Gout flares occur when urate crystals trigger an acute inflammatory response4,12
Flares are intense signals of gouty arthritis3
Gout flare severity can be variable, with mild flares subsiding in several hours to a few days and severe flares lasting many days to several weeks.5 Over time, gout may lead to repeated flares.
Stages of gouty arthritis3
Adapted from Klippel 2008. Edwards NL. Gout. A. Clinical features. In: Klippel JH, Stone JH, Crofford LJ, White PH, eds. Primer on the Rheumatic Diseases. 13th ed. New York: Springer; 2008:241-249.9
Gout is a crystal-induced arthritis caused by hyperuricemia3,34
- Acute gout flares occur when urate crystals, which form above the solubility threshold of uric acid, activate an acute inflammatory response4,10,12
- Factors such as increases or decreases in uric acid levels, dietary indiscretions, and joint trauma may disrupt the stable microenvironment of crystal deposits and provoke a flare3
Review details on inflammation and flares »
- Hyperuricemia promotes deposition and accumulation of monosodium urate crystals in the joints and soft tissue10
- In gout patients, crystal deposition and low-grade inflammation can continue during intercritical periods, with or without acute inflammatory responses4,6-8,10,11
Find out more about gout and hyperuricemia »
COLCRYS (colchicine, USP) does not treat hyperuricemia. ULORIC (febuxostat) and COLCRYS have not been shown to prevent chronic joint destruction and tissue deformities, and effects on tophi have not been established.
Help manage gouty arthritis with a joint approach
Maintaining uric acid levels <6 mg/dL is the key to managing gout. Preventing and reducing the frequency of gout flares while taking medicines that lower uric acid levels provides patients with a joint approach.
Read more about managing gout »
Important Safety Information for COLCRYS (colchicine, USP)
- COLCRYS is contraindicated in patients with renal or hepatic impairment who are currently prescribed P-gp inhibitors or strong inhibitors of CYP3A4. In these patients, life-threatening and fatal colchicine toxicity has been reported with colchicine taken in therapeutic doses. Dose adjustments of COLCRYS may be required when co-administered with P-gp or CYP3A4 inhibitors in patients with normal renal and hepatic function.
- Fatal overdoses, both accidental and intentional, have been reported in adults and children who have ingested colchicine. Keep COLCRYS out of the reach of children.
- Blood dyscrasias such as myelosuppression, leukopenia, granulocytopenia, thrombocytopenia, pancytopenia, and aplastic anemia have been reported in patients taking colchicine at therapeutic doses.
- Colchicine-induced neuromuscular toxicity and rhabdomyolysis have been reported with chronic treatment in therapeutic doses, especially when colchicine is prescribed in combination with other drugs known to cause this effect. Patients with renal dysfunction and elderly patients, even those with normal renal and hepatic function, are at increased risk.
- Monitor for toxicity and if present consider temporary interruption or discontinuation of colchicine.
- The most common adverse reactions in clinical trials were diarrhea (23%) and pharyngolaryngeal pain (3%).
Please click here for complete Prescribing Information and Medication Guide for COLCRYS (colchicine, USP) »
COLCRYS (colchicine, USP) 0.6 mg tablets are indicated in adults for the prophylaxis of gout flares and treatment of acute gout flares when taken at the first sign of a flare.
COLCRYS is not an analgesic medication and should not be used to treat pain from other causes.
Important Safety Information for ULORIC (febuxostat)
- ULORIC is contraindicated in patients being treated with azathioprine or mercaptopurine.
- An increase in gout flares is frequently observed during initiation of anti-hyperuricemic agents, including ULORIC. If a gout flare occurs during treatment, ULORIC need not be discontinued. Prophylactic therapy (i.e. – NSAIDs or colchicine) upon initiation of treatment may be beneficial for up to six months.
- Cardiovascular Events: In randomized controlled studies, there was a higher rate of cardiovascular thromboembolic events (cardiovascular deaths, non-fatal myocardial infarctions, and non-fatal strokes) in patients treated with ULORIC [0.74 per 100 P-Y (95% CI 0.36-1.37)] than allopurinol [0.60 per 100 P-Y (95% CI 0.16-1.53)]. A causal relationship with ULORIC has not been established. Monitor for signs and symptoms of MI and stroke.
- Hepatic Effects: Postmarketing reports of hepatic failure, sometimes fatal, have been received. Causality cannot be excluded. During randomized controlled studies, transaminase elevations greater than three times the upper limit of normal (ULN) were observed (AST: 2%, 2%, and ALT: 3%, 2% in ULORIC and allopurinol-treated patients, respectively). No dose-effect relationship for these transaminase elevations was noted.
Obtain liver tests before starting treatment with ULORIC. Use caution in patients with liver disease. If liver injury is detected, promptly interrupt ULORIC and assess patient for probable cause, then treat cause if possible, to resolution or stabilization. Do not restart treatment if liver injury is confirmed and no alternate etiology can be found.
