Current Concepts In Managing Chronic Gout

Start Page: 46
51
Author(s): 
Scott Neville, DPM

References
1. Li-Yu J, Clayburne G, Sieck M, et al. Treatment of chronic gout. Can we determine when urate stores are depleted enough to prevent attacks of gout? J Rheumatol. 2001; 28(3):577-80.
2. Perez-Ruiz F, Calabozo M, Fernandez-Lopez MJ, et al. Treatment of chronic gout in patients with renal function impairment: an open, randomized actively controlled study. J Clin Rheumatol. 1999; 5(2):49-55.
3. Neogi T. Clinical practice: gout. New England J Med. 2011; 364(5):443-52.
4. Terkeltaub R. Update on gout: new therapeutic strategies and options. Nature Reviews Rheumatology 2010; 6(1):30-8.
5. Zhang W, Doherty M, Bardin T, et al. EULAR evidence based recommendations for gout. Part II: Management. Report of a task force of the EULAR Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis. 2006; 65(10):1312-24.
6. Khanna, Dinesh et al. American College of Rheumatology guidelines for management of gout, part 1 & 2. Arthritis Care Research. 2012; 64(10): 1431-1461.
7. Jordan KM, Cameron JS, Snaith M, et al. British Society for Rheumatology and British Health Professionals in Rheumatology guideline for the management of gout. Rheumatology. 2007; 46(8):1372-4.
8. Perez-Ruiz F, Calabozo M, Pijoan JI, Herrero-Beites AM, Ruibal A. Effect of urate-lowering therapy on the velocity of size reduction of tophi in chronic gout. Arthritis Rheum. 2002; 47(4):356-60.
9. Singh JA, Reddy SG, Kundudkulam J. Risk factors for gout and prevention: a systematic review of the literature. Curr Opin Rheumatol. 2011; 23(2):192-202.
10. Zhang Y, Woods R, Chaisson CE, Neogi T, Niu J, McAlindon TE, et al. Alcohol consumption as a trigger of recurrent gout attacks. Am J Med 2006; 119(9):800.e13-8.
11. Choi HK, Atkinson K, Karlson EW, Curhan G. Obesity, weight change, hypertension, diuretic use, and risk of gout in men: the healthcare professionals follow-up study. Arch Int Med. 2005; 165(7):742-8.
12. Becker MA, Schumacher HR, Espinoza LR, Wells AF, McDonals P, Loyd E, et al. The urate lowering efficacy and safety of febuxostat in the treatment of hyperuricemia of gout: the CONFIRMS trial. Arthritis Res Ther 2010; 12(2):R63.
13. Sundy JS, Baraf HS, Yood RA, et al. Efficacy and tolerability of pegloticase for the treatment of chronic gout in patients refractory to conventional therapy. JAMA. 2011; 306(7):711-720.

   For further reading, see “Recognizing And Treating Lower Extremity Gout” in the February 2012 issue of Podiatry Today.

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Susan Salak, D.P.M.says: June 7, 2013 at 2:17 pm

Your article states that the goal is to reduce uric acid levels quickly. Previous articles that I have read from Podiatry Management indicate that reducing the uric acid level too quick can precipitate continued gout flares. Also, is it safe to state to patients that diet plays a small role in precipitating a gout attack since your article states that exogenous factors account for only 10%?

Please advise.

Reply to this comment »
Scott Neville, DPMsays: June 20, 2013 at 11:25 pm

The article never suggests that reducing the serum uric acid quickly is the goal. In the article, I discussed how to properly titrate allopurinol up slowly to help reduce mobilization flares. I also covered the topic of mobilization flares in the section entitled, "What You Should Know About The Urate Lowering Therapy Paradox." It says:

"It is important to educate patients that paradoxically, the initiation of urate lowering therapy can trigger acute gouty attacks. This is thought to be secondary to the rapid decrease in the serum uric acid that causes a large change in the concentration gradient. This concentration gradient causes mobilization of the urate, which is thought to increase so-called “mobilization flares.”

Therefore, one must utilize concomitant use of nonsteroidal anti-inflammatory medications when initiating urate lowering therapy. It is important to note colchicine (Colcrys, Takeda), given at 0.6 mg PO q.d. or b.i.d., is the only FDA approved medication for gout prophylaxis."

To address your second question, I think it is important to understand that the audience for this article was physicians, not patients. I do not believe it would be wise to downplay the importance of dietary modifications to your patients, but I also believe it is important that patients have a realistic expectation of what they can hope to obtain with dietary modifications alone. Patient education about dietary modifications can be effective without urate lowering therapy as long as the serum uric acid is under 7 mg/dL. If you have a serum uric acid of 7 mg/dL and you reduce the serum uric acid by 10% with dietary modification, the serum uric acid will still be a sub-therapeutic 7.3 mg/dL. I think it is extremely important that both patients and physicians understand this because in many cases, urate lowering therapy will need to be utilized in conjunction with dietary modifications.

Reply to this comment »
Lewis Stuttardsays: June 17, 2013 at 5:14 am

As a podiatric surgeon and a gout sufferer, Ihave only one question. How does one ensure the serum uric acid stays below 6 mg/dl ( or 5 in UK )?

Regards,
Lewis Stuttard

Reply to this comment »
Scott Neville DPMsays: June 20, 2013 at 3:42 pm

One of the main reasons why serum uric acid is persistently sub-therapeutic is inappropriate dosing of urate lowering therapy. For instance, in multiple studies, allopurinol is consistently under-dosed, resulting in sub-therapeutic serum uric acid levels.

If we assume that a patient is on an appropriate urate lowering therapy at the appropriate dose and that patient continues to be symptomatic, that is the definition of refractory chronic gout. Krystexxa is the only FDA-approved medication for refractory chronic gout.

I would encourage such a patient to seek out a local Krystexxa representative to find a physician in the area who is knowledgeable about Krystexxa.

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