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Research Articles

Clinical features and biomarker differences of severe intrinsic and extrinsic atopic dermatitis

ORCID Icon, ORCID Icon & ORCID Icon
Pages 97-103 | Received 08 Aug 2023, Accepted 27 Dec 2023, Published online: 23 Jan 2024
 

Abstract

Objectives

Atopic dermatitis (AD) can be classified into intrinsic AD(IAD) and extrinsic AD(EAD). However, the differences in clinical features and pathogenesis between these two subtypes of AD are currently unclear. This study aimed to analyse the differences in clinical features and peripheral blood biomarkers between Chinese patients with severe IAD and EAD in order to elucidate the physiopathogenesis of AD.

Materials and methods

A total of 316 hospitalised patients definitively diagnosed with severe AD were included in this study. There were 72 cases of severe IAD and 244 cases of severe EAD. The clinical features of the patients were recorded in details. Serum total IgE, IgA, IgG, IgM, complementC3/C4, peripheral blood cell counts, lactate dehydrogenase (LDH), C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), IL-2R, IL-6, IL-8, and TNF-α in AD patients and 60 age-matched healthy controls were analysed. IAD and EAD had similar severity/Scoring Atopic Dermatitis (SCORAD) scores.

Results

Compared with healthy controls, IAD patients had significantly higher total IgE, eosinophils, monocytes, LDH, CRP, IL-2R, IL-6, IL-8 and TNF-α, and lower IgM and C4. EAD patients had significantly higher total IgE, IgA, eosinophils, white blood cell (WBC) counts, neutrophils, monocytes, basophils, LDH, CRP, IL-2R, IL-6, IL-8, TNF-α and lower IgM than healthy controls. IAD patients had a higher percentage of rural/urban living and female/male, a shorter course of disease and lower total IgE, eosinophils, WBC counts, neutrophils, monocytes, basophils, LDH, IgG and C4 than EAD patients. SCORAD scores, eosinophils, LDH expression levels increased with total IgE uniquely in patients with EAD.

Conclusions

IAD and EAD exhibit specific clinical features and molecular changes. IAD has a more complex physiopathogenesis, and deserves further investigation.

Acknowledgements

The authors thank Professor Yunhua Deng, for his very valuable support. In memory of our teacher, colleague, and friend.

Ethical approval

This study was approved by the ethics committee of Tongji Hospital (TJ-IRB20221280). All patients or their parents provided written informed consent.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

The Knowledge Innovation Project of the Wuhan Science and Technology Bureau, Grant/Award Number: 2022020801020528. Project of the Beijing Science and Innovation Foundation for Medical Development, Grant/Award Number: KC2022-JX-0165.

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