Addressing Disparities in Health Care

Gout and African Americans: Reducing disparities

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LIFESTYLE MODIFICATION

Dietary modification is a useful initial step toward reducing uric acid levels (Table 1).27 The following measures are recommended:

Reduce alcohol intake. Alcoholic beverages, particularly beer, are strongly linked to hyperuricemia, according to a 2013 meta-analysis.31 Although alcohol consumption is lower in African Americans than in whites, mortality rates from cirrhosis and other alcohol-related diseases are 10% higher, suggesting metabolic differences that render African Americans more susceptible to the negative health effects of alcohol.32

Avoid sugary drinks. Sweetened beverages, especially those rich in fructose, are also implicated in hyperuricemia and gout. NHANES found an increase in serum uric acid of 0.33 mg/dL (95% CI, 0.11–0.73) in those consuming one to three sugar-sweetened drinks per day compared with nonconsumers, adjusting for total energy intake, age, sex, medications, hypertension, and GFR.33 A prospective study also found a relative risk of 1.85 for those who drink two or more sugar-sweetened beverages per day compared with those who drink fewer than one per month (95% CI 1.08–3.16).34

Unfortunately, African Americans consume a disproportionate amount of sugar from all sources: 17% of African Americans are considered heavy consumers vs 9% of whites.35

Limit foods rich in purines. Red meat, seafood, and some vegetables, including asparagus, spinach, peas, cauliflower, and mushrooms, are associated with increased serum uric acid levels. NHANES found that greater meat and seafood consumption was associated with increased uric acid levels. Choi et al36 found that the risk of gout increased by 21% with each additional daily serving of meat; the relative risk of developing gout was 1.41 (95% CI 1.07–1.86) in the fifth quintile of meat intake compared with the first quintile, and 1.51 (95% CI 1.17–1.95) in the fifth quintile of seafood consumption.

Despite these associations with high-purine food consumption and gout, many purine-rich foods may not contribute to hyperuricemia, and therefore a low-purine diet may not be protective. Interestingly, purine-rich vegetable protein intake is not associated with increased gout risk.37

Increase dairy consumption. Dairy in the diet is associated with a lower incidence of gout, with a decrease of 0.21 mg/dL (95% CI –0.37 to –0.04) in serum uric acid levels between the highest and lowest quintiles of dairy consumption.38 A randomized controlled trial found a 10% reduction in serum uric acid levels with milk consumption.39

Enjoy coffee. Coffee intake has been inversely correlated with gout. Daily intake of 4 to 5 cups of coffee is associated with a relative risk of 0.60 (95% CI 0.41–0.87) vs no coffee.40

Vitamin C and cherry juice41,42 have also been linked to lower gout risk, but the data are less robust.

Control weight. Primary care providers should advise patients to increase physical activity and maintain a healthy weight.

In a prospective study, Choi et al43 found that, in men, the risk of gout increased with the BMI. Compared with men with BMIs in the range of 21 to 22.9 kg/m2, the relative risks were:

  • 1.95 (95% CI 1.44–2.65) at BMI 25 to 29.9 kg/m2
  • 2.33 (95% CI 1.62–3.36) at BMI 30 to 34.9 kg/m2
  • 2.97 (95% CI 1.73–5.10) at BMI > 35 kg/m2.

In addition, those who gained more than 13.6 kg since age 21 had a relative risk of 1.99 (95% CI 1.49–2.66) of developing gout compared with those whose weight remained within 1.8 kg.

For those who cannot achieve weight loss through conservative measures, bariatric surgery has shown promise. In a prospective study of 60 obese patients (BMI > 35 kg/m2) with gout and type 2 diabetes mellitus, uric acid steadily declined during the first year after bariatric surgery.44

TREATMENT OF ACUTE ATTACKS

Gout can be effectively managed in most patients. Behavioral and pharmacologic interventions are cheap and effective and have been shown to halt further damage to joints as well as retard the progression of renal disease and reduce cardiovascular morbidity.

During acute attacks, anti-inflammatory medications, principally glucocorticoids, nonsteroidal anti-inflammatory drugs, and colchicine, should be given promptly to reduce the intensity and duration of flares.

Although traditional teaching has been that urate-lowering therapy should not be initiated during an acute gout attack because it could prolong the duration of the attack, guidelines now permit it, based on studies showing that therapy does not prolong attacks.45,46

AGGRESSIVE URATE-LOWERING THERAPY FOR PROPHYLAXIS

Long-term treatment of gout is aimed at reducing uric acid levels by mitigating modifiable risk factors and through urate-lowering therapy.46 For many patients, conservative management with dietary and other behavioral changes is not sufficient to prevent further attacks of gout, necessitating urate-lowering therapy. Comorbid diseases such as obesity, hypertension, chronic kidney disease, and diabetes should also be addressed because they promote hyperuricemia and gouty attacks.47

A number of organizations have issued gout management guidelines over the past decade, including the American College of Rheumatology (ACR) in 2012, the European League Against Rheumatism (2006, updated in 2014), and the British Society of Rheumatology (2007). All recommend urate-lowering therapy to prevent gout flares.

