Lakhasly

Pathogenesis of acute gouty arthritis Deposition of UA crystals in the joint cavity is the triggering cause of gout.Interestingly, it is thought that may even end the inflammatory phase by engulfing the crystals and the inflammatory debrisThis involves the triggering of G protein, phospholipase A2, C and D, tyrosine kinase and other kinases such as mitogen-activated kinases (ERK1/ERK2, p38) and c-Jun N-terminal kinase.While less-differentiated monocytes produce abundant amounts of TNF, IL-1, IL-6 and IL-8 along with endothelial activation following phagocytosis of urate crystals.The pathogenesis of gouty arthritis involves initial activation of monocytes and mast cells followed by neutrophils.

Pathogenesis of acute gouty arthritis
Deposition of UA crystals in the joint cavity is the triggering cause of gout. These crystals initiate the inflammatory process by being engulfed by synovial phagocytic cells leading to release of lysosomal enzymes and production of inflammatory chemokines. Another mechanism is that UA crystals change the stability of cell membrane of phagocytic cells by direct crosslinkage with membrane lipids and glycoproteins. This involves the triggering of G protein, phospholipase A2, C and D, tyrosine kinase and other kinases such as mitogen-activated kinases (ERK1/ERK2, p38) and c-Jun N-terminal kinase. This interaction leads to increased IL-8 in phagocytes resulting in activation of neutrophils [25], [26].

The pathogenesis of gouty arthritis involves initial activation of monocytes and mast cells followed by neutrophils. Before the first attack of gout and in the inter-critical period, macrophages engulf UA crystals. Well-differentiated macrophages have the capability to contain these crystals without inducing an inflammatory response. While less-differentiated monocytes produce abundant amounts of TNF, IL-1, IL-6 and IL-8 along with endothelial activation following phagocytosis of urate crystals. Also, mast cells are key players in inducing the acute gouty attack by producing histamine and IL-1. This results in increasing vascular permeability and vasodilatation. Interestingly, it is thought that may even end the inflammatory phase by engulfing the crystals and the inflammatory debris