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[Gout, beyond the joint: How should we treat it?]
M A Pou1, D Martinez-Laguna2, C Diaz-Torne3
1EAP Encants, Institut Català de la Salut, Barcelona, España; Grupo de Investigación en Enfermedades del Aparato Locomotor en Atención Primaria (GREMPAL).
Gout management is poor despite advances, with genetics and kidney function being key factors. Effective treatment involves lowering uric acid levels to below 6mg/dl to dissolve crystals and cure the disease.
Area of Science:
- Rheumatology
- Nephrology
- Cardiology
Background:
- Gout, caused by monosodium urate crystal deposition, is often poorly managed due to its presentation and misconceptions.
- Despite increased knowledge, less than 30% of gout patients receive adequate treatment.
- Prevalence in Spain is 2.5% and rising, underscoring a significant public health issue.
Purpose of the Study:
- To review the pathogenesis of gout and hyperuricemia.
- To emphasize the roles of genetics and renal function over diet.
- To discuss gout's systemic consequences, including cardiovascular risk.
Main Methods:
- Review of current literature on gout pathogenesis, crystal deposition, and treatment strategies.
- Analysis of factors influencing hyperuricemia, including genetic and renal aspects.
- Examination of therapeutic approaches, focusing on hypouricemic agents.
Main Results:
- Genetics and renal function significantly influence hyperuricemia more than diet.
- Gout is an independent cardiovascular risk factor beyond joint and renal manifestations.
- Sustained uricemia below 6mg/dl is crucial for dissolving crystals and achieving disease remission.
Conclusions:
- Hypouricemic therapy is the cornerstone for gout treatment, aiming for crystal dissolution and cure.
- Comprehensive management includes addressing cardiovascular risks, preventive measures, flare treatment, and patient education.
- Optimizing patient adherence to lifestyle modifications and pharmacotherapy is essential for long-term gout control.
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