The American and European guidelines recommend a target uric acid level below 6 mg/dL, and the British guidelines recommend a target below 5 mg/dL.48 For patients with palpable and visible tophi, the ACR guidelines state that lowering to below 5 mg/dL may be needed.46

First-line agents for urate-lowering therapy are xanthine oxidase inhibitors, which include allopurinol (costing $0.48 per generic 100-mg tablet or $0.92 per 300-mg tablet), and febuxostat ($5.38 per 40-mg or 80-mg tablet). For patients with contraindications or intolerances to allopurinol or febuxostat, probenecid ($1.15 per 500-mg tablet), which functions as a uricosuric agent (ie, increases urinary excretion of uric acid), may be used.

Losartan ($1.68 per 25-mg tablet) and fenofibrate ($1.91 per 48-mg tablet) are also often used to reduce uric acid levels, but they have only modest effects and are not approved for this indication in the United States.49

MANAGE CHRONIC CASES WITH CONTINUED THERAPY

ACR guidelines strongly emphasize continuing prophylaxis in case of ongoing gout activity (ie, detection of tophi on examination, recent gout attacks, or chronic gouty arthritis) (Table 3). The following durations have been proposed for prophylaxis:

  • 6 months after an attack
  • 6 months after achieving target uric acid level in patients with evidence of tophi
  • 3 months after achieving target uric acid level in patients with resolved tophi.

Two randomized controlled trials support the use of the anti-inflammatory agent colchicine ($4.30 per tablet) for prophylaxis when initiating urate-lowering therapy.50,51

Monitor uric acid levels, renal function, adverse effects

The initial dosage of urate-lowering agents depends on the presence of kidney disease (Table 3).

Allopurinol is typically started at 50 mg to 100 mg oral daily, and titrated upward in increments of 100 mg depending on uric acid levels. According to the ACR guidelines, uric acid levels should be measured every 2 to 5 weeks.46 The Febuxostat vs Allopurinol Streamline Trial found that 97% of patients reached target uric acid levels within two titrations.52

Especially during the first months of therapy, physicians should be vigilant for adverse effects of allopurinol, including hypersensitivity reaction (rash, fever, Stevens-Johnson syndrome), hepatotoxicity, and myelotoxicity (bone marrow suppression), and for effects of febuxostat, such as rash, diarrhea, elevations in aminotransferase levels, and upper respiratory tract infections.53 Although the maximum acceptable dose of allopurinol is 800 mg even in chronic kidney disease, regularly monitoring for hypersensitivity reactions and other adverse effects is needed if doses are above 300 mg per day.46

Routine follow-up is essential

Adherence to therapy should be assessed at every visit. Patients should be counseled that gout is a chronic disease and that they should continue on urate-lowering therapy even if they are not having acute attacks. Adverse effects of medications should be monitored and addressed, although for allopurinol and febuxostat these are rare beyond the first few months of initiation and titration. If worsening of gout or uric acid levels occurs, therapy should be augmented and contributors to hyperuricemia reviewed. In refractory cases, rheumatology consultation may be needed; medications such as pegloticase ($16,800/mL) may be deemed necessary for severe tophaceous gout or for patients who need more rapid reduction of urates.49

STRATEGIES TO ADDRESS DISPARITIES

Creative approaches are needed to engage African American communities to reduce the burden of gout. No trials have been published evaluating methods for reducing health disparities with gout, but strategies for other chronic conditions may be applicable.

Incorporate guidelines better. Although setting and disseminating guidelines should ensure that care is standardized, studies have found that primary care physicians and rheumatologists frequently do not implement them.3,54 Reasons cited for poor adherence to gout guidelines include their relatively recent release, poor patient adherence, lack of measurement tools, and inadequate education of primary care physicians. Incorporating the guidelines as “best practice advisories” into electronic medical record systems has been proposed to improve their implementation.46

Use a team approach. Some quality improvement projects have used pharmacists and nurses to help implement gout guidelines. In two studies, empowering nurses and pharmacists to better educate patients and implement standardized protocols for titrating urate-lowering medications led to sustained improvements in maintaining serum uric acid levels less than 6 mg/dL.55–57

Multidisciplinary involvement by nutritionists, physicians, and community health workers have been found to help improve glycemic control in African Americans.58 Similar efforts can be undertaken to improve control of uric acid levels through dietary modification and improved compliance.

Address patient concerns. Substantial gaps exist in knowledge about gout between providers and the general population, although large studies specifically focusing on African Americans are lacking.59 Qualitative studies suggest that patient experience of gout may vary depending on race, with African Americans more likely than whites to rank the following concerns regarding gout as high: dietary restrictions, emotional burden, severe pain, the need for canes or crutches during flares, and gout bringing their day to a halt.60 Another study among African Americans with gout found concerns about the effectiveness of urate-lowering therapy, side effects of medications, polypharmacy, pill size, cost, refill issues, and forgetting to take medications regularly.61

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