The NSAIDs largely have supplanted colchicine as the treatment of choice, and many NSAIDs have been used successfully. These agents are most effective when given within the first 24 hours of the onset of pain. Most studies have shown similar results among agents, and all NSAIDs are considered to be effective. Doses at the higher end of the therapeutic range are often needed.13
Indomethacin was used traditionally, but its relative cyclooxygenase-1 (COX-1) selectivity theoretically increases its gastropathy risk. Thus other generic NSAIDs may be preferred. Adverse effects of NSAIDs include gastropathy (primarily peptic ulcers), renal dysfunction, and fluid retention.14 NSAIDs generally should be avoided in patients at risk for peptic ulcers, those taking warfarin, and those with renal insufficiency or uncontrolled hypertension or heart failure.
Cyclooxygenase-2 (COX-2)-selective inhibitors produce results comparable with those of traditional NSAIDs. However, cardiovascular safety concerns and the high cost of COX-2 inhibitors argue against their use for this disorder. NSAIDs are usually continued until 24 hours after symptoms subside.
First-line treatment NSAID second-line treatment colchicine
Consider IA injection of corticosterods for monoarticular attack (see Table 59-1 lor agents/doses)
FIGURE 59-2. Treatment algorithm for gout and hyperuricemia. Renal insufficiency is defined as an estimated creatinine clearance (CrCl) of less than 30 mL/min. (IA, intra-articular; NSAID, nonsteroidal anti-inflammatory drug.)
Colchicine has a long history of successful use and was the treatment of choice for many years. It is used infrequently today because of its low therapeutic index. Col-chicine is thought to exert its anti-inflammatory effects by interfering with the function of mitotic spindles in neutrophils by binding of tubulin dimers; this inhibits phagocytic activity. 5
Oral colchicine is absorbed rapidly from the GI tract and metabolized extensively in the liver. About two-thirds of patients with acute gout respond favorably if it is given within the first 24 hours of symptom onset. Unfortunately, more than 80% of patients experience adverse effects. GI effects (e.g., nausea, vomiting, diarrhea, and abdominal pain) are most common and are considered a forerunner of more serious systemic toxicity, including myopathy and bone marrow suppression (usually neut-ropenia). Some clinicians still use the strategy of continuous dosing until either pain relief or GI side effects occur. However, systemic toxicity can occur with oral col-
chicine without prior GI effects, especially in patients with renal insufficiency.16,17 Because of these problems, oral colchicine should be reserved for patients who are at risk for NSAID-induced gastropathy or who have failed NSAID therapy. IV colchicine was removed from the U.S. market due to an increased risk of serious and
potentially fatal systemic effects when administered by this route. Table 59-1 Dosage Regimens for Acute Gout and Antihyperuricemic Treatment
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