Gout is an inflammatory arthritis that is caused by the body's immune response to monosodium urate crystals in the joints. Uric acid is the product of purine metabolism and can settle out of solution. Several signs of gout include podagra and tophi. Gout should not be confused for pseudogout which is caused by calcium pyrophosphate. The difference between the two can be seen when observing the crystals. The negative birefringement urate crystals are needle-shaped.
The treatment of gout begins with treatment of symptoms. This includes NSAIDs, corticosteriods, colchicine, and ACTH. Colchicine inhibits inflammatory responses by inhibiting microtubule polymerization and inflammatory mediators.
Patients with gout who present with tophi, frequent attacks, and urolithiasis, may be started on ULT (urate lowering therapy). Allopurinol (hypersensitivity associated with HLA-B allele) is a competitive inhibitor of xanthine oxidase and febuxostat is a non-purine inhibitor of xanthine oxidase. Both will lower the production of uric acid. Uricosuric agents compete with uric acid at the transporters for reabsorption. These include probenecid (reduces excretion of penicillins) and lesinurad.
The transitioning treatment to ULT includes an anti-inflammmatory and a ULT drug.
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