The independence and stability of socioeconomic predictors of morbidity in systemic lupus erythematosus
Article first published online: 9 DEC 2005
Copyright © 1995 American College of Rheumatology
Arthritis & Rheumatism
Volume 38, Issue 2, pages 267–273, February 1995
How to Cite
Karlson, E. W., Daltroy, L. H., Lew, R. A., Wright, E. A., Partridge, A. J., Roberts, W. N., Stern, S. H., Straaton, K. V., Wacholtz, M. C., Grosflam, J. M. and Liang, M. H. (1995), The independence and stability of socioeconomic predictors of morbidity in systemic lupus erythematosus. Arthritis & Rheumatism, 38: 267–273. doi: 10.1002/art.1780380217
- Issue published online: 9 DEC 2005
- Article first published online: 9 DEC 2005
- Manuscript Accepted: 1 SEP 1994
- Manuscript Received: 11 MAR 1994
- NIH. Grant Numbers: AR-36308, AR-39921, AI-07306, AR-07530
Objective. We studied the relationship between systemic lupus erythematosus (SLE) morbidity and socioeconomic status (SES) at 5 centers.
Methods. Ninety-nine patients who met American College of Rheumatology criteria for SLE were randomly sampled at each center, balancing by race and insurance status. Subjects were interviewed for current and past SES factors, such as insurance, occupation, employment, education, and income. SLE disease activity was measured by the SLE Activity Measure (SLAM).
Result. Higher education, private insurance/Medicare, and higher income were associated with less disease activity at diagnosis. Controlling for SES, race, and center, the best predictors of less active disease at diagnosis were private insurance/Medicare (P = 0.002) and higher education (P = 0.007). From the time of diagnosis to the study visit (mean 3.5 years), insurance, income, and employment status changed for a significant number of subjects (37%, 16%, and 21%, respectively).
Conclusion. Private insurance or Medicare and higher education are associated with less active disease at diagnosis of SLE. Health insurance, income, and employment status are unstable measures of socio-economic status and may explain the variability in conclusions of previous studies on the role of SES in SLE.