Gout is the most common inflammatory type of arthritis affecting adults. The clinical syndrome of gout arises from deposition of urate crystals in joints,where they cause an inflammatory response, and in soft tissues where they do not. Crystal deposition occurs when serum becomes saturated with urate,the final breakdown product of purine metabolism.It is characterized by chronic hyperuricemia which is defined as serum urate levels above 6.8mg/dl,the level above which the physiological saturation threshold is exceeded.Typically gout produces an acute monoarthritis of rapid onset,often waking patients from sleep. Gout manifests itself as microscopic or macroscopic soft tissue deposit of monosodium monohydrate crystal which triggers severe,but …show more content…
All the above agents are non-selective inhibitors for the neutrophil driven inflammation that occurs in acute gout. 1. Colchicine - Colchicine has been found to be efficacious when compared to placebo in randomised controlled trial. It has also been very clearly confirmed that high and low dose of colchicine has similar effectiveness, but low dose of colchicine carries a better safety profile as compared to the high dose. Accordingly, high dose of colchicine should be avoided which carries significant gastrointestinal side effects. The usual dose should be 2-4 tablets a day, which has similar efficacy, but with much less risk of side effect. Intravenous colchicine is associated with potential fatal adverse event and should be avoided. Also, there is a drug interaction between CYP3A4E-glycoprotein inhibitors and colchicine in particular in the presence of hepatic and renal dysfunction which should be taken into consideration on using colchicine. In mild to moderate renal impairment with GFR >30 ml/min colchicine can be used in reduced