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    Asymptomatic hyperuricaemia: a silent activator of the innate immune system. Joosten Leo A B,Crişan Tania O,Bjornstad Petter,Johnson Richard J Nature reviews. Rheumatology Asymptomatic hyperuricaemia affects ~20% of the general population in the USA, with variable rates in other countries. Historically, asymptomatic hyperuricaemia was considered a benign laboratory finding with little clinical importance in the absence of gout or kidney stones. Yet, increasing evidence suggests that asymptomatic hyperuricaemia can predict the development of hypertension, obesity, diabetes mellitus and chronic kidney disease and might contribute to disease by stimulating inflammation. Although urate has been classically viewed as an antioxidant with beneficial effects, new data suggest that both crystalline and soluble urate activate various pro-inflammatory pathways. This Review summarizes what is known about the role of urate in the inflammatory response. Further research is needed to define the role of asymptomatic hyperuricaemia in these pro-inflammatory pathways. 10.1038/s41584-019-0334-3
    Optimal uric acid levels by febuxostat treatment and cerebral, cardiorenovascular risks: post hoc analysis of a randomized controlled trial. Rheumatology (Oxford, England) OBJECTIVES:Hyperuricaemia is recognized as an independent risk marker for cardiovascular and renal diseases. However, uric acid is a powerful free-radical scavenger, and the optimal level of serum uric acid (SUA) determining outcomes is unknown. This study explored whether interventional treatments for excessive SUA reduction were harmful and what constituted the optimal lowering of SUA levels for the prevention of events in patients with asymptomatic hyperuricaemia. METHODS:This was a post hoc analysis of a randomized trial (Febuxostat for Cerebral and CaRdiorenovascular Events PrEvEntion StuDy [FREED]) in which 1070 older patients with asymptomatic hyperuricaemia were enrolled and allocated to febuxostat (n = 537) or non-febuxostat treatment group (n = 533). We assessed the relationship between the endpoint (withdrawal or study completion) SUA levels and clinical outcomes. Primary endpoint was defined as a composite of all-cause mortality, cerebral and cardiorenovascular events. RESULTS:In the febuxostat group, patients achieving SUA levels ≤4 mg/dl (hazard ratio: 2.01 [95% CI: 1.05, 3.87]), >4 to ≤5 mg/dl (2.12 [1.07, 4.20], >6 to ≤7 mg/dl (2.42 [1.05, 5.60]), and >7 mg/dl (4.73 [2.13, 10.5]) had significantly higher risks for a primary composite event than those achieving SUA levels >5 to ≤6 mg/dl (P = 0.003 [log-rank test]). This J-shaped relationship applied to patients with renal impairment (P = 0.007 [Gray's test]) and was not significant in the non-febuxostat treatment group (P = 0.212 [log-rank test]). CONCLUSION:Optimal SUA level by febuxostat treatment is 5-6 mg/dl for reducing all-cause mortality, cerebral, cardiovascular and renal events. Excessive SUA reduction may be harmful in older hyperuricaemic populations. TRIAL REGISTRATION:ClinicalTrial.gov, https://clinicaltrials.gov, NCT01984749. 10.1093/rheumatology/keab739
    Role of asymptomatic hyperuricemia in the progression of chronic kidney disease and cardiovascular disease. Waheed Yousuf,Yang Fan,Sun Dong The Korean journal of internal medicine Previous research has investigated whether hyperuricemia serves as an independent risk factor for cardiovascular and renal diseases. Hyperuricemia is defined as an abnormally high level of uric acid (UA; i.e., serum urate level > 6.8 mg/dL). Hyperuricemia has been considered a complication of chronic kidney disease (CKD). However, it seems to play a pathogenic role in the progression of renal diseases. There has been increasing focus on the link between hyperuricemia and CKD. The results of randomized controlled trials have implied independent associations between hyperuricemia and the progression of cardiovascular and renal morbidities. These associations may be mediated by renin-angiotensin system activation, nitric oxide synthase inhibition, and macrovascular/microvascular disease development. There remains controversy regarding the use of serum UA level as an indirect index of renal vascular disease. This literature review focuses on the role of asymptomatic hyperuricemia in the progression of CKD, as well as the association between hyperuricemia and cardiovascular disease. It also provides a general overview of the physiological metabolism of UA. 10.3904/kjim.2020.340
    The shrinking toe sign in gout. Bardin Thomas,Nguyen Quang D,Hieu Nghia L,Tran Khoi M,Dalbeth Nicola,Do Minh D,Ea Hang-Korng,Richette Pascal,Resche-Rigon Matthieu,Bousson Valérie Seminars in arthritis and rheumatism OBJECTIVE:To describe the frequency, clinical presentation and understand the pathophysiology of toe shortenings during urate-lowering treatment (ULT) of gout, a feature we called the shrinking toe sign. METHODS:Sequential foot photographs and radiographs of 1141 consecutive gouty patients followed-up for at least 6 months under ULT were retrospectively scrutinized. Features from patients with toe shortenings were extracted from anonymized files. Tophi adjacent to the shortening sites were semi quantified on foot photographs and toe shortenings were measured on radiographs with the Corel draw software (Corel corporation, Canada). Measurement concordance was assessed by concordance correlation coefficients (CCC) and correlation between tophus scores and toe shortenings was analyzed by using linear model with a patient random effect. 97 patients who did not develop toe shortening during ULT were analyzed as controls. RESULTS:Shrinking toes were observed in 10 patients (0.9%) with tophaceous gout at joints with baseline destructive arthropathy. The first and second toes and metatarsophalangeal joints were predominantly involved. The sign was observed after serum urate had been lowered below the 300 and 360 µmol/l targets, in 8 and 2 patients, respectively. Measured shortenings (CCC: 0.99) correlated (p < 10) with decreases in tophus score (CCC: 0.91). Sequential radiograph analysis revealed that toe shortening was mainly due to lytic bone collapse during articular tophus dissolution. Comparison with controls showed that the sign developed in severe gout and in joints with more severe erosion score at baseline. CONCLUSION:The shrinking toe appears as rare feature of severe tophaceous gout, triggered by dissolution of bone-replacing tophi. Our findings reinforce the need to treat gout early, before destruction of bone scaffold by extensive tophi, as MSU crystal dissolution by ULT may further weaken these areas and induce their collapse. 10.1016/j.semarthrit.2022.151981