How can I get my patients to understand that gout is a chronic disease?

When I began my rheumatology career decades years ago, I commonly encountered patients with chronic, crippling arthritis as the result of long-standing gout. In addition to the severe deformities of their hands and feet, these individuals were distinguished by large tophaceous deposits scattered over the joints and ears. With advances in understanding gout pathophysiology and the availability of effective urate-lowering medications, that scenario is fortunately now rare. However, chronic gout continues to be a significant medical problem despite being the only rheumatic disease considered to be “curable.”

It is important for clinicians to educate patients on the differences between acute gout and chronic gout, including their unique mechanisms and treatment approaches. The only treatment goal for acute gout is to quickly alleviate the severe pain and swelling from crystal-induced joint inflammation, using medications such as colchicine, glucocorticoids, or NSAIDs. Obtaining a serum uric acid at the time of an acute attack of gout may help to confirm clinical suspicion of gout but urate-lowering medications should not be started until at least a few weeks after the acute attack subsides.

Discussing gout as a chronic disease, directly related to hyperuricemia, should begin at follow-up, shortly after the initial gout episode. Gout risk factors, including diet, alcohol intake and obesity, as well as comorbidities, including chronic renal disease, hypertension, and cardiovascular disease, should be evaluated and their management role in gout explained in detail. (Editor’s Note: An upcoming clinical challenge will address medication and lifestyle modifications to treat refractory gout.) Some patients may choose to modify these risk factors before beginning urate-lowering medications. Patients with more gout risk factors, such as substantial alcohol intake, obesity, and chronic renal disease, should be encouraged to begin urate-lowering medications earlier.

The decision to begin urate lowering therapy should be individualized since otherwise healthy patients may go months or years gout-free after their first attack. It is recommended that urate-lowering medications be initiated in any patient with more than 2 gout attacks in a year, especially if the serum uric acid is consistently >7-8 mg/dl. Absolute indications for urate-lowering therapy include radiographic evidence of gout joint damage, presence of tophi on physical examination, a history in patients with uric acid stones or moderate to severe chronic kidney disease.

Overall, it is essential that patients understand that joint damage will very likely progress with each subsequent gout attack. In stark contrast, if the serum uric acid normalizes (<6 mg/dl), the joint damage will not progress and will often reverse (this is known as treating to target). There is also evidence that cardiovascular and renal disease will improve with optimal urate control. Chronic, tophaceous gout should be a thing of the past and currently is likely the result of patient non-adherence or inadequate healthcare communication.