The management of hyperuricemia with urate deposition

Desideri, Giovambattista; Puig, Juan; Richette, Pascal

doi:10.1185/03007995.2015.1087982

Cited by 15 publications

(11 citation statements)

References 39 publications

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“… 38 The main recommendations for optimal management of silent hyperuricemia to prevent gout development and possible cardiorenal sequelae according to current guidelines are resumed in Table 2 . 1 , 40 , 50 …”

Section: Management Of Hyperuricemiamentioning

confidence: 99%

An evidence-based review on urate-lowering treatments: implications for optimal treatment of chronic hyperuricemia

Bove¹,

Cicero²,

Veronesi³

et al. 2017

VHRM

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Several studies suggest that chronic hyperuricemia, the main precursor of gout, is involved in the pathogenesis of different systemic disorders that affect cardiovascular and renal systems, such as hypertension, obesity, hypercholesterolemia, atherosclerosis, metabolic syndrome, chronic heart failure, and chronic kidney disease. Recent epidemiological evidence has shown an increasing trend in the prevalence of hyperuricemia and gout in the Western world: a number of population-based studies estimate a prevalence of up to 21% for hyperuricemia and 1%–4% for gout. As such, early detection and careful management of this pathological condition is required, starting from lifestyle changes (mainly based on a diet low in red meat, sugars, and alcoholic beverages, with increased intake of vegetables, water, and vitamin C sources), adding specific drugs to lead serum uric acid (SUA) levels under the target value of 7 mg/dL. In particular, nonselective and selective XO inhibitors (allopurinol, oxypurinol, febuxostat) reduce SUA levels and the overproduction of reactive oxygen species, mainly related to XO overactivity that often causes inflammatory damage to the vascular endothelium. The effect of lowering SUA levels via XO inhibition includes an attenuation of oxidative stress and related endothelial dysfunction that largely contribute to the pathophysiology of metabolic syndrome and cardiovascular diseases. Therefore, the inhibition of XO overactivation seems to be an excellent therapeutic option to limit the harmful effects of excess UA and reactive oxygen species. In conclusion, rapid diagnosis and correct therapy for hyperuricemia may also improve the prevention and/or treatment of serious and multifactorial diseases. The available evidence supports the importance of promoting new experimental clinical trials to confirm the emerging antioxidant role of XO inhibitors, which could effectively contribute to cardiovascular and chronic kidney disease prevention.

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Section: Management Of Hyperuricemiamentioning

confidence: 99%

An evidence-based review on urate-lowering treatments: implications for optimal treatment of chronic hyperuricemia

Bove¹,

Cicero²,

Veronesi³

et al. 2017

VHRM

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“…The prevalence of asymptomatic hyperuricemia in the general population is estimated of 2% to 13%, and is augmented in recent decades [5]. The increase in serum UA levels may be linked to the rising prevalence of overweight and obesity, as well as, the increased consumption of sugar-sweetened beverages, foods rich in purine or alcohol [6,7]. Accumulating evidences show that increased UA level represents a risk factor for metabolic syndrome and cardiovascular diseases [8,9].…”

Section: Introductionmentioning

confidence: 99%

Hyper-homocysteinemia Inducing Hyperuricemia: What are the Mechanisms?

Cacciapuoti

2017

J Rheum Dis

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Hyperuricemia is related to metabolic syndrome, and is defined as an over-production or under-excretion of uric acid (UA), with increased UA serum concentration. Among other causes, Hyper-homocysteinemia (H-Hcy) can be responsible for hyperuricemia. The mechanisms underlying the association between these two conditions are unclear, but increased UA serum levels can be a consequence of renovascular atherosclerosis, with reduced UA excretion. An alternative hypothesis is the overproduction of UA from adenosine (originating from S-adenosyl-homocysteine). Genetic polymorphism (C677T) of methylenetetrahydrofolate reductase (MTHFR) may contribute. A possible mechanism is purines biosyinthesis originating from this gene variant. However, the results obtained from several studies and meta-analyses of the relationship between H-Hcy and hyperuricemia are ambivalent, and broader research is needed. (J Rheum Dis 2017;24:127-130)

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“…In addition to the unclear ACR and ACP guidelines of AH management, the literature contains conflicting reports regarding the usefulness of treating AH, both to reduce the risk of progression to gout and to prevent complications such as renal deposits of urate crystals 15-19. Cost-benefit analyses for both symptomatic treatments and ULT should be taken into consideration 14…”

mentioning

confidence: 99%

Knowledge and practice in the management of asymptomatic hyperuricemia among primary health care physicians in Jeddah, Western Region of Saudi Arabia

Alqarni

Hassan

2018

SMJ

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Objectives:To assess knowledge and practice levels in asymptomatic hyperuricemia (AH) and investigate predictors of urate-lowering therapy (ULT) misprescribing among primary health care (PHC) physicians.Methods:A cross-sectional study was conducted among 201 PHC physicians from December 2017 to May 2018. A based clinical guidelines for hyperuricemia management from American Professional Organizations, a semi-structured questionnaire was administered to collect demographic and professional data; knowledge and practice levels in management of AH; and barriers to the management of hyperuricemia and gout, with focus of the misprescribing of ULT in AH. A 2-stage stratified sampling technique was used to select 4 PHC centers were from each of the 5 advisory sectors in Jeddah, Kingdom of Saudi Arabia; and to recruit a minimum of 10 eligible participants per primary health care center (PHCC). Binary logistic regression was used to analyze predictors of ULT misuse in AH.Results:Only 32.8% participating physicians had adequate knowledge about AH. Regarding practice, while majority (88.1%) correctly recommended a low-purine diet and lifestyle changes to patients, almost half misprescribed ULT and 10.9% misprescribed non-steroid anti-inflammatory drugs. Lack of knowledge and awareness about guidelines were the most frequently self-reported barriers to adequate practice. Predictors of ULT misuse included the percentage of patients having gout (1-10%: OR=5.40, p=0.047) or receiving ULT (>10-20%: OR=20.02, p=0.001)among patients seen in clinic, attendance of rheumatology conferences (OR=2.55, p=0.017), and having a close relative with hyperuricemia or gout (OR=2.45, p=0.026).Conclusion:There are inadequate levels of knowledge regarding AH among Saudi PHC physicians increasing risk of malpractice including misprescription of ULT and anti-inflammatory medications.

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The management of hyperuricemia with urate deposition

Cited by 15 publications

References 39 publications

An evidence-based review on urate-lowering treatments: implications for optimal treatment of chronic hyperuricemia

An evidence-based review on urate-lowering treatments: implications for optimal treatment of chronic hyperuricemia

Hyper-homocysteinemia Inducing Hyperuricemia: What are the Mechanisms?

Knowledge and practice in the management of asymptomatic hyperuricemia among primary health care physicians in Jeddah, Western Region of Saudi Arabia

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