT has also increased significantly and was higher than that of gout.

Efficacy and cost-effectiveness of nurse-led care involving education and engagement of patients and a treat-to-target urate-lowering strategy versus usual care for gout: a randomised controlled trial

SummaryBackgroundIn the UK, gout management is suboptimum, with only 40% of patients receiving urate-lowering therapy, usually without titration to achieve a target serum urate concentration. Nurses successfully manage many diseases in primary care. We compared nurse-led gout care to usual care led by general practitioners (GPs) for people in the community.MethodsResearch nurses were trained in best practice management of gout, including providing individualised information and engaging patients in shared decision making. Adults who had experienced a gout flare in the previous 12 months were randomly assigned 1:1 to receive nurse-led care or continue with GP-led usual care. We assessed patients at baseline and after 1 and 2 years. The primary outcome was the percentage of participants who achieved serum urate concentrations less than 360 μmol/L (6 mg/dL) at 2 years. Secondary outcomes were flare frequency in year 2, presence of tophi, quality of life, and cost per quality-adjusted life-year (QALY) gained. Risk ratios (RRs) and 95% CIs were calculated based on intention to treat with multiple imputation. This study is registered with www.ClinicalTrials.gov, number NCT01477346.Findings517 patients were enrolled, of whom 255 were assigned nurse-led care and 262 usual care. Nurse-led care was associated with high uptake of and adherence to urate-lowering therapy. More patients receiving nurse-led care had serum urate concentrations less than 360 μmol/L at 2 years than those receiving usual care (95% vs 30%, RR 3·18, 95% CI 2·42–4·18, p<0·0001). At 2 years all secondary outcomes favoured the nurse-led group. The cost per QALY gained for the nurse-led intervention was £5066 at 2 years.InterpretationNurse-led gout care is efficacious and cost-effective compared with usual care. Our findings illustrate the benefits of educating and engaging patients in gout management and reaffirm the importance of a treat-to-target urate-lowering treatment strategy to improve patient-centred outcomes.FundingArthritis Research UK.