Current Concepts In Managing Chronic Gout

Scott Neville, DPM

With recently published guidelines and emerging medications, this author offers a closer look at key principles in diagnosing and treating chronic gout.

When patients are diagnosed with gout, they often have many questions. One of the most frequently asked questions pertains to whether this gouty attack is a one-time event or whether it is chronic gout that needs prophylactic treatment. Thankfully, due to the new 2012 American College of Rheumatology guidelines and other research, the treatment of chronic gout has recently become clearer.

   Not so long ago my management of gout patients left a lot to be desired. I thought gout was easy. We have all treated the extraordinarily painful, red hot, swollen, acute gout foot with success. We give an injection or write a prescription and shortly thereafter, the patient thinks you are a hero. You have a grateful patient. Case closed and you can move on to the next patient. This treatment plan may sound familiar to some of you.
Here is the problem with that line of thinking. Just because the patient is in an intercritical and asymptomatic period does not mean our job has ended. Treating all podagra patients symptomatically without regard to their total body uric acid is a recipe to create chronic gout.

Pertinent Insights On Debulking The Total Body Urate Pool

Gout is a progressive disorder with acute attacks followed by intercritical periods. If the serum uric acid is above the level of solubility, the total body urate pool is increasing as urate precipitates out in tissues. As the total body urate pool increases, the acute gouty attacks become more and more frequent. These attacks also become more aggressive and longer lasting. Elevated total body urate is also associated with tophi formation as well as polyarticular disease. The understanding that gout is a progressive disorder is critical if we are going to treat acute or chronic gout appropriately.

   There is significant evidence that debulking the total body urate pool leads to fewer gout attacks. There have been multiple studies that support this idea but Li-Yu and colleagues performed one of the most compelling studies in 2001.1 This study revealed that patients with a serum uric acid of greater than 6 mg/dL experienced a mean of six acute gouty attacks per year while patients who had a serum uric acid below 6 mg/dL for 12 months had a mean of one attack per year. Half of those patients had no attacks at all. Perez-Ruiz and colleagues performed a similar study, revealing that after two years of controlling the serum uric acid below 6 mg/dL, acute gouty attacks had been completely eradicated.2

What Is The Optimal Serum Uric Acid Target?

Imagine a cold glass of iced tea on a hot summer day. As you add sweetener to the glass, it dissolves into the iced tea until you reach the solubility limit. Any sweetener one adds over the solubility limit will be visible as precipitate at the bottom of the glass. This analogy is similar to what happens physiologically with hyperuricemia. Uric acid above the solubility limit precipitates out in the soft tissue, increasing the total body urate pool. By decreasing the serum uric acid to below the solubility limit, monosodium urate crystals can dissolve, most often leading to resolution of the symptoms associated with gout.

   The solubility of uric acid at physiologic temperature and pH is 6.8 mg/dL.3,4 With this knowledge, it makes sense that the therapeutic target for serum uric acid is below 6 mg/dL. The European League against Rheumatism Task Force for Gout and the American College of Rheumatology guidelines have both set the therapeutic target for serum uric acid at 5,6 The British Society of Rheumatology, however, has published more stringent guidelines, setting the target for serum uric acid at 7


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.

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.

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 )?

Lewis Stuttard

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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