Joy Wan1, Nandita Mitra2, Ole J Hoffstad3, Albert C Yan4, David J Margolis5. 1. Department of Dermatology, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania; Section of Pediatric Dermatology, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania. Electronic address: joywan@pennmedicine.upenn.edu. 2. Department of Biostatistics, Epidemiology and Informatics, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania; Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania. 3. Department of Biostatistics, Epidemiology and Informatics, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania. 4. Section of Pediatric Dermatology, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania. 5. Department of Dermatology, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania; Department of Biostatistics, Epidemiology and Informatics, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania; Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania.
Abstract
BACKGROUND: Wide variation exists in the timing of atopic dermatitis (AD) disease onset among children. Distinct trajectories of early-onset, mid-onset, and late-onset AD have been previously described. OBJECTIVE: To evaluate longitudinal disease control and persistence with respect to age at onset of AD. METHODS: A cohort study was performed using the Pediatric Eczema Elective Registry, a prospective observational cohort of subjects with childhood-onset AD. AD control and persistence were assessed biannually for up to 10 years. RESULTS: A total of 8015 subjects with 41,934 person-years of follow-up were included. In longitudinal analyses using generalized linear latent and mixed modeling, older age at onset of AD was associated with better disease control and less-persistent AD. For each additional year of age at onset of AD, the adjusted odds ratios for poorer AD control and for persistent AD were 0.93 (95% confidence interval, 0.91-0.94) and 0.84 (95% confidence interval, 0.80-0.88), respectively. Differences in AD control and persistence among subjects with early-, mid-, and late-onset AD were most pronounced from early adolescence onward. LIMITATIONS: Misclassification bias may arise from using self-reported data on age at onset. Attrition and missing data in longitudinal studies may introduce bias. CONCLUSION: Early-, mid-, and late-onset pediatric AD appear to be clinically distinct subtypes of the disease.
BACKGROUND: Wide variation exists in the timing of atopic dermatitis (AD) disease onset among children. Distinct trajectories of early-onset, mid-onset, and late-onset AD have been previously described. OBJECTIVE: To evaluate longitudinal disease control and persistence with respect to age at onset of AD. METHODS: A cohort study was performed using the Pediatric Eczema Elective Registry, a prospective observational cohort of subjects with childhood-onset AD. AD control and persistence were assessed biannually for up to 10 years. RESULTS: A total of 8015 subjects with 41,934 person-years of follow-up were included. In longitudinal analyses using generalized linear latent and mixed modeling, older age at onset of AD was associated with better disease control and less-persistent AD. For each additional year of age at onset of AD, the adjusted odds ratios for poorer AD control and for persistent AD were 0.93 (95% confidence interval, 0.91-0.94) and 0.84 (95% confidence interval, 0.80-0.88), respectively. Differences in AD control and persistence among subjects with early-, mid-, and late-onset AD were most pronounced from early adolescence onward. LIMITATIONS: Misclassification bias may arise from using self-reported data on age at onset. Attrition and missing data in longitudinal studies may introduce bias. CONCLUSION: Early-, mid-, and late-onset pediatric AD appear to be clinically distinct subtypes of the disease.
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