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Association of Malassezia to Atopic Dermatitis

  • Fungal Infections of Skin and Subcutaneous (A Bonifaz, Section Editor)
  • Published:
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Abstract

Purpose of Review

Atopic dermatitis (AD) is a common chronic, inherited, relapsing, inflammatory skin condition. A multifactorial etiology has been postulated, including genetic and immunological factors, impaired skin barrier function and environmental triggers, all of them are relevant in the pathogenesis. Malassezia spp. is the most common fungi of the skin microbiome. Most of the studies comparing the skin colonization with Malassezia spp. in healthy people and AD patients did not show difference between both groups. This review aims to show the studies carried out in this regard and the reported evidence about the role of Malassezia spp. in the pathogenesis of AD.

Recent Findings

The rate of IgE-mediated sensitization Malassezia spp. is very high in AD patients, mainly in adult patients and in patients with involvement in the head and neck. Different mechanisms have been postulated to explain the interaction of Malassezia spp. with human skin cells and immune cells and how its interaction contributes to the inflammation process in AD. Systemic and topical azole antifungals have been used with doubtful results showing beneficial effects in some AD patients.

Summary

There is no clear explanation for the high frequency of Malassezia spp. sensitization in AD patients in relation with healthy individuals. Further research is necessary to determine the specific role of Malassezia in AD and the indication for the use of antifungals in this disease.

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Correspondence to Mirna Toledo-Bahena.

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This article does not contain any studies with human or animal subjects performed by any of the authors.

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This article is part of the Topical Collection on Fungal Infections of Skin and Subcutaneous Tissue

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Valencia-Herrera, A., Toledo-Bahena, M., Ramírez-Cortés, E. et al. Association of Malassezia to Atopic Dermatitis. Curr Fungal Infect Rep 12, 201–206 (2018). https://doi.org/10.1007/s12281-018-0330-0

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  • DOI: https://doi.org/10.1007/s12281-018-0330-0

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