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학습 자료 둘러보기 →An acute gout attack is a sterile inflammatory arthritis triggered by monosodium urate crystal deposition in the joint. The hallmark is a sudden, often nocturnal onset of excruciating monoarticular pain, peaking within 12–24 hours. The affected joint is typically erythematous, hot, and exquisitely tender—even the pressure of a bedsheet can be intolerable.
The inflammatory cascade is driven by crystal activation of the NLRP3 inflammasome, which releases IL-1beta. This cytokine mediates intense vasodilation, increased vascular permeability, and direct stimulation of pain fibers, producing the classic signs of inflammation. The first metatarsophalangeal joint (podagra) is the most common site, but ankles, knees, and wrists can also be affected.
Do not confuse an acute gout flare with a septic joint (bacterial arthritis), which is a medical emergency. Both can present with a hot, swollen, painful joint. If systemic signs like fever, chills, or leukocytosis are present, or the patient has risk factors for infection, arthrocentesis with synovial fluid analysis and culture is mandatory to rule out sepsis before initiating gout-specific therapy.
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