Gout: Evaluation and Management

Uric acid is a byproduct of purine nucleotide metabolism, primarily synthesized in the liver and less frequently in other tissues. Hyperuricemia, characterized by elevated uric acid levels, can lead to gout and nephrolithiasis. It is also associated with conditions such as hypertension, metabolic syndrome, cardiovascular disease, and chronic kidney disease. Gout is an inflammatory disease marked by the deposition of monosodium urate (MSU) crystals in joints and tissues. It commonly affects the metatarsophalangeal joint, followed by other lower extremity joints, making it the most prevalent inflammatory arthritis. The pathophysiology of gout involves pro-inflammatory cytokines, lipid mediators, and the complement system, which contribute to the initiation and exacerbation of gout flares. Diagnosis relies on clinical evaluation, the identification of MSU crystals, and radiological imaging. Treatment encompasses acute gout flare management, prophylaxis, dietary modifications, and urate-lowering therapies. Common therapeutic agents include nonsteroidal anti-inflammatory drugs, colchicine, glucocorticoids, adrenocorticotropic hormone, and anti-IL-1β biological agents.