Gout Pathophysiology
People frequently conflate pseudogout and gout. Pseudogout symptoms are very similar to those of gout, but pseudogout attacks are typically less severe. The significant distinction between pseudogout and gout is that calcium pyrophosphate crystals, not uric acid crystals, may irritate the joints in pseudogout. Pseudogout requires a distinct treatment than gout. In addition, pseudogout is caused by the formation of calcium pyrophosphate crystals in the joint synovial fluids.
Under-excretion of urate by the gut or extra-renal organs also contributes to the development of gout or hyperuricemia. Symptomatic gout and crystal deposition are the next criterion for the formation of MSU crystals in certain individuals. MSU crystals elicit a transient inflammatory response that is sterile and self-limiting, mediated by the innate activation of the immune system. Interleukin 1 beta is the main cytokine responsible for the acute inflammatory response, which is triggered by MSU crystals. In some patients, the progression of gout is accompanied by structural joint injury. In gout, structural joint damage is caused by the direct effect of MSU crystals on joint tissues and the indirect impact of joint inflammation. In addition to their central function in the pathogenesis of gout, MSU crystals play a physiological role in immune surveillance, specifically as a danger signal or adjuvant.
Several interdependent milestones are involved in the pathophysiology of gout. A high uric acid level is an essential risk factor for the development of gout and a necessary condition for the formation of monosodium urate (MSU) crystals. In the majority of individuals, hyperuricemia is caused by inadequate urate excretion via intestinal and renal mechanisms. Numerous metabolic, genetic, and environmental factors are associated with serum urate and alter the synthesis or transport of urate in one way or another. Urate supersaturation is the most important factor in MSY crystal formation. Other factors, such as components of connective tissue, temperature, and pH, also play a significant role in crystal formation.
Changes in the regulatory processes of the inflammatory response to MSU crystal formation may influence an individual’s susceptibility to develop gout. Leucine-rich nucleotide increases pyrin protein 3 inflammasome binding oligomerization. The formation of tophus is the defining characteristic of the progression of gout, and both the inflammatory tissue component and MSU crystals of tophus contribute to the development of joint injury that leads to gout. Interleukin 1 beta is an essential cytokine that, along with other immune system components, serves a significant role in the inflammatory response to crystal formation. Extreme levels of structural joint injury result in the appearance and onset of symptoms that have a significant impact on a gout patient’s quality of life.
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