Addressing Disparities in Health Care

Gout and African Americans: Reducing disparities

Author and Disclosure Information

ABSTRACTAfrican Americans are more likely to suffer from gout and are less likely to receive optimal treatment for it. Physicians should be aware of risk factors for gout and professional guidelines for treating acute attacks and high uric acid levels, and should help develop strategies to reduce disparities in healthcare delivery.


  • Gout is more common in African Americans mainly because of their higher prevalence of risk factors such as obesity, diabetes, chronic kidney disease, and hypertension.
  • Gout significantly reduces quality of life, economic productivity, and physical function and increases the risks of cardiovascular and renal disease.
  • Although professional guidelines and effective medications are widely available, studies have found low physician compliance with providing optimal gout treatment, especially for African American patients.
  • Treatment for gout in African Americans is the same as for all patients. Acute attacks should be treated promptly with anti-inflammatory agents, and uric acid levels should be aggressively lowered with drug therapy and diet modification.



Despite the historic association of gout with royalty and “rich eating,” gout disproportionately affects those of lower socioeconomic status.1 Risk factors for gout, including obesity, chronic kidney disease, diabetes, and hypertension, are more common in African Americans, resulting in a higher prevalence of the disease. In addition, African Americans are less likely to receive the aggressive treatment for gout advocated by professional societies, such as anti-inflammatory medications during flares and prophylactic urate-lowering therapy.

This article reviews the epidemiology of gout and its pathophysiology, risk factors, and optimal management, focusing on African Americans and strategies to reduce healthcare disparities in this patient population.


Gout is the most common inflammatory arthritis in the United States today, affecting 4% of the adult US population.2 It is a chronic disease associated with high levels of uric acid, usually manifesting as intermittent attacks of painful monoarthritis, although multiple joints may be involved.

Despite a popular misconception that gout is merely an episodic nuisance, it is a serious disease that can significantly affect physical function and quality of life.3 A 2013 systematic review found that quality of life was significantly reduced in patients with gout, particularly those with polyarticular gout, tophi, comorbidities, and radiographic damage.4

Economic costs include decreased worker productivity and increased absences from work.5,6 From 2001 to 2005, an estimated 2 million visits were made to primary care providers due to gout.7 Because gout frequently coexists with diabetes, hypertension, coronary artery disease, and kidney disease, it is often overlooked during routine clinic visits.3


Uric acid, a product of purine metabolism, is the key mediator of gouty arthritis. Accumulation of uric acid in joints and other tissues leads to an exuberant inflammatory response manifesting as a gouty attack. When uncontrolled, uric acid may crystallize in joints and other structures, leading to tophi formation, which can cause chronic deforming and erosive arthritis, known as chronic tophaceous gout.8

Although gout is considered to be a musculoskeletal disorder, recent evidence indicates that hyperuricemia plays an important role in the development of renal disease and contributes to cardiovascular morbidity and death.9 Several studies have found that reducing uric acid levels lowers cardiovascular mortality rates and retards the progression of chronic kidney disease.10


Large-scale epidemiologic surveys have established that prevalence varies widely among population groups. Premenopausal women are less likely to be affected than men, presumably due to the effect of female hormones on renal tubular excretion of uric acid.11

Certain Asian populations (Filipinos, Taiwanese, Micronesians, the Maoris of New Zealand, Hmong Chinese immigrants in Minnesota) and African Americans have a high prevalence, while people from several sub-Saharan African countries have a very low prevalence. These differences are likely due to a variety of reasons, including genetic predisposition; diet (Table 1); risk factors such as obesity, diabetes, and hypertension; less access to healthcare resources; and inappropriate treatment.12,13


“African Americans” are a highly heterogeneous group making up about 13% of the US population. Most scholars now consider racial identity largely a product of socioeconomic and political circumstances rather than a scientific concept.14 The US Census Bureau defines African Americans (or “blacks”) as those having origins in the black racial groups of Africa,15 but even this is problematic, since it combines people as diverse as descendants of 17th, 18th, and 19th century enslaved Africans with recent first-generation African immigrants, as well as with Caribbean- and Latino-Americans of African heritage.

