Purpose of review This review highlights the available data describing racial and ethnic health disparities among patients with rheumatoid arthritis in the United States from an epidemiological, disease activity, and wider socioeconomic standpoint. Recent findings Despite centralized government initiatives to include more underrepresentative minority populations into research, many of the studies that examined rheumatoid arthritis still fail to include sizeable cohorts of races or ethnic groups other than whites. Evidence is slowly mounting that individual, provider, and system-level barriers exist and contribute to unequal care that leads to poorer outcomes amongst patients with rheumatoid arthritis. As rheumatoid arthritis is a progressive disease, early treatment is crucial to delay functional decline – a narrow window for many minority patients who are disproportionality affected by disability. Summary To combat the inequality that exists amongst rheumatoid arthritis patients we must focus on why discrepancies exist on every level, system, physician, patient, and illness. Further research is needed to tease the complex interplay between race, social economic status, medical access, and outcomes to explain the disparities found in rheumatoid arthritis.

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Purpose of review Hyperuricemia is highly prevalent, affecting approximately 38 million individuals in the United States. However, the significance of asymptomatic hyperuricemia – hyperuricemia in the absence of gout – continues to be debated. Recent findings Asymptomatic hyperuricemia results in monosodium urate crystal deposition in tissues, which may promote chronic inflammation. Intracellularly, hyperuricemia inhibits the master regulator adenosine monophosphate (AMP)-associated protein kinase and may condition innate immune responses through durable epigenetic modifications. At the population level, asymptomatic hyperuricemia is associated with multiple comorbidities, including hypertension, chronic kidney disease, coronary artery disease, and diabetes; limitations of these studies include that most are retrospective and some do not rigorously distinguish between asymptomatic hyperuricemia and gout. Treatment studies suggest that urate lowering may reduce the risk of incidence or progression of some of these comorbidities; unfortunately, many of these treatment studies are small or flawed, and not all study results are consistent. Summary Accumulating evidence suggests that asymptomatic hyperuricemia contributes to the comorbidities with which it associates and that proper asymptomatic hyperuricemia treatment may reduce future risk. Additional prospective trials are needed to definitely establish causality and support decision-making as to whether, and which patients with asymptomatic hyperuricemia would warrant urate-lowering treatment.