SNOWMASS, COLO. – A disturbing proportion of gout cases are mismanaged by primary care physicians, and the blame falls squarely upon rheumatologists, according to one prominent gout expert.
"As rheumatologists, gout is our disease. The cause and pathophysiology are well understood, we can make the diagnosis with absolute certainty, and we’ve got great medicines. Yet today we all see people with tophi. That’s tragic. It shouldn’t exist. One of our biggest mistakes has been not being able to educate primary care physicians that having a tophus is bad, that it’s eroding cartilage and bone, and that it’s something we can prevent if we start urate-lowering therapy soon enough," Dr. Robert L. Wortmann said at the conference.
Dr. Robert L. Wortmann
An estimated 8.3 million Americans have gout. Yet, the pharmaceutical industry says only 3.1 million of them are prescribed urate-lowering drugs. Five different studies show that a mere 40% of those on allopurinol are prescribed a dose sufficient to drive serum uric acid below 6 mg/dL, a key tenet of gout management, noted Dr. Wortmann, professor of medicine at Dartmouth Medical School in Hanover, N.H.
Moreover, poor treatment adherence is a huge problem in gout. A study of close to 4,200 gout patients started on urate-lowering drug therapy found that 56% of them were nonadherent (Arthritis Res. Ther. 2009;11(2):R46).
"I charge you all to go back from this meeting and try to communicate with all the primary care physicians you can about the principles of managing gout. People shouldn’t suffer from this," the rheumatologist declared.
He offered these major take home points:
Don’t prescribe urate-lowering drugs for asymptomatic hyperuricemia: This practice hasn’t been shown to prevent the future development of gout, yet it exposes patients to the risk of drug toxicities.
But don’t ignore asymptomatic hyperuricemia, either: Epidemiologic studies have linked asymptomatic hyperuricemia, defined by a serum urate in excess of 6.8 mg/dL, to increased risks of hypertension, cardiovascular disease, diabetes, chronic kidney disease, and all-cause mortality. The big unanswered question is whether using medications to lower serum urate in individuals with asymptomatic hyperuricemia reduces the risk of any of these conditions. That’s the subject of ongoing large clinical trials in high-risk patients. If those studies prove positive, clinical practice will change.
While awaiting the outcome of the prevention trials, it’s worth bearing in mind that Framingham Heart Study data indicate that individuals with a serum uric acid level above 9 mg/dL have a 22% chance of developing gout within the next 5 years. The major contributors to asymptomatic hyperuricemia include obesity, metabolic syndrome, and heavy consumption of fructose-containing beverages or alcohol. Those issues should be addressed.
Losartan is the only antihypertensive agent that’s uricosuric. Fenofibrate is the sole uricosuric drug indicated for dyslipidemia. Preferential consideration could be given to the use of these drugs in hypertensive and/or hyperlipidemic patients with asymptomatic hyperuricemia.
The important thing is not which oral agent you use for treatment of acute gout, it’s to initiate therapy as early as possible, at the first hint of an attack. Colchicine, maximum-dose NSAIDs, and oral prednisone dosed at 20 mg BID until symptoms have been gone for 1 week followed by another week at 20 mg/day – they’re all effective. And since they work by different mechanisms, they can beneficially be combined in refractory patients.
The old-school colchicine dosing regimen most physicians were taught has been cast aside of late. It had a high rate of diarrhea, an inhumane side effect in gout patients hobbled by a foot too sore to walk on. The former regimen has been replaced by 1.2 mg, given in a single dose, followed by 0.6 mg 1 hour later.
"This lower dose is just as effective as the old high-dose regimen of two 0.6-mg pills given at once and then one per hour for the next 5 hours. And the lower-dose program has the same side effect profile as placebo," Dr. Wortmann said.
Get the gout patient’s serum urate below 6 mg/dL using the lowest effective dose of the urate-lowering drug you’ve selected. Physicians have traditionally started gout patients on allopurinol at the standard dose of 300 mg/day. Recently, it has been demonstrated that the risk of developing allopurinol hypersensitivity syndrome is greatly reduced by starting off at 150 mg/day, checking the urate level 2 weeks later, then increasing to 300 mg/day if the serum urate isn’t below 6 mg/dL. After 2 weeks at 300 mg/day, check the urate again, and if it still isn’t below 6 mg/dL then bump the dose to 400 mg/day. Continue testing and titrating every 2 weeks until the serum urate is less than 6 mg/dL – and preferably less than 4 mg/dL if the patient has tophi – or until the maximum approved dose of 800 mg/day is reached.