Current Concepts In Managing Chronic Gout
- Volume 26 - Issue 6 - June 2013
- 6431 reads
- 4 comments
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 mg/dL.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.