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Musculoskeletal Last reviewed:

Gout

Also known as: urate arthropathy, monosodium urate crystal arthropathy

Reviewed by the Black Health editorial team Last reviewed

7.0% in Black men

U.S. age-standardized prevalence in Black men (NHANES 2007-2016), vs. 5.4% in white men

Overview

Gout is the most common form of inflammatory arthritis in the United States, and Black adults carry a disproportionate share of it. Black men are about 1.3 times more likely to have gout than white men; Black women are 1.8 times more likely than white women. What makes this disparity more troubling is that gout is highly treatable. The drug that controls it, allopurinol, costs a few dollars a month and has decades of evidence behind it. Yet research shows Black patients are dramatically less likely to receive it or stay on it. This page explains what gout is, what drives it in Black adults, and what effective treatment actually looks like.

How Gout affects Black patients

In the most recent nationally representative NHANES data (2007-2016, n=18,693), age-standardized gout prevalence was 7.0% in Black men versus 5.4% in white men, and Black women had higher rates than white women as well (PMC9379746). The hyperuricemia gap, meaning elevated serum urate before any flare happens, was roughly two-fold in age-adjusted analyses. Much of the disparity attenuates after adjusting for poverty, diet, BMI, and chronic kidney disease, which is the point: the gap is downstream of social and clinical risk factors that disproportionately load on Black patients, not a fixed feature of being Black.

Once Black patients have gout, the treatment gap takes over. In Medical Expenditure Panel Survey and Veterans Administration cohorts, Black patients are about half as likely as white patients to maintain high adherence to allopurinol (odds ratio roughly 0.49), are more often started on subtherapeutic doses, and are less likely to be titrated to the serum urate target of less than 6 mg/dL. The downstream signal is more emergency department visits and hospitalizations for flares that should never have happened on adequate urate-lowering therapy.

Two genetics points specific to people of African descent. First, HLA-B*58:01, the allele that predicts severe cutaneous reactions to allopurinol (Stevens-Johnson syndrome, toxic epidermal necrolysis, DRESS), shows up in roughly 3 to 6% of African Americans, higher than in white or Hispanic populations. The 2020 American College of Rheumatology gout guideline conditionally recommends HLA-B*58:01 testing before starting allopurinol in patients of Southeast Asian and African descent (PMID 32391934). This is not optional fine print; the reaction can be fatal, and the test is a one-time cheek swab. Second, APOL1 high-risk variants drive a large share of the excess kidney disease seen in Black adults, and reduced kidney function is itself a major driver of high uric acid. I could not verify a direct causal link between APOL1 variants and gout incidence in primary sources; the AASK cohort found uric acid trajectories predicted CKD progression independent of APOL1 status. The honest framing is that APOL1-related CKD raises uric acid through impaired excretion, and that mechanism matters for Black patients with both diagnoses.

Symptoms

  • Sudden severe joint pain, usually starting overnight, often in the big toe
  • Joint that is hot, red or dusky, swollen, and exquisitely tender, even bedsheets hurt
  • Attacks peaking within 12 to 24 hours and lasting several days to a week or two
  • Recurrences in the same joint or spreading to ankles, knees, wrists, fingers, elbows
  • Low-grade fever during a flare
  • Hard lumps under the skin (tophi) on ears, fingers, elbows, or over joints in long-standing disease
  • Kidney stones, sometimes the first sign of high uric acid
  • Stiffness and lingering soreness in the joint between attacks

When to see a doctor

Same week if you have a first attack of acute joint pain that fits the picture above. Same day or emergency department if the joint is hot and swollen and you have a fever, if multiple joints are involved, if you have a prosthetic joint, or if you cannot rule out septic arthritis, which can destroy a joint in days and is treated very differently from gout. Same week if you have known gout and have had two or more flares in a year, visible tophi, kidney stones, or chronic kidney disease, because those are firm indications to start urate-lowering therapy under the 2020 ACR guideline. Bring a list of current medications. Diuretics, low-dose aspirin, cyclosporine, and tacrolimus all raise serum urate.

