Possible protective effect of hydroxychloroquine on delaying the occurrence of integument damage in lupus: LXXI, data from a multiethnic cohort.

Abstract

To determine the features predictive of time to integument damage in patients with systemic lupus erythematosus (SLE) from a multiethnic cohort (LUpus in MInorities, NAture versus nurture [LUMINA]). LUMINA SLE patients (n = 580) age > or =16 years, with a disease duration of < or =5 years at baseline (T0), of African American, Hispanic, and Caucasian ethnicity were studied. Integument damage was defined per the Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (scarring alopecia, extensive skin scarring, and skin ulcers lasting at least 6 months); factors associated with time to its occurrence were examined by Cox proportional univariable and multivariable (main model) hazards regression analyses. Two alternative models were also examined: in model 1, all patients, regardless of when integument damage occurred (n = 94), were included; in model 2, a time-varying approach (generalized estimating equation) was employed. Thirty-nine (6.7%) of 580 patients developed integument damage over a mean +/- SD total disease duration of 5.9 +/- 3.7 years, and were included in the main multivariable regression model. After adjusting for discoid rash, nailfold infarcts, photosensitivity, and Raynaud's phenomenon (significant in the univariable analyses), disease activity over time (hazard ratio [HR] 1.17, 95% confidence interval [95% CI] 1.09-1.26) was associated with a shorter time to integument damage, whereas hydroxychloroquine use (HR 0.23, 95% CI 0.12-0.47) and Texan-Hispanic (HR 0.35, 95% CI 0.14-0.87) and Caucasian ethnicities (HR 0.37, 95% CI 0.14-0.99) were associated with a longer time. Results of the alternative models were consistent with those of the main model, although in model 2, the association with hydroxychloroquine was not significant. Our data indicate that hydroxychloroquine use is possibly associated with a delay in integument damage development in patients with SLE.