In addition, many African Americans trace their ancestry to other racial and ethnic groups, especially European and Native American. A study of nine European DNA markers among 10 African American populations in the United States and one population of Jamaicans of African descent found a range of frequencies from 7% among Jamaicans to 23% among African Americans living in New Orleans.16

Although such diversity argues against generalizing healthcare needs for the entire African American community, some evidence indicates that genetic markers for gene-disease associations may be consistent across traditional racial boundaries.17


Several small studies have found evidence of genetic factors mediating the risk for hyperuricemia and gout. Twin studies indicate that hyperuricemia is highly heritable,18 although they do not show a concordance in the heritability of gout, suggesting that environmental factors also have an important role in developing clinical manifestations of the disease.12

Genome-wide association studies have identified 28 separate loci influencing uric acid levels, including genes for uric acid transporters (eg, SLC2A9 and ABCG2), and metabolic pathway regulators (eg, PDZK1, SCL22A12, and PRPSAP1), but the distribution among African Americans is largely unknown.19 One important exception is SLC2A9, a renal tubular transporter of uric acid: variants of SLC2A9 were found exclusively in African Americans, but the clinical significance of this association is unclear.20

Several epidemiologic studies have looked at gout in African Americans.

In the Coronary Artery Risk Development in Young Adults study,21 young African Americans had lower levels of uric acid than whites after adjusting for body mass index (BMI), glomerular filtration rate (GFR), diet, and medications. But after up to 20 years of follow-up, the risk of hyperuricemia was 2.3 times higher in African American women than in white women (95% confidence interval [CI] 1.34–3.99). Such differences were not found between African American and white men.

The National Health and Nutritional Examination Survey (NHANES) found that African American adolescents had lower uric acid levels than white adolescents after taking into account sugar intake, GFR, BMI, and onset of puberty.22

The Multiple Risk Factor Intervention Trial23 also found that among those with high cardiovascular risk, the incidence of hyperuricemia and gout was lower in African Americans than in whites.


Despite some evidence that African Americans have genetic factors that are protective against gout, they have a much greater frequency of acquired risk factors for gout, including obesity, physical inactivity, hypertension, diabetes mellitus, renal failure, high intake of seafood, elevated blood lead levels, and use of antihypertensive medications (Table 2).

Hochberg et al24 examined the incidence of gout in 352 African American and 571 white physicians and found higher rates in African Americans (9% vs 5%). The authors suggested different rates of hypertension as an explanation, although the use of antihypertensive medications such as diuretics that promote hyperuricemia confounds the strength of this conclusion.


Unlike for heart failure, in which subgroup analyses of large prospective studies have found different efficacies of medications in African Americans than in whites, no such data exist for gout. Although there is a higher risk of allopurinol hypersensitivity in ethnic groups that express the HLA-B*5801 polymorphism (eg, Han Chinese, Korean, Thai, Japanese, Portuguese), African Americans are not known to be at greater risk.25 There are also no special precautions for using febuxostat or probenecid in African Americans.

Absent any compelling reason, gout management should be the same regardless of ethnicity.26 Patients should be counseled on primary prevention measures such as dietary and behavioral modification and, if necessary, started on aggressive urate-lowering therapy.27


African Americans with gout are less likely to receive urate-lowering therapy.28 According to the 2002 National Ambulatory Medical Care Survey in the United States, African Americans with gout are far less likely to receive allopurinol than whites (42% vs 80%; odds ratio [OR] 0.18; 95% CI 0.04–0.78).23 Even when therapy is prescribed, rates of nonadherence are greater in African Americans than in whites (OR 1.86, 95% CI 1.52–2.27), though the authors do not speculate why this is so.29 No studies have compared rates of prescribing febuxostat to African Americans vs whites.

African Americans are also less likely to receive ongoing routine care for their gout. A 2007 study30 of 663 veterans found that physicians were 1.41 times less likely to adhere to three selected quality indicators when dealing with nonwhite than white patients (95% CI 0.52–3.84). The three quality indicators studied were:

  • Lowering of daily allopurinol dose to below 300 mg/day in the presence of renal insufficiency (no longer considered a quality measure)
  • Monitoring of serum urate level at least once during the first 6 months of continued use of a xanthine oxidase inhibitor, such as allopurinol
  • Monitoring of complete blood cell count and creatinine kinase at least every 6 months in patients with renal impairment receiving long-term prophylactic oral colchicine (> 0.5 mg/day for at least 6 months).

The finding was independent of age, comorbidity index, healthcare access, and utilization characteristics (eg, number of inpatient and outpatient visits, type of physician, most frequently seen physician).

Next Article:

Geographic tongue

Related Articles