Screening

There is no population screening program for gout. Diagnosis during a flare is clinical plus a serum urate level, with joint aspiration to look for monosodium urate crystals under polarized light when the diagnosis is uncertain or septic arthritis is on the table. The serum urate target for anyone on urate-lowering therapy is less than 6 mg/dL, and less than 5 mg/dL is often used when tophi are present (PMID 32391934). A single normal urate during a flare does not rule out gout, urate often drops acutely; recheck two weeks after the flare resolves. For Black patients being considered for allopurinol, the ACR conditionally recommends HLA-B*58:01 genotyping before the first dose; a positive test means use a non-allopurinol agent.

Treatment overview

The 2020 American College of Rheumatology guideline is the current standard (PMID 32391934). It splits cleanly into two jobs: stop the flare, then lower the urate so flares stop coming back.

Flares. First-line options, given equal weight, are colchicine, an NSAID, or glucocorticoids (oral, intra-articular, or intramuscular). Pick based on comorbidities. Colchicine needs dose reduction in kidney disease and interacts with statins and clarithromycin. NSAIDs are off the table for many patients with CKD, heart failure, or ulcer history. Glucocorticoids are usually the safest pick in CKD. Start treatment within 24 hours of onset; earlier is better.

Urate-lowering therapy. Strongly recommended for anyone with one or more tophi, radiographic damage from gout, or two or more flares per year. Allopurinol is first-line, including for patients with CKD. Start low (no more than 100 mg/day, lower if eGFR is reduced) and titrate up gradually to the dose that achieves serum urate less than 6 mg/dL; many patients need 300 to 600 mg/day or higher, and underdosing is the most common reason therapy fails. Febuxostat is an alternative when allopurinol is not tolerated. Probenecid is an option in patients with adequate kidney function. Anti-inflammatory prophylaxis with low-dose colchicine, NSAID, or prednisone is co-prescribed for at least 3 to 6 months when starting urate-lowering therapy, because dropping urate triggers flares before it prevents them.

Refractory disease. Pegloticase, an IV recombinant uricase, is reserved for patients with frequent flares or unresolved tophi despite maximal oral therapy. It is strongly NOT recommended as a first switch when xanthine oxidase inhibitors fail without ongoing frequent flares or tophi.

Lifestyle. The guideline conditionally recommends limiting alcohol, purine-rich foods, and high-fructose corn syrup, and weight loss in patients with overweight or obesity. Diet alone rarely gets serum urate to target; it is an adjunct, not a substitute, for urate-lowering therapy in anyone who meets indications.

Questions to ask your doctor

Bring this list to your next appointment.

  • What is my serum uric acid level right now, and what is the target we are aiming for with treatment?
  • Should I be on urate-lowering therapy given how many flares I have had, and if not, why not?
  • Do I need HLA-B*58:01 testing before starting allopurinol?
  • Can you prescribe colchicine for me to keep on hand so I can take it within the first 24 hours of my next flare?
  • What does my kidney function look like, and does it affect which gout medication is best for me?
  • How often should I have my uric acid level checked once I start treatment?

Find care for gout

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The numbers

  • Among those who are prescribed allopurinol, only 35.2% of all gout patients achieve high adherence. Black patients are significantly less likely to achieve this: odds ratio of 0.49 (95% CI, 0.33 to 0.73), meaning they are about half as likely as white patients to maintain consistent treatment. (Rheumatology Advisor: Gout Treatment Gaps Persist)

What it is

Gout is caused by hyperuricemia: too much uric acid in the blood. Uric acid is a natural byproduct of the body breaking down purines, which are found in red meat, shellfish, organ meat, alcohol (especially beer), and high-fructose corn syrup. Normally, uric acid dissolves in the blood and is excreted by the kidneys. When levels remain elevated for years, uric acid can crystallize and deposit in joint spaces, especially in the feet, ankles, knees, and wrists.

When crystals trigger an immune response, the result is a gout flare: sudden, intense joint pain, often described as the joint being on fire. The big toe is the classic site (the medical term is podagra), but flares can occur in any joint. Flares typically peak within 24 hours and resolve over 7 to 10 days without treatment, but they become more frequent and more severe without preventive management.

Over time, untreated gout leads to tophi (hard uric acid deposits under the skin), chronic joint destruction, and accelerated kidney damage. Gout is also independently associated with increased risk of cardiovascular disease.

