What lies ahead?
Clearly, much can still be accomplished toward improving the long-term management of hyperuricemia with currently available forms of ULT. Adherence to treatment and greater educational efforts directed at both patients and clinicians would go a long way toward preventing the morbidity associated with gout. But even under the very best of conditions, an estimated 100,000-300,000 of the nearly 5 million U.S. patients with gout would not be adequately managed by current therapies.15 These patients are the target population for new and innovative ways to lower serum uric acid.
While the majority of gout patients do not achieve adequate control of their hyperuricemia or symptoms, they are not truly treatment failures. These patients are generally victims of inadequate prescribing, poor compliance, or both. The term “treatment-failure gout” should be reserved for those symptomatic patients with contraindications to the currently available urate-lowering medications or when the maximum medically appropriate dose of those agents does not control hyperuricemia.
Continue Reading
Two new urate-lowering medications are very close to gaining FDA approval (the first ones since the release of allopurinol more than 40 years ago). Pegloticase offers the promise of urate lowering through a mechanism totally different from the excretion-enhancing probenecid or the synthesis-blocking medications allopurinol and the soon-to-be-released febuxostat.
Finally, enhanced educational efforts directed at clinicians ought to emphasize:
1. Prompt and aggressive treatment of acute gout
2. An accepted target for urate lowering (serum uric acid level <6.0 mg/dL) to prevent gout and perhaps a lower goal in certain comorbidities
3. Recognition that allopurinol dosing >300 mg/day is often required to achieve this goal. The widely published guidelines restricting the maximum dose of allopurinol in patients with chronic kidney disease is not warranted and will not be sufficient in many cases.
4. The involvement of patients in lifestyle changes (e.g., dietary restriction of purine-rich food and drink, limiting fructose intake, and the control of metabolic syndrome) is essential to stem this epidemic. The Gout & Uric Acid Education Society has a reliable and noncommercial Web site created by experts in the field to educate patients and professionals about gout and hyperuricemia (www.gouteducation.org).
As these tenets become better recognized by providers and the general public and as new therapies are developed, gout treatment may finally emerge from the dark ages.
Ms. McTigue is a physician assistant in the Division of Rheumatology at the University of Florida College of Medicine and the Veterans Affairs Medical Center in Gainesville.
References
1. Lawrence RC, Helmick CG, Arnett FC, et al. Estimates of the prevalence of arthritis and selected musculoskeletal disorders in the United States. Arthritis Rheum. 1998;41:778-799.
2. St.-Onge MP, Keller KL, Heymsfield SB. Changes in childhood food consumption patterns: a cause for concern in light of increasing body weights. Am J Clin Nutr. 2003;78:1068-1073.
3. Mikuls T, Farrar J, Bilker W, et al. Gout epidemiology: results from the UK General Practice Research Database, 1990-1999. Ann Rheum Dis. 2005;64:267-272.
4. Johnson RJ, Kivlighn SD, Kim YG, et al. Reappraisal of the pathogenesis and consequences of hyperuricemia in hypertension, cardiovascular disease, and renal disease. Am J Kidney Dis. 1999;33:225-234.
5. Caspi D, Lubart E, Graff E, et al. The effect of diuretics on renal function and uric acid handling in elderly patients. Arthritis Rheum. 2000;43:103-108.
6. Choi H, Atkinson K, Karlson E, et al. Alcohol intake and risk of incident gout in men: a prospective study. Lancet. 2004;363:1277-1281.
7. Nakagawa T, Hu H, Zharikov S, et al. A causal role for uric acid in fructose-induced metabolic syndrome. Am J Physiol Renal Physiol. 2006;290:F625-F631.
8. Hahn P, Edwards NL. Management of hyperuricemia. In: Koopman WJ, Moreland LW, eds. Arthritis and Allied Conditions. 15th ed. Baltimore, Md.:Williams and Wilkins; 2004:2341-2356.
9. Celebrex [package insert]. New York, N.Y.: Pfizer Inc.; 2008.
10. Perez-Ruiz FCM, Calabozo M, Fernandez-Lopez, MJ, et al. Treatment of chronic gout in patients with renal function impairment. An open, randomized, actively controlled trial. J Clin Rheumatol. 1999;5:49-55.
11. McGonagle D, Tan AL, Madden J, et al. Management of treatment resistant inflammation of acute on chronic tophaceous gout with anakinra. Ann Rheum Dis. 2007;66:1683-1684.
12. Pascual E, Sivera F. Why is gout so poorly managed? Ann Rheum Dis. 2007;66:1269-1270.
13. Hande KR, Noone RM, Stone WJ. Severe allopurinol toxicity. Description and guidelines for prevention in patients with renal insufficiency. Am J Med. 1984;76:47-56.
14. Vázquez-Mellado J, Morales EM, Pacheco-Tena C, Burgos-Vargas R. Relationship between adverse events associated with allopurinol and renal function in patients with gout. Ann Rheum Dis. 2001;60:981-983.
15. Singh JA, Hodges JS, Toscano JP, Asch SM. Quality of care for gout in the US needs improvement. Arthritis Rheum. 2007;57:822-829.
All electronic documents accessed October 7, 2008.
