Gout is a prevalent, chronic condition that affects more than 9.2 million people in the US.1 Yet, as our understanding of gout has increased, the use of urate-lowering therapies has not.
Last year, the American College of Rheumatology (ACR) issued new guidelines for managing gout, including for the treatment of patients with gout whose condition is not being controlled by urate-lowering medications, those who are continuing to experience frequent gout flares and subcutaneous tophi, and in whom serum urate target is not being achieved.
We know that achieving a minimum serum uric acid level of 6 mg/dL can reduce flares and tissue deposition of urate. When left untreated or undertreated, serious long-term or even permanent damage to the bones, joints, and organs can occur. We also understand the correlation between uncontrolled gout and other comorbid conditions such as chronic kidney disease, diabetes, and heart disease.
However, hyperuricemia may not be the only important target. The impact of gout on patients’ quality of life may be influenced by other factors. As Becker et al found in their study, “[Patients’] perceptions of their overall gout-related pain and functioning were highly correlated to [health-related quality of life] and disability.” Also, the presence of tophi was negatively correlated with quality of life measures.2
A 2011 study published in the Journal of Medical Economics also indicated that gout flares “significantly affect[ed] patient work productivity and social activities.”3
So, the question arises – what is the true “target?”
Start a Dialogue
This question presents the physician and the patient with a critical issue – the need for an open dialogue and clear communication about the treatment goal. Not only do treating physicians need to educate the patient about the burden and comorbidities associated with gout, but also they need to listen to the patient about their specific gout-related symptoms or the dysfunctions that they may be experiencing.
Many personal factors also influence the patient’s acceptance and adherence to the treatments proposed, which can make the conversation even more difficult, especially with the many myths surrounding gout. Patients may be resistant to initiate conversations about gout given the associated stigma and assumption that they are to blame for lifestyle choices that can cause gout flares without realizing that factors, like genetics and preexisting conditions, play a much larger role. In addition, primary care physicians may not appreciate gout as a potentially erosive and debilitating disease.
In short, patient shame and physician misunderstandings can interfere with achieving an effective therapeutic plan for those living with the condition.
Commit to the Conversation
There are many things that can be done to debunk myths about gout and improve the physician-patient dialogue. Most importantly, health care providers and patients should be better educated on the advances in gout research. An example is how dual-energy computed tomography scans have allowed us to visualize the true burden of uric acid build-up in anatomic locations of the body that may be missed in a physical exam.4-6
We also know that damage from tophi deposits occurs even when a patient is not experiencing pain. This “intercritical” phase of gout can be deceiving for both the patient and the physician. Focusing on the frequency or symptomology of gout flares may not be effective since chronic gout can present with either a lower grade or no pain and lead to more chronic disability. Another advancement in our understanding of gout treatment is the importance of the speed at which we reduce the urate burden.7
Pegloticase, a recombinant uricase enzyme, has revolutionized treatment of gout by allowing us to rapidly reduce and clear the tophaceous burden in the body.8 Awareness of this treatment option is still lagging in the primary care and patient communities, and there’s a critical need to close this knowledge gap.
I challenge clinicians to open the dialogue with their patients with gout and become stronger advocates for proper diagnosis and treatment of this chronic condition as it is the medical community’s responsibility to take this condition more seriously and recognize its impact on quality of life, while educating patients on its detrimental effects.
- Chen-Xu M, Yokose, C, Rai SK, Pillinger MH, Choi HK. Contemporary prevalence of gout and hyperuricemia in the united states and decadal trends: the National Health and Nutrition Examination Survey 2007-2016. Arthritis Rheumatol. 2019;71(6):991-999. doi:10.1002/art.40807
- Becker MA, Schumacher R, Benjamin KL, et al. Quality of life and disability in patients with treatment-failure gout. J Rheumatol. 2009;36;1041-1048. doi:10.3899/jrheum.071229
- Edwards NL, Sundy JS, Forsythe A, Blume S, Pan F, Becker MA. Work productivity loss due to flares in patients with chronic gout refractory to conventional therapy. J Med Econ. 2011;14(1):10-15. doi:10.3111/13696998.2010.540874
- Choi HK, Al-Arfaj AM, Eftekhari A, et al. Dual energy computed tomography in tophaceous gout. Ann Rheum Dis. 2009;68:1609-1612. doi:10.1136/ard.2008.099713
- Edwards NL. Gout. A. Clinical features. In: Klippel JH, Stone JH, Crofford L, White PH, eds. Primer on the Rheumatic Diseases. 13th ed. Springer; 2008:241-249.
- Bongartz T, Glazebrook KN, Kavros SJ, et al. Dual-energy CT for the diagnosis of gout: an accuracy and diagnostic yield study. Ann Rheum Dis. 2015;74:1072-1077.
- Schett G, Schauer C, Hoffmann M, Herrmann M. Why does the gout attack stop? A roadmap for the immune pathogenesis of gout. RMD Open. 2015;1(suppl 1):e000046. doi:10.1136/rmdopen-2015-000046
- Pegloticase. Prescribing information. KRYSTEXXA. 2010. Updated April 2012. Accessed May 24, 2021. https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/125293s034lbl.pdf
This article originally appeared on Clinical Advisor