Why it is different for Black adults

Chronic kidney disease drives the disparity in men. Kidneys excrete roughly two-thirds of the body's uric acid. When kidneys are damaged, uric acid accumulates. Black men have dramatically higher rates of chronic kidney disease (CKD), driven largely by untreated hypertension and diabetes. Research shows that after adjusting for poverty, BMI, diet, and CKD together, the racial disparity in gout in men disappears statistically, suggesting CKD and metabolic disease are the primary mediators. (PMC: Racial and Sex Disparities in Gout Prevalence Among US Adults, PMC9379746)

Poverty and BMI drive the gap in women. In Black women, poverty and body mass index account for much of the excess risk. Both factors raise uric acid production and reduce renal excretion. The practical implication: the structural conditions shaping food access, economic stability, and chronic disease burden are the upstream drivers. Treating gout without addressing these factors produces incomplete results.

Treatment access is the central failure. Even controlling for disease severity, Black patients with gout receive urate-lowering therapy at rates far below white patients. Studies have documented structural barriers including: clinicians less likely to initiate preventive treatment in Black patients, Black patients less likely to receive follow-up uric acid monitoring, and out-of-pocket costs even for inexpensive generics creating adherence gaps. Qualitative research has found that Black patients with gout also report receiving less education about the role of diet and medication from their providers. (PMC: Facilitators and Barriers to Adherence to Urate-Lowering Therapy in African-Americans with Gout, PMC4060486)

HLA-B testing before allopurinol. The American College of Rheumatology and others recommend offering HLA-B*58:01 testing to patients of Southeast Asian and African American descent before starting allopurinol, because this genetic variant is associated with a rare but serious hypersensitivity reaction (severe skin reactions including Stevens-Johnson syndrome). The test is inexpensive, and a negative result means allopurinol is safe to use. Black patients should ask whether this test is appropriate for them before starting the medication.

Treatment, plainly

Gout treatment has two distinct goals: stopping acute flares and preventing the next one.

Stopping a flare: Colchicine, taken early in a flare (within 24 hours of onset), is highly effective and reduces severity significantly. NSAIDs (ibuprofen, indomethacin, naproxen) are an alternative if there are no kidney or cardiovascular contraindications. Corticosteroids (prednisone) are used when colchicine and NSAIDs are not appropriate. None of these medications lower uric acid; they only treat the inflammation.

Preventing future flares: urate-lowering therapy (ULT). The goal of long-term treatment is to lower serum uric acid below 6.0 mg/dL, the threshold at which crystals dissolve over time and flares stop occurring. Allopurinol is the standard first-line option, started at a low dose and titrated upward while monitoring uric acid levels. Febuxostat is an alternative for patients who cannot tolerate allopurinol. Probenecid is occasionally used in patients with preserved kidney function who underexcrete uric acid rather than overproduce it.

The ACR recommends starting ULT in anyone with: - Two or more gout flares per year - Tophi - Gout with CKD Stage 2 or worse - Gout with a history of kidney stones

Starting allopurinol can temporarily trigger flares during the early weeks as crystals mobilize. Low-dose colchicine or an NSAID is typically prescribed alongside ULT for 3 to 6 months to prevent this.

Dietary modification reduces uric acid modestly. Limiting red meat, shellfish, organ meat, alcohol, and high-fructose corn syrup (especially soda sweetened with HFCS) is recommended. Increasing low-fat dairy, coffee, and staying well hydrated all have evidence of mild uric acid reduction. Diet alone rarely brings uric acid to target; it works alongside medication, not instead of it.

How to find care

Sources

  1. PMC: Racial and Sex Disparities in Gout Prevalence Among US Adults (PMC9379746)
  2. PMC: Racial and Gender Disparities in Patients with Gout (PMC3545402)
  3. Rheumatology Advisor: Gout Treatment Gaps Persist in US, Black and Southern-Residing Patients Most Affected
  4. PMC: Facilitators and Barriers to Adherence to Urate-Lowering Therapy in African-Americans with Gout (PMC4060486)
  5. AAFP: Management of Gout: Update from the American College of Rheumatology
  6. PMC: Can Racial Disparities in Optimal Gout Treatment Be Reduced? (PMC3337326)
  7. Mass General: Research Spotlight: Racial and Sex Disparities in the Prevalence of Gout Among US Adults
  8. Renal and Urology News: Racial Disparity in Gout Prevalence Revealed

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Medical disclaimer

This content is for informational and educational purposes only. It is not a substitute for professional medical advice, diagnosis, or treatment. Always consult a qualified healthcare provider with questions about a medical condition. If you are experiencing a medical emergency, call 911 or your local emergency number immediately.

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