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More yeast, more problems?: reevaluating the role of Malassezia in seborrheic dermatitis

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Abstract

Seborrheic dermatitis (SD) is an inflammatory skin disorder and eczema subtype increasingly recognized to be associated with significant physical, psychosocial, and financial burden. The full spectrum of SD, including dandruff localized to the scalp, is estimated to affect half of the world’s population. Despite such high prevalence, the exact etiopathogenesis of SD remains unclear. Historically, many researchers have theorized a central, causative role of Malassezia spp. based on prior studies including the proliferation of Malassezia yeast on lesional skin of some SD patients and empiric clinical response to antifungal therapy. However, upon closer examination, many of these findings have not been reproducible nor consistent. Emerging data from novel, targeted anti-inflammatory therapeutics, as well as evidence from genome-wide association studies and murine models, should prompt a reevaluation of the popular yeast-centered hypothesis. Here, through focused review of the literature, including laboratory studies, clinical trials, and expert consensus, we examine and synthesize the data arguing for and against a primary role for Malassezia in SD. We propose an expansion of SD pathogenesis and suggest reframing our view of SD to be based primarily on dysregulation of the host immune system and skin epidermal barrier, like other eczemas.

Key points

  1. 1.

    Seborrheic dermatitis is a common inflammatory skin disease with poorly understood pathogenesis.

  2. 2.

    Seborrheic dermatitis is commonly considered to be a disease resulting from Malassezia yeast proliferation, though studies supporting this are limited and inconsistent.

  3. 3.

    Emerging evidence suggests that immune dysregulation and skin barrier function are likely central to SD pathogenesis, with Malassezia functioning as a secondary, associated factor

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Data availability

The authors confirm that the data supporting the findings of this study are available within the article.

Abbreviations

SD:

Seborrheic dermatitis

TCI:

Topical calcineurin inhibitors

PDE-4:

Phosphodiesterase-4

cAMP:

Cyclic adenosine monophosphate

IGA:

Investigator’s global assessment

FDA:

Food and Drug Administration

NDA:

New Drug Application

PDUFA:

Prescription Drug User Fee Act

GWAS:

Genome-wide association study

ZNF750:

Zinc finger protein 750

MPZL3:

Myelin protein zero-like 3

Th17:

Type 17T helper cell

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Funding

RC received funding from NIH grant number K12 HS026385.

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RC had full access to all the data in the study and takes responsibility for the integrity of the data and accuracy of the data analysis. Study concept and design: RC. Acquisition of Data: RC, CHC. Analysis and interpretation of data: RC, CHC. Drafting of the manuscript: RC, CHC. Critical revision of the manuscript for important intellectual content: RC, CHC. Statistical analysis: RC, CHC.

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Correspondence to Raj Chovatiya.

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Conflict of interests

RC has served as an advisory board member, consultant, and/or investigator for AbbVie, Apogee Therapeutics, Arcutis, Argenx, ASLAN Pharmaceuticals, Beiersdorf, Boehringer Ingelheim, Bristol Myers Squibb, Cara Therapeutics, Dermavant, Eli Lilly and Company, FIDE, Galderma, Genentech, Incyte, Janssen, LEO Pharma, L’Oréal, Nektar Therapeutics, Novan, Inc., Opsidio, Pfizer Inc., Regeneron, RAPT, Sanofi, and UCB. CHC has no conflicts to disclose.

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Chang, C.H., Chovatiya, R. More yeast, more problems?: reevaluating the role of Malassezia in seborrheic dermatitis. Arch Dermatol Res 316, 100 (2024). https://doi.org/10.1007/s00403-024-02830-7

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