Why are gout flares typically self limited?
The following mechanisms have been postulated:
- • Inflammation allows for an influx of apolipoprotein-B into the joint, where it coats crystals and reduces their inflammatory potential.
- • Phagocytosis and clearance by neutrophils decreases the crystal burden; neutrophil extracellular traps (NETs) are formed, NET-related proteases digest inflammatory mediators, followed by apoptosis of inflammatory cells.
- • Heat generated from inflammation enhances urate solubility.
- • Adrenocorticotropic hormone (ACTH) secretion in response to pain/stress suppresses inflammatory responses.
- • Proinflammatory cytokines (IL-1 and TNF) are balanced by the production of cytokine inhibitors and regulatory cytokines such as transforming growth factor-β.
