Article Text
Abstract
Background Systemic lupus erythematosus (SLE) disproportionately affects racial/ethnic minorities and is an independent risk factor for pneumonia, infections, renal disease and cardiovascular diseases (CVD). There are also racial/ethnic differences in these common comorbidities. There is limited understanding of how much inequality or heterogeneity SLE confers independently of the underlying disease pathways of comorbidities between race/ethnic groups. We examined the patterns, strength and direction of the risk of comorbidities in race/ethnic groups with SLE compared to controls. We hypothesized that those with SLE will have increased risk of comorbidities and that these associations will be strongest for racial minorities and weakest for non-Hispanic whites (NHW).
Methods We defined a cohort using electronic health records data (2005–2016) from a large healthcare organization in California serving patients of diverse racial/ethnic backgrounds. The eligible population included SLE patients and age-sex-race/ethnicity matched non-SLE patients (≥18 years of age). SLE diagnosis was the primary exposure defined using ICD9: 710.0 and ICD10: M32.1, M32.8, and M32.9. The following outcomes were identified: pneumonia, infections, renal disease and CVD. For each racial/ethnic group, we calculated the proportion of incident comorbidities among SLE cases and controls, and then built adjusted logistic regression models for each outcome with SLE as the exposure.
Results We identified 1,290 SLE cases and 12 900 controls. The median age at baseline was 43 years and 92% of the cohort was female. Among SLE cases, 38% were NHW, 13% were Hispanic, 4% were Black, and 25% were Asian/Pacific Islander. Compared to controls, SLE cases had higher incidence of pneumonia (32% vs 18%), infections (46% vs 26%), renal disease (16% vs 3%) and CVD (45% vs 22%). The association persisted with odds ratio (OR) of 1.5 to 3, after adjusting for confounders (p<0.01). In subgroups analysis, ORs were similar across all racial/ethnic groups. We found no evidence for heterogeneity in the patterning of increased odds of the comorbidities between race/ethnic groups. For example, NHW, Blacks, Hispanics and Asians with SLE had between 2–3 times increased odds of CVD compared to controls.
Conclusions Our findings suggest that SLE similarly increases the risk of pneumonia, infections, renal disease and cardiovascular diseases (CVD) across racial/ethnic groups. Understanding the reasons for the lack of heterogeneity is important for targeting preventative interventions among patients with SLE.
Acknowledgements The authors would like to gratefully acknowledge the National Heart, Lung, and Blood Institute for funding this research.