Acute gout steroids

Acute gout attacks can be managed with nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, or corticosteroids (intra-articular injection or systemic). All three agents are appropriate first-line therapy for acute gout. Therapy should be initiated within 24 hours of onset. The drug selection is dictated by the patient's tolerance of those medications and the presence of any comorbid diseases that contraindicates the use of a specific drug. For patients with severe or refractory gout attacks, practitioners can try combining agents. If all of these medications are contraindicated in a patient, narcotics may be used short term to relieve pain until the acute attack has resolved. Long-term use of narcotics should be avoided.

Nonsteroidal antiinflammatory drugs are frequently used as initial therapy in acute gout. In select cases, however, colchicine has been recommended as an alternative therapy. A review of the literature raises significant concerns regarding the cost to benefit ratio of using colchicine in this setting. A survey of alternative forms of therapies showed few studies investigating the efficacy and side effects of a short course of oral steroids, and little support for this modality in standard textbooks. Our preliminary study suggests that a short course of oral corticosteroid therapy can be used effectively for acute gout when NSAIDs are contraindicated. The use of prednisone 30 to 50 mg or its equivalent initially, and gradually tapered over 10 days, results in clinical resolution without rebound arthropathy or steroid complications in most patients. As a result, we rarely use colchicine in the management of acute gout in our practice.

Hyperuricemia is a classic feature of gout, but nearly half of the time gout occurs without hyperuricemia and most people with raised uric acid levels never develop gout. [8] [37] Thus, the diagnostic utility of measuring uric acid levels is limited. [8] Hyperuricemia is defined as a plasma urate level greater than 420 μmol/l ( mg/dl) in males and 360 μmol/l ( mg/dl) in females. [38] Other blood tests commonly performed are white blood cell count , electrolytes , kidney function and erythrocyte sedimentation rate (ESR). However, both the white blood cells and ESR may be elevated due to gout in the absence of infection. [39] [40] A white blood cell count as high as ×10 9 /l (40,000/mm 3 ) has been documented. [11]

In addition, medications are available that may help prevent ulcers in people who need to take NSAIDs. Proton-pump inhibitors (PPIs) are the first drug of choice for preventing ulcers in high-risk individuals. They have been shown to reduce NSAID-ulcer rates by as much as 80% compared with no treatment. Types of these drugs include omeprazole (Prilosec), esomeprazole (Nexium), lansoprazole (Prevacid), rabeprazole (AcipHex ), and pantoprazole (Protonix). Prevacid is the first proton-pump inhibitor specifically approved for protecting against ulcers in chronic NSAID users.

Acute gout steroids

acute gout steroids

In addition, medications are available that may help prevent ulcers in people who need to take NSAIDs. Proton-pump inhibitors (PPIs) are the first drug of choice for preventing ulcers in high-risk individuals. They have been shown to reduce NSAID-ulcer rates by as much as 80% compared with no treatment. Types of these drugs include omeprazole (Prilosec), esomeprazole (Nexium), lansoprazole (Prevacid), rabeprazole (AcipHex ), and pantoprazole (Protonix). Prevacid is the first proton-pump inhibitor specifically approved for protecting against ulcers in chronic NSAID users.

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