In this study of an ethnically diverse population of 498 adults with RA, we found significant variation by race/ethnicity in disease activity and function. Most striking, the relationship between race/ethnicity and RA outcomes differed between two clinic settings, with significant racial and ethnic disparities in disease activity and function observed only at the university hospital clinic. Whites were observed to have less disease activity and better function than non-Whites, and English speakers compared to non-English speakers as well as U.S.-born compared to immigrants also had less disease activity at the university hospital clinic; these differences were not observed at the county clinic.
This is the first U.S. study to examine whether variation in disease activity among diverse racial/ethnic groups with RA is moderated by clinic setting. Our study population included a significant number of subjects of Asian/Pacific Islander ethnicity, and with non-English proficiency and immigrant status. The fact that clinically and statistically significant disparities in outcomes persisted even after adjusting for medication use indicates that variation in current treatment – an important indicator of quality of care--did not explain these differences.
Possible mechanisms for the clinic-level differences in outcomes observed in our sample include differences in patient characteristics and preceding events (e.g., residual effects of low socioeconomic status, communication barriers such as health literacy and LEP, or genetic/biologic differences), patient behavior (e.g., adherence or preferences for medication), or delivery system structure (e.g., variation in time to initial rheumatology care and access to treatment). Research in other chronic diseases indicates that limited English language proficiency can contribute to health disparities(29
), and ours is the first study to demonstrate this in RA. Of note, the addition of language to the race/ethnicity models in this study had no effect on the race/ethnicity-outcomes associations, suggesting that language does not substantially explain the racial and ethnic disparities observed in our study. While there is significant language diversity in our cohort, the county hospital clinic is staffed with full-time in-person interpreters which may substantially mitigate the contribution of language to disparities at that clinic site. Given the small numbers of non-Hispanic Whites as well as small numbers of English-speaking Hispanics or Asian/Pacific Islanders, our analysis may have been underpowered to distinguish between the effects of language and race/ethnicity at the county hospital.
Significant progress in the field of genetic epidemiology has revealed ethnic differences in the genetic predisposition to RA between persons of European and Asian ancestries(31
). While genetics may be one mechanism by which variation in outcomes occur, it is unlikely to be the sole factor(32
). Racial/ethnic differences in disease activity within the university but not in the public hospital setting does not support a genetic or biologic basis for observed racial/ethnic differences.
Patient preference is another possible mechanism by which disparities may occur(33
). In the 2003 report, Unequal Treatment: Confronting Racial and Ethnic Disparities in Health Care
, the Institute of Medicine notes that patient preferences based on inaccurate understanding may be a source of racial disparity in care(35
). Constantinescu, et al. found that African Americans with RA were more risk-averse than Whites(34
). Difference in rates of biologic use across settings may also be a reflection of insurance coverage for biologics, a patient’s ability to pay, or of sociodemographic differences within all racial/ethnic groups between patients at the university and county hospital clinics, such that university hospital clinic patients have increased access to subspecialty care and fewer barriers to obtaining biologic agents (e.g., lower rates of latent tuberculosis). Despite the fact that we found large differences in rates of biologic agents across clinic sites (more than twice the rate of use for all subgroups at the university hospital compared to the county clinic), differences in outcomes persisted in multivariable models controlling for current treatment, indicating that variation in preferences or access cannot fully explain the differences in RA outcomes.
Our study parallels findings from the United Kingdom where patients from socially deprived areas and those with lower individual-level SES had higher disease activity and poorer function(11
). In a U.S. study, Bruce et al. observed worse function, pain and global health among Hispanics and African Americans compared to non-Hispanic Whites but only found statistically significant differences in pain after adjusting for age, gender, education, disease duration, comorbidities, and DMARDs(13
). In contrast to our study, that sample was predominantly White and patients were cared for in numerous community and university clinics. A study by Yazici et al examined racial and ethnic differences in baseline clinical status measures in 118 DMARD-naive subjects with early RA (<3 years) at one site(14
); Hispanics had statistically significantly higher (worse) HAQ scores, longer morning stiffness and higher psychological distress scores compared to African Americans and Whites adjusting for age and disease duration. While our study found racial/ethnic differences in patient-reported measures of function and patient global assessments similar to the study by Yazici, we also saw differences in ESR and the DAS-28. Therefore we conclude that racial/ethnic differences are observed in “objective” outcomes beyond those that are patient-reported. Prior examples of racial/ethnic differences in ESR have been reported. Del Rincon et al. found higher ESR levels in Hispanic and African American RA patients compared to non-Hispanic Whites from multiple clinical sites in Texas(32
Our study has several limitations. The cross-sectional design does not allow inferences regarding causation. If minority RA patients with milder disease tend not to seek or receive subspecialty care, this could lead to an overestimation of disparities. By contrast, the public hospital clinic we studied is staffed with interpreters and routinely utilizes drug-assistance programs for biologic therapies, which may mitigate disparities that could occur in other settings. Our co-variates did not include potential confounders related to SES, including prior access to care, insurance status, and income. However, our main measure of SES was education level, previously shown to be a more reliable measure of long-term SES as it remains relatively constant throughout adult life(38
). Given the main findings of our study, that Whites at the university hospital clinic had significantly lower disease activity and better function than non-Whites, this may be explained in part by higher educational attainment among Whites at the university. The pattern of educational attainment by race/ethnicity was the same at both clinic sites with Whites having higher educational levels than other race/ethnic groups. We therefore performed additional analyses which categorized education into four levels rather than three, and then further subdivided the top category of BA degree or higher into college graduate and post-graduate education. The results presented herein were not affected by either change. Due to the limited number of non-Hispanic white subjects at the county hospital (n=19), this study may have been underpowered to detect a true difference between the racial and ethnic groups at the county hospital. It should be noted however, that the relationship between the other sociodemographic variables of language and immigrant status (which included greater numbers of subjects in each category) with disease activity and function at the county hospital were also not significant which is consistent with the race/ethnicity finding. Another potential limitation is that given the cross-sectional design we are unable to account for variation in disease activity among patients over time (early, potentially un- or undertreated vs. later disease, better controlled) and whether that may differ based on the length of time treated at either clinic. However, disease duration is included in the multivariable models, and descriptively, the majority of patients had longer disease duration with only 15% having less than 12 months and 50% with disease duration greater than seven years. Lastly, we cannot determine whether disparities resulted from problems with delays in diagnosis or initial treatment, access, or self-management (e.g., adherence).
By including a diverse sample of patients who received care from a uniform set of university-employed rheumatologists, this study confirms prior research by demonstrating that racial/ethnic disparities exist in patient-reported and “objective” outcomes (e.g., inflammatory markers). It also extends prior research by demonstrating that disparities exist for Asians/Pacific Islanders as well as for immigrants and non-English speakers, and that clinic setting/context can influence overall disease severity and modify the relationships between race/ethnicity and RA outcomes. The next steps will be to explore whether these across-clinic differences occur as a result of differences in recognition, access, and quality of care in early disease, from the stress associated with disadvantaged circumstances, from challenges in self-management or communication barriers once specialty care is underway, or from some combination of these factors. An additional challenge is to discover how characteristics of patients, providers, and local policies associated with different healthcare systems can affect outcomes and either contribute to or eliminate disparities.