Asymptomatic hyperuricemia: is it time to intervene?

Abstract

Whether to treat hyperuricemia uncomplicated by articular gout, urolithiasis, or uric acid nephropathy is an exercise in clinical judgment and universal agreement is lacking. Patients with coronary artery disease, chronic kidney disease, and early onset hypertension with persistent hyperuricemia are likely to be benefited with urate-lowering therapy. The paradigm of the causative association of hyperuricemia with cardiovascular and chronic kidney diseases seems to have progressed from skepticism to increasing evidence of a true relationship. Although such evidences are mounting, they are not enough to support pharmacotherapy for all patients with asymptomatic hyperuricemia. Further studies are needed to determine which patients are likely to get beneficial effects from pharmacotherapy and the minimum threshold of uric acid level required to experience clinical benefits.

Risk of Acute Myocardial Infarction Among New Users of Allopurinol According to Serum Urate Level: A Nested Case-Control Study

“…The reduced risk of AMI with allopurinol use was particularly observed in patients with gout, but it is noteworthy that we also observed a protective effect in patients with asymptomatic hyperuricemia provided that treatment was prolonged and SUA levels maintained below 7 mg/dL. Whether the protective effect observed in these patients should change the general recommendation of not using allopurinol in them [6][7][8][9], is a question beyond the scope of the present research and should be addressed in specific studies considering the risks of allopurinol, in particular severe cutaneous reactions [35][36][37][38].…”

“…Allopurinol, a xanthine oxidase inhibitor (XOI), is the first-line ULT for patients with gout to prevent acute flares [6,7]. Often, it is also used to treat asymptomatic hyperuricemia, though this practice is generally not supported [8,9]. In the last few years, many studies have provided evidence on the cardiovascular benefits of allopurinol [5,10].…”

Genome‐Wide Association and Functional Studies Reveal Novel Pharmacological Mechanisms for Allopurinol

“…These attacks are typically caused by chronically high concentrations of serum uric acid (SUA), or hyperuricemia, and are characterized by the extreme pain and discomfort they cause for patients . The painful and debilitating attacks associated with this disease as well as the underlying hyperuricemia have been shown to be risk factors for various diseases, including coronary heart disease, stroke, and especially chronic kidney disease, which represents the greatest comorbidity risk for gout patients . Thus, management of gout and hyperuricemia has become increasingly important in the prevention of life‐threatening cardiac and renal diseases.…”

“…have been shown to be risk factors for various diseases, including coronary heart disease, stroke, and especially chronic kidney disease, which represents the greatest comorbidity risk for gout patients. [2][3][4][5][6] Thus, management of gout and hyperuricemia has become increasingly important in the prevention of life-threatening cardiac and renal diseases.…”

Tratamento da hiperuricemia assintomática: revisão baseada na evidência

“…Ainda que evidência convincente do papel do AU apenas exista para a gota e nefrolitíase, 7 associações a condições não articulares têm vindo a ser demonstradas há já vários anos, como é o caso da doença renal crónica, da hipertensão, da doença cardiovascular e da resistência insulínica. 8 Num estudo, Obermayr e colaboradores seguiram 21.475 voluntários saudáveis ao longo de sete anos e confirmaram, após ajuste para múltiplos fatores de risco confundidores, uma duplicação de risco de incidência de doença renal na presença de concentrações séricas de AU entre 7-8,9mg/dL. 9 Jalal e colaboradores, numa revisão de 2013, avaliaram 24 estudos e os resultados obtidos demonstraram a hiperuricemia com fator de risco independente para a progressão de doença renal crónica.…”