Redefining Gout: No Longer a “Disease of Kings,” Rather a “Disease of the Masses”

Friday, 12 June 2015

Think gout is the medieval disease of kings? Think again. Gout is the most common form of inflammatory arthritis1 and affects more than 15.8 million people in the United States, France, Germany, Italy, Spain, the United Kingdom and Japan.2 This is predicted to grow to 17.7 million diagnosed cases by 2021.2 That’s more than the population of New York City!3 It is an extremely painful, chronic disease that is caused when uric acid levels increase to a point where uric acid crystal deposits are formed and settle throughout the body — in the joints, tendons, kidneys and other organs.1

With so many individuals affected worldwide,2 it’s rather astonishing that misconceptions about the disease still abound. In particular, the belief that gout is predominately caused by diet and lifestyle is a myth.4 Excessive alcohol consumption and regular indulgence in rich foods, such as red meat and high-fat dairy, are often blamed.5 Yet gout is known to run in families and is often caused by a genetic predisposition.5 Simply put, diet is not a cause of gout — rather, it can contribute to increasing patients’ already high serum uric acid (sUA) levels, and trigger a painful flare in joints.4 Elevated sUA occurs mainly when the body does not remove enough uric acid (inefficient removal in approximately 90% of patients) or in some people who make too much sUA (over-production in approximately 10% of patients).6

A painful burden

The pain of these flares is often so immense that many patients with podagra – when the condition involves the big toe – can’t even bare the simple weight of a bedsheet on their foot. This pain can be debilitating to the point where people are missing work7 and have limited physical activity.8 However, there is more to gout than the flares. Patients without flares are at risk, too.1 Over time, the chronic nature of gout can have a serious impact throughout the entire body – causing permanent joint destruction and bone erosion, if not appropriately treated.1 Ongoing elevated sUA levels may result in uric acid crystals causing local and systemic inflammation, the development of tophi, and eventually permanent bone and joint damage and disability.1 And if that’s not enough, gout is often associated with serious comorbidities such as hypertension, chronic kidney disease, cardiovascular disease, and metabolic syndromes including diabetes.1,5

Gout is chronic, progressive, and debilitating, but it can be controlled with the right treatment

With all this said, there is hope for individuals living with gout. Gout can be successfully managed with proper treatment.9 Uric acid-lowering medication aims to reduce a patient’s sUA levels to the target levels set forth by the American College of Rheumatology (ACR) and the European League Against Rheumatism (EULAR) of <6.0 mg/dL (<360 µmol/L).9,10 Those with greater disease severity may need to achieve an even lower target level of <5.0 mg/dL (<300 µmol/L).9,10

Over the past 30 years, there have been limited treatment options for the millions of patients suffering from gout who fail to reach target sUA levels on the current standard of therapy, xanthine oxidase inhibitors (XOIs). In fact, approximately 50% of patients do not achieve recommended sUA goals with the current standard of care of an XOI alone.11-14 Both ACR and EUALR guidelines recommend a combination therapy when target sUA levels aren’t achieved on an XOI.9,10

The unmet need for an efficacious therapeutic option is clear. That is why AstraZeneca saw the potential in the work being done at Ardea Biosciences. Their talented team in San Diego is focused on developing innovative new treatments that focus on the primary underlying cause of gout – inefficient removal of uric acid. Simply put, this is an exciting opportunity for the millions of individuals living with gout worldwide, and we’re optimistic about the promise of this new research.

Together, AstraZeneca and Ardea are committed to advancing the new science of gout and to developing treatments that will help patients better manage their disease. We are looking forward to future developments that have the potential to improve lives for the better, and hope you are, too.

Scott W. Baumgartner, MD
Vice President, Medical Affairs


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  3. United States Census Bureau. (2015, April 22). New York (city), New York. Retrieved from (Guidance on using the Census website can be found at 
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  11. Schumacher HR, Jr., Becker MA, Wortmann RL, et al. Effects of febuxostat versus allopurinol and placebo in reducing serum urate in subjects with hyperuricemia and gout: a 28-week, phase III, randomized, double-blind, parallel-group trial. Arthritis Rheum. 2008;59(11):1540-1548.
  12. Becker MA, Schumacher HR, Jr., Wortmann RL, et al. Febuxostat compared with allopurinol in patients with hyperuricemia and gout. N Engl J Med. 2005;353(23):2450-2461.
  13. Becker MA, Schumacher HR, Espinoza LR, et al. The urate-lowering efficacy and safety of febuxostat in the treatment of the hyperuricemia of gout: the CONFIRMS trial. Arthritis Res Ther. 2010;12(2):R63.
  14. Edwards NL. Febuxostat: a new treatment for hyperuricaemia in gout. Rheumatology (Oxford). 2009;48(suppl 2):ii15-ii19.