In addition, gout is indicated by excessively high levels of uric acid, which is referred to as hyperuricemia in an individual. The primary cause of hyperuricemia is underexcretion of the kidneys (Buttaro, Trybulski, Bailey, & Sandberg-Cook, 2013). Although not the sole indicator, hyperuricemia is a good indication of gout disease. However, not all individuals who have hyperuricemia will develop gout. In order to diagnose gout disease, the urate levels in the serum must be 7 mg/dL for men and 6 mg/dL for women, which are subsequently used as an indicator of gout disease or a risk factor for developing gout disease in the patient (De Miguel et al., 2012).
Actual gout disease is not diagnosed until the uric acid levels accumulate in sufficient …show more content…
Monosodium urate (MSU) crystals stimulate cells called toll-like receptors 2 and 4 (TLR2, TLR4), formation of C5 and complement membrane attack complex (C5b-9), cytokines, chemokines and other inflammatory mediators causing an influx of neutrophils to that particular joint (Doherty, 2009). The TLR2, TLR4, and the TLR adaptor protein MyD88 stimulate phagocytosis of the MSU crystals. When the TLR2 and TLR4 recognize the MSU crystals, MYD88, Rac1, and AKt signaling transducer activates the transcription factor nuclear factor-KB and multiple other pro-inflammatory mediators (Doherty, 2009; Moi, Sriranganathan, Edward, & Buchbinder, 2013). The mediators contain neutrophilic cytosolic proteins, such as prostanoids and leukotrienes, which are chemotactic and magnify the inflammatory response. When the MSU crystals are being phagocytized, it triggers the assembly of the cytosolic NACHT-LRR-PYD-containing protein (NALP)3 (cryopyrin) inflammasome protein complex in the intracellular (Doherty, 2009; Moi, Sriranganathan, Edward, & Buchbinder, 2013) . In addition, the caspase-1 activation is activated which causes the Il-1B to mature and release into the phagocytes which cause the MSU crystal-induced NALP3 inflammasome protein complex assembly to be suppressed high concentrations microtubule inhibitor colchicine. This indicates that a high concentration of
Actual gout disease is not diagnosed until the uric acid levels accumulate in sufficient …show more content…
Monosodium urate (MSU) crystals stimulate cells called toll-like receptors 2 and 4 (TLR2, TLR4), formation of C5 and complement membrane attack complex (C5b-9), cytokines, chemokines and other inflammatory mediators causing an influx of neutrophils to that particular joint (Doherty, 2009). The TLR2, TLR4, and the TLR adaptor protein MyD88 stimulate phagocytosis of the MSU crystals. When the TLR2 and TLR4 recognize the MSU crystals, MYD88, Rac1, and AKt signaling transducer activates the transcription factor nuclear factor-KB and multiple other pro-inflammatory mediators (Doherty, 2009; Moi, Sriranganathan, Edward, & Buchbinder, 2013). The mediators contain neutrophilic cytosolic proteins, such as prostanoids and leukotrienes, which are chemotactic and magnify the inflammatory response. When the MSU crystals are being phagocytized, it triggers the assembly of the cytosolic NACHT-LRR-PYD-containing protein (NALP)3 (cryopyrin) inflammasome protein complex in the intracellular (Doherty, 2009; Moi, Sriranganathan, Edward, & Buchbinder, 2013) . In addition, the caspase-1 activation is activated which causes the Il-1B to mature and release into the phagocytes which cause the MSU crystal-induced NALP3 inflammasome protein complex assembly to be suppressed high concentrations microtubule inhibitor colchicine. This indicates that a high concentration of