期刊連結：http://www.gouthyperuricemia.org
Purpose: Acute gouty arthritis has a very unique clinical presentation compared to other arthritides in that it has a very rapid onset and subsequent termination. The purpose of this review is to probe the mechanism of inflammatory initiation and termination in acute gouty arthritis.
Findings: Symptoms are initiated when resident macrophages of the joint ingest monosodium urate (MSU). This process triggers the activation of inflammasomes followed by the release of inflammatory cytokines. Cytokines recruit neutrophils that amplify the inflammatory process after ingestion of MSU. After MSU phagocytosis, neutrophils form neutrophil extracellular traps (NETosis) that not only induces neutrophil apoptosis but also traps and degrades cytokines. Finally, aggregated NETosis rapidly terminates the inflammatory process.
Conclusion: The hallmark of acute gouty arthritis is its rapid course initiated by macrophages after phagocytosis of MSU and terminated by infiltrating neutrophils after the formation of aggregated NETosis.