Recognizing And Treating Lower Extremity Gout

Author(s): 
Nicholas Romansky, DPM, FACFAS

Key Pearls On Intercritical And Chronic Gout Therapy

For the purpose of comprehensiveness, one can conceivably use IL-1 antagonist/inhibitors. These include anakinra, canakinumab and rilonacept.16-18 For intercritical and chronic gout, it is critical to prevent further crystal accumulation and recurrent gouty flare-up episodes.

   Therapy should begin immediately after the acute attack. Many suggest giving patients the option of initiating the next course of therapy because if they do not, they may risk another episode of an acute flare-up. As mentioned previously, one should redo lab work two to four weeks after the acute episode.

   It is generally accepted that in patients with tophi or with two or more attacks in one year, one should initiate therapy for chronic gout. The key in the urate lowering therapy is the reduction and maintenance of a serum uric acid level of less than 6.0 mg/dL. At this level, there is a decreased number of flares, less uric crystal accumulation in joints and dissolved tophi.

   Two classes of drugs for long-term therapy/maintenance of the reduction of serum uric acid include xanthine oxidase inhibitors and uricosurics. Allopurinol (Zyloprim) is a xanthine oxidase inhibitor and is most commonly used to reduce hyperuricemia regardless of its etiology. The dosing of allopurinol is individually based. Typically, the initial dose of allopurinol is 100 mg but again, depending on the severity, 100 mg 1 to 3 tabs p.o. can be a starting dose. Hypersensitivity syndrome and refractoriness to the drug (2 percent of patients on allopurinol have hypersensitivity syndrome or refractoriness) could create an erythematous rash, hepatitis, eosinophilia, fever, declining renal function or even fatality.19

   Febuxostat (Uloric, Takeda) has been approved as a non-purine selective inhibitor of both oxidized and reduced forms of xanthine oxidase.20,21 Febuxostat has not been recommended for the treatment of asymptomatic hyperuricemia. Liver enzymes may elevate the use of this drug. Clinical trials have shown a higher rate of cardiovascular thromboembolic events with febuxostat in comparison to patients tested with allopurinol. Low-dose NSAIDs and colchicines can be used as prophylaxis with the concomitant use of a urate lowering agent until the serum uric acid level is stable at less than 6.0 mg/dL.21

   Seven clinical trials showed that febuxostat 40 mg/dL was inferior to allopurinol 300 mg/dL in lowering the serum level to less than 6.0 mg/dL.21 The febuxostat dosage of 80 mg/dL was superior when researchers tested it against allopurinol. Although febuxostat 40 mg/dL and 80 mg/dL were well tolerated, liver enzyme elevations, nausea, arthralgias and rash may occur. Multiple studies show that febuxostat 80 mg/dL has more effectively lowered and maintained serum uric acid levels to a level less than 6.0 mg/dL, typically within two to four weeks, in comparison to allopurinol 300 mg/dL.20

   If patients do not tolerate xanthine oxidase inhibitors, then probenecid can be the first drug of choice. Concurrent use of aspirin will block the effect of probenecid. The use of probenecid can block the excretion of penicillin, increase the serum concentration of generic furosemide and may extend heparin metabolism.

   Once the patient has become asymptomatic and the intercritical phase has begun, the use of chronic therapy and follow-up visits are important especially in the very beginning following the acute phase. Until a second acute episode occurs, many patients do not want to modify their lifestyle even after receiving education about the joint destruction effects of gout. The effects of gout are even more critically important because of the greater occurrence of metabolic syndrome, cardiovascular disease, obesity and stress in America.

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