Current Concepts In Managing Chronic Gout

Scott Neville, DPM

   As the serum uric acid falls into the therapeutic range, the total body urate can start to decrease but this process is slow unless the gradient is high according to Le Chatelier’s principle. Perez-Ruiz and coworkers confirmed this in 2002.8 They noted that the speed of tophi resolution was inversely proportional to the serum uric acid level. Therefore, the lower serum uric acid is, the quicker the debulking of the total body urate will occur.

A Closer Look At Nonpharmacological Options For Gout

After making the diagnosis of gout and getting the acute flare under control, our job is not complete. The American College of Rheumatology guidelines recommend a multipronged nonpharmacological approach for all patients who have been diagnosed with gout.6 Among these are patient education, consideration of secondary causes of hyperuricemia and elimination of nonessential prescription medications.

   Patient education about the disease as well as dietary and lifestyle modifications have been partially efficacious. Studies have shown a 10 to 18 percent reduction in serum uric acid with exercise and dietary modification alone. However, in patients with serum uric acid above 7 mg/dL, this is often not adequate to decrease the serum uric acid to under the target of 6,9 The reason for this is fairly simple. Ninety percent of uric acid in the body is from endogenous sources while only 10 percent is from exogenous sources. In other words, only 10 percent of the uric acid is from dietary purines and 90 percent is from tissue purine synthesis. That is why controlling gout by diet alone often fails, necessitating urate lowering therapy.

What About Secondary Causes Of Hyperuricemia?

It is also important that we consider secondary causes of hyperuricemia and seek to modify these when possible. Some of the most common secondary causes of hyperuricemia include obesity, diabetes mellitus, hypertension, hyperlipidemia, excessive alcohol intake, chronic renal disease and lead intoxication.9,10 Clearly, coordination of the patient’s care with the entire healthcare team is critical to the success in addressing the secondary causes of gout. Often, specialists are maligning these secondary causes of gout and despite optimal treatment, the serum uric acid continues to be uncontrolled.

   Several medications are associated with hyperuricemia. In a 2005 study, there was a 77 percent increase in relative risk for gout in men who were taking thiazide diuretics.11 This was true even after controlling for other risk factors associated with gout. Other urate elevating prescriptions include loop diuretics, niacin and pyrazinamide. In some situations, treating hyperuricemia may be as easy as discontinuing the offending medication. In consultation with the prescribing provider, consider elimination of any nonessential urate elevating prescription medications.

Key Insights On Urate Lowering Therapy

The American College of Rheumatology guidelines have identified four situations in which one should initiate urate lowering therapy.6 The first situation is having tophus or tophi present upon examination or imaging studies. The second is frequent gouty attacks defined as more than one acute attack per year. The third indication for urate lowering therapy is chronic kidney disease of stage II or worse. Lastly, patients with past urolithiasis should start on urate lowering therapy. Many of the patients presenting to my office with an acute gouty attack qualify for the initiation of urate lowering therapy. It is incumbent upon us either to treat the patient’s hyperuricemia or refer the patient to a primary care provider or rheumatologist who will manage the patient’s chronic gout appropriately.


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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