ACR2012 Highlights: Gout Treatment


Among the revelations about gout treatment at this year’s meeting: Confusion among physicians about the definition of “control,” misunderstandings among gout patients about their own disease, and new drug options.

Among the revelations at this year’s meeting: Confusion among physicians about the definition of “control,” misunderstandings among gout patients about their own disease, and new drug options. (To see the entire abstract mentioned in an item below, please click on the abstract number that follows it.)

•   In gout, physicians think that “controlled” can mean more than 2 flares, serum uric acid (sUA) of 7 mg/dL, or continued tophi. A survey interviewed 125 rheumatologists and 124 primary care physicians, audited the charts of their 1,245 gout patients, and asked, “Do you consider this patient to be well controlled on their current urate lowering therapy?” meaning “No desire to increase the dose to achieve better control.” Among these “controlled” patients, 278 (32%) were treated with a xanthine oxidase inhibitor but had at least two flares in the previous year, had sUA of 7.0 mg/dL, and 30% had tophi. Factors predicting flares were kidney disease, alcoholism, depression, anti-hyperglycemic agents, and tophi. Of 621 patients treated with allopurinol, only 26% were free of flares. (Abstract #140)

•   Gout patients assessed for their knowledge about gout didn’t understand their disease, and had poor adherence to medication. In this study from investigators at the University of Michigan 24 patients, most of them seeing primary care physicians, participated in focus groups after being enrolled based on responses to an online screening survey. The themes that emerged were that patients:

--  didn’t understand the natural history of gout;

--. didn’t realize that recurrent acute flares resulted in chronic joint damage;

--  lacked knowledge of treatment options and duration of therapy;

--  felt their physicians didn’t spend enough time explaining the disease;

--  didn’t grasp the need for chronic urate lowering therapy to avoid complications and disability; and

--  weren’t aware of the treatment goals for hyperuricemia.

Not surprisingly, rates of adherence to medication were poor. Adherence was low among 38% and medium among 42% of participants. (Abstract #158)

•   Unexpectedly, levotofisopam lowers serum urate – by half. In phase I trials, this optical isomer of an established anti-anxiety drug that is used outside the United States produced unanticipated reductions in serum urate. This led Duke University physicians to launch a separate study of gout patients. The gout study stopped early after demonstrating efficacy. The mean sUA for 13 patients went from 8.0 mg/dL at baseline to 4.1 mg/dL (a 49% reduction) at 7 days. All 13 patients reached <6.0 mg/dL. (Abstract #818).

•   Rilonacept reduced flares in chronic kidney disease, with acceptable safety. The PRESURGE phase III clinical trials had 126 patients with chronic kidney disease, initial sUA ≥7.5 mg/dL, and ≥2 flares/year. In a post-hoc analysis, among all patients with low kidney function at baseline (eGFR ≥60 ml/min/1.73m2 ) the number of flares per patient declined from 1.5 to below 0.5. Among patients with poorer kidney function (eGFR ≥30 and <60), the number of flares dropped from 2.2 to less than 1. Serious adverse effects were more frequent in the group with eGFR <60.  (Abstract #813)

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