Open AccessLeukocyte Telomere Length and Childhood Onset of Systemic Lupus Erythematosus in the Black Women's Experiences Living with Lupus Study
Author(s) -
Bridges John,
Chung Kara W.,
Martz Connor D.,
Smitherman Emily A.,
Drenkard Cristina,
Wu Calvin,
Lin Jue,
Lim S. Sam,
Chae David H.
Publication year - 2022
Publication title -
acr open rheumatology
Language(s) - English
Resource type - Journals
ISSN - 2578-5745
DOI - 10.1002/acr2.11411
Subject(s) - medicine , systemic lupus erythematosus , confidence interval , lupus erythematosus , disease , age of onset , pediatrics , demography , immunology , antibody , sociology
Objective The study objective was to compare leukocyte telomere length (LTL) among patients with systemic lupus erythematosus (SLE) diagnosed in childhood versus adulthood. Methods Data are from the Black Women's Experiences Living with Lupus (BeWELL) study. Multivariable linear regression analyses that examined childhood diagnosis of SLE (diagnosed before 18 years of age), age, and their interaction in relationship to LTL were conducted, adjusting for a range of demographic, socioeconomic, and health‐related covariates. Results The total analytic sample size was 415. Forty participants (9.6%) were diagnosed in childhood. There was no main effect of childhood diagnosis on LTL (b = 0.007; 95% confidence interval [CI]: −0.089 to 0.103). However, the interaction between age and childhood diagnosis was significant (b = −0.008; 95% CI: −0.016 to −0.001), indicating a steeper inverse association between age and LTL among those diagnosed in childhood compared with those diagnosed in adulthood. This interaction remained statistically significant ( P = 0.024) after controlling for disease duration measured dichotomously (less than 10 years vs. 10 years or more); it was marginally significant ( P = 0.083) when controlling for disease duration measured continuously. Conclusion This cross‐sectional analysis suggests that Black women with childhood‐onset SLE may undergo accelerated LTL shortening compared with their adult‐onset counterparts. This relationship persisted even after controlling for differences in SLE damage and disease duration. These findings inform research on immunosenescence mechanisms of SLE.