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Interpreting the Link Between Hyperuricemia and Cardiometabolic Disorders and Management

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Dr Alan Almeida, Mumbai    06 March 2021

  • Hyperuricemia is reported in 13 of 21 Global Burden of Diseases (GBD) regions. It is more prevalent in Asia.
  • The prevalence is higher in patients with comorbidities.
  • Risk factors – Uric acid is the end-product of purine metabolism. Purines can be endogenously produced or may be obtained exogenously from diet. Sedentary lifestyle and obesity are also risk factors for hyperuricemia.
  • About 90% of hyperuremic cases are due to decreased uric acid excretion. The etiology includes: Overproduction of uric acid; decreased uric acid excretion; genetic disorders and in-born errors of metabolism; genetic disorders.
  • More than two-thirds of patients with hyperuricemia remain asymptomatic. Symptoms are those of gout and nephrolithiasis.
  • Comorbidities associated with hyperuricemia include cardiovascular (CV) disorders, hypertension, metabolic disorders, diabetes, chronic kidney disease (CKD) and obesity.
  • Guidelines cut-off values of uric acid for hyperuricemia – Women: >6 mg/dL; Men: >7 mg/dL; Children and adolescents: >5.5 mg/dL.
  • Uric acid levels 7-9 mg/dL double the risk for incident kidney disease. Levels >9 mg/dL triple the risk of incident kidney disease.
  • PERL study – There was no evidence of clinically meaningful benefits of serum urate reduction with allopurinol in kidney outcomes in patients with type 1 diabetes and early to moderate diabetic kidney disease.
  • CKD-FIX study – Urate lowering treatment with allopurinol did not halt decline in eGFR in patients with high risk of progression of CKD.
  • Obesity is recognized as an associated risk factor with a variety of adverse health consequences including diabetes, hypertension and CV events. The positive correlation between elevated serum uric acid and obesity in adults has been examined by many studies.
  • Management of hyperuricemia– 
  • Detailed history: Investigate causes (alcohol consumption, obesity, drugs that increase urate levels)
  • Physical examination: Comorbidities like obesity, dyslipidemia and hypertension, and its aggressive treatment
  • Complete laboratory investigations: CBC, LFT, HbA1c, lipid profile, RFT, calcium, phosphate levels
  • Radiological investigation: Identify MSU deposits
  • Lifestyle modification
  • Pharmacotherapy.
  • Management simplified – Serum uric acid level 7-8 mg/dL: Lifestyle modification; 8-9 mg/dL + comorbidities: Lifestyle modification + pharmacotherapy; >9 mg/dL with or without comorbidities: Lifestyle modification + pharmacotherapy.
  • CARES study prompted FDA boxed warning on febuxostat.
  • CARES trial on febuxostat vs. allopurinol – In patients with gout and major CV coexisting conditions, febuxostat was non-inferior to allopurinol with respect to rates of adverse CV events. All-cause mortality and CV mortality were increased with febuxostat vs. allopurinol.
  • FAST trial on febuxostat vs. allopurinol – Febuxostat was noninferior to allopurinol with respect to the primary CV endpoint. Long-term febuxostat use was not associated with an increased risk of death or serious adverse events compared with allopurinol.
  • FAST study prompted to reconsider and modify the advice to avoid the use of febuxostat in patients with CV disease.

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