- Adverse reactions occurring in at least 1% of ULORIC-treated patients, and, at least 0.5% greater than placebo, are liver function abnormalities, nausea, arthralgia, and rash.
Please click here for complete Prescribing Information for ULORIC (febuxostat) »
ULORIC is a xanthine oxidase (XO) inhibitor indicated for the chronic management of hyperuricemia in patients with gout. ULORIC is not recommended for the treatment of asymptomatic hyperuricemia.
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- Edwards NL. Clinical gout. In: Hochberg MC, Silman AJ, Smolen JS, Weinblatt ME, Weisman MH, eds. Rheumatology. 6th ed. Philadelphia, PA: Mosby Elsevier; 2014:1569-1574.
- Wortmann RL. Gout and hyperuricemia. In: Firestein GS, Budd RC, Harris ED Jr, McInnes IB, Ruddy S, Sergent JS, eds. Kelley’s Textbook of Rheumatology. Vol 2. 8th ed. Philadelphia, PA: Saunders Elsevier; 2009:1481-1506.
- Becker MA, Jolly M. Clinical gout and the pathogenesis of hyperuricemia. In: Koopman WJ, Moreland LW, eds. Arthritis and Allied Conditions: A Textbook of Rheumatology. Vol 2. 15th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005:2303-2339.
- McCarthy GM, Barthelemy CR, Veum JA, Wortmann RL. Influence of antihyperuricemic therapy on the clinical and radiographic progression of gout. Arthritis Rheum. 1991;34:1489-1494.
- Pascual E, Batlle-Gualda E, Martínez A, Rosas J, Vela P. Synovial fluid analysis for diagnosis of intercritical gout. Ann Intern Med. 1999;131:756-759.
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- Schumacher HR Jr. The pathogenesis of gout. Cleve Clin J Med. 2008;75(suppl 5):S2-S4.
- Pascual E. Persistence of monosodium urate crystals and low-grade inflammation in the synovial fluid of patients with untreated gout. Arthritis Rheum. 1991;34:141-145.
- McLean L, Becker MA. Etiology and pathogenesis of gout. In: Hochberg MC, Silman AJ, Smolen JS, Weinblatt ME, Weisman MH, eds. Rheumatology. 5th ed. Philadelphia, PA: Mosby Elsevier; 2011:1841-1857.
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- Busso N, So A. Mechanisms of inflammation in gout. Arthritis Res Ther. 2010;12:206.
- Rose DM, Liu-Bryan R. Innate immunity in triggering and resolution of acute gouty inflammation. Curr Rheumatol Rep. 2006;8:209-214.
- Liu-Bryan R, Scott P, Sydlaske A, Rose DM, Terkeltaub R. Innate immunity conferred by Toll-like receptors 2 and 4 and myeloid differentiation factor 88 expression is pivotal to monosodium urate monohydrate crystal-induced inflammation. Arthritis Rheum. 2005;52:2936-2946.
- Cronstein BN, Terkeltaub R. The inflammatory process of gout and its treatment. Arthritis Res Ther. 2006;8(suppl 1):S3.
- Phelps P. Polymorphonuclear leukocyte motility in vitro. IV. Colchicine inhibition of chemotactic activity formation after phagocytosis of urate crystals. Arthritis Rheum. 1970;13:1-9.
- Pope RM, Tschopp J. The role of interleukin-1 and the inflammasome in gout: implications for therapy. Arthritis Rheum. 2007;56:3183-3188.
- COLCRYS (colchicine, USP) Prescribing Information and Medication Guide. Takeda Pharmaceuticals.
- Terkeltaub RA, Furst DE, Bennett K, Kook KA, Crockett RS, Davis MW. High versus low dosing of oral colchicine for early acute gout flare: twenty-four-hour outcome of the first multicenter, randomized, double-blind, placebo-controlled, parallel-group, dose-comparison colchicine study. Arthritis Rheum. 2010;62:1060-1068.
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- Dore RK. The gout diagnosis. Cleve Clin J Med. 2008;75(suppl 5):S17-S21.
- ULORIC (febuxostat) Prescribing Information. Takeda Pharmaceuticals.
- Allopurinol full prescribing information, October 2009.
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- Loeb JN. The influence of temperature on the solubility of monosodium urate. Arthritis Rheum. 1972;15:189-192.
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- Data on file, Takeda Pharmaceuticals U.S.A., Inc.
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- Schumacher HR, Becker MA, Wortmann RL, et al. Effects of febuxostat versus allopurinol and placebo in reducing serum urate in subjects with hyperuricemia and gout: a 28-week, phase III, randomized, double-blind, parallel-group trial. Arthritis Rheum. 2008;59:1540-1548.
- Becker MA, Schumacher HR, Wortmann RL, et al. Febuxostat compared with allopurinol in patients with hyperuricemia and gout. N Engl J Med. 2005;353:2450-2461.
- Becker MA, Schumacher HR, Espinoza LR, et al. The urate-lowering efficacy and safety of febuxostat in the treatment of the hyperuricemia of gout: the CONFIRMS trial. Arthritis Res. 2010;12:R63.