Treatment of pain and inflammation can be achieved with NSAIDs, colchicine, or corticosteroids (systemic or intra-articular). The choice of which treatment is the right one for a particular patient should be made on the basis of the patient’s co-morbid medical conditions, other medications, and side effect profile.
NSAIDS: Commonly used NSAIDs during an acute gout attack include ibuprofen 800 mg three to four times daily or indomethacin 25 to 50 mg four times daily. Treatment should be discontinued when symptoms resolve.
Colchicine: Intravenous colchicine is associated with serious toxicities and side effects, so it should be used as an oral formulation only. High dose oral colchicine (1.2 mg followed by 0.6 mg every hour for 6 doses) is generally poorly tolerated because of GI side effects. Lower doses are much better received and may be used in combination with NSAIDs.
Corticosteroids: In patients with contraindications to NSAID use, corticosteroids are the next choice. Corticosteroids can be administered as an injection into the effected joint (intra-articular steroids) or given systemically (orally, such as prednisone or medrol). Intra-articular steriods are useful if only one or two joints are affected and the treating physician is proficient in injecting those joints. Oral corticosteroids can be used starting at 30-40 mg daily tapering over 10-14 days.
Patients who have multiple episodes of acute gout attacks per year or who have tophi on exam are candidates for uric acid lowering therapy. Use of uric acid lowering agents will reduce the frequency of gout attacks and over time, reduce tophi formation, and diminish the risk of joint destruction. The following are indications for uric acid lowering therapy:
tophi or chronic arthritis on exam
failure of colchicine prophylaxis of acute gouty arthritis
Prior to chemotherapy as prophylaxis of tumor lysis syndrome
Extremely high levels of serum uric acid (>12 mg/dl)
Uric acid is the end product of purine (nucleic acid component of DNA) metabolism and is produced normally by the body during tissue remodeling and breakdown. About 20% of uric acid is derived from purines ingested in food. Causes of hyperuricemia can be divided into two major categories: decreased clearance of uric acid from the kidney and increased synthesis of uric acid.