Abstract

Atopic dermatitis (AD) is associated with allergic comorbidities, such as asthma, allergic rhinitis (AR), and allergic contact dermatitis (ACD). The etiology of keloid is largely unknown; however, AD and keloid share inflammatory pathways characterized by T-helper cell 2 cytokines and increased dermal fibroblast activity. The prevalence of keloids has been reported to increase in patients with AD, but it remains controversial. This study aimed to estimate the prevalence of keloids in patients with AD, and compare it with the prevalence of other comorbidities of AD. We assessed the Korean National Health Information Database and medical records including coexisting asthma, AR, and ACD. Single and multiple logistic regression models were created for keloids and each allergic disease. The prevalence of keloids was higher in the AD group than in the control group. Among patients with AD, adolescents and adults had a higher prevalence of keloids than infants and children. The risk of keloids was high with AD alone, and coexisting asthma significantly increased the risk. Similarly, the risk of keloids was higher in AR associated with AD and ACD associated with AD than in AD alone. Thus, among Koreans, patients with AD have a higher risk of keloid development, with coexisting allergic diseases increasing the risk.

Highlights

  • Atopic dermatitis (AD) is associated with allergic comorbidities, such as asthma, allergic rhinitis (AR), and allergic contact dermatitis (ACD)

  • In patients with AD, 26.01% of patients were younger than 5 years, and 51.88% were younger than 20 years of age

  • Our results demonstrate that the prevalence of keloids increases with coexisting allergic diseases, such as asthma, AR, and ACD

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Summary

Introduction

Atopic dermatitis (AD) is associated with allergic comorbidities, such as asthma, allergic rhinitis (AR), and allergic contact dermatitis (ACD). Among Koreans, patients with AD have a higher risk of keloid development, with coexisting allergic diseases increasing the risk. The mechanism underlying the pathological development of keloids is largely unknown; it is mainly characterized by an overproduction of extracellular matrix and high activity of fibroblasts during the inflammatory and remodeling phases of scar formation, resulting in the excessive accumulation of c­ ollagen[4,5]. These processes are observed in fibroblasts among patients with ­AD6. The severity of AD was associated with a higher prevalence of comorbid allergic disorders and increased severity of ­comorbidities[10]

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