during an AD flare.44 However, potent topical corticosteroids are commonly avoided on the face due to deleterious side effects, contributing to poorer disease control of facial eczema compared with body eczema.45 Furthermore, steroid withdrawal can follow prolonged inappropriate use of moderate-to-potent topical steroids primarily in the face and genital regions.29 Topical steroid withdrawal following discontinuation of topical steroids can lead to a rebound dermatitis, which has been confused with head and neck dermatitis.29 This is important to consider when trying to manage facial eczema with topical steroids.
The management of facial vs body eczema not only contributes to their differences but is important to recognize when suggesting treatment recommendations to patients. While gentle skin care is important in the management of all eczema, it is especially important in facial eczema when options for treatment with high potency topical steroids are more limited. Facial eczema treatments can focus on skin hydration, including use of a towel gently draped over the head and neck in the bathtub and prioritizing baths over showers to better hydrate the skin.25 Non-steroid topicals like calcineurin inhibitors have been shown to be a safe alternative to topical steroids in the treatment of sensitive sites such as the head and neck.46 A double-blinded randomized controlled trial assessing the safety and efficacy of pimecrolimus cream 1% in patients with AD on the face and neck who were dependent or intolerant of topical steroids demonstrated that it was effective at clearing facial AD, especially in eyelid dermatitis, and additionally helped to reverse skin thinning.47
The management of facial vs body eczema not only contributes to their differences but is important to recognize when suggesting treatment recommendations to patients. While gentle skin care is important in the management of all eczema, it is especially important in facial eczema when options for treatment with high potency topical steroids are more limited. Facial eczema treatments can focus on skin hydration, including use of a towel gently draped over the head and neck in the bathtub and prioritizing baths over showers to better hydrate the skin.25 Non-steroid topicals like calcineurin inhibitors have been shown to be a safe alternative to topical steroids in the treatment of sensitive sites such as the head and neck.46 A double-blinded randomized controlled trial assessing the safety and efficacy of pimecrolimus cream 1% in patients with AD on the face and neck who were dependent or intolerant of topical steroids demonstrated that it was effective at clearing facial AD, especially in eyelid dermatitis, and additionally helped to reverse skin thinning.47
CONCLUSIONS
This article highlights the multifactorial pathophysiology of AD and its contribution to the differences between facial and body eczema. Exposure to environmental triggers and host factors results in alterations in the microbiome and skin barrier function. Despite the rising prevalence of AD, there is little research investigating the causative factors contributing to the difference in facial and body eczema. The face and the body not only differ topographically, but also differ in their environmental exposures. Both of these factors contribute to different levels of skin barrier disruption and microbiome alteration.
Biological and environmental factors account for the differences in facial and body eczema (Figure 1). The topographical diversity of the skin results in differing regional environments and therefore the organisms that can reside in the regions. The face and the body are exposed to differing levels of aeroallergens, UV radiation, and personal hygiene and cosmetic products.
Although it is important to recognize the conditions that trigger AD, and how these conditions differ based on location, it is also important to focus attention on preserving the skin microbiome and skin barrier despite such exposures. With increased evidence of the importance of commensal organisms in maintaining structural integrity of the skin, future research should investigate the role of probiotics, both topical and oral, in treatment for both facial and body eczema. In addition to supporting the development of a robust microbiome at the site of AD, further research is needed on maintaining the integrity of the skin barrier through the use of products to replenish NMF levels. Understanding differences in structure and environmental exposures can be used in the management of facial vs body eczema, as well as for the development of new AD treatments.
Biological and environmental factors account for the differences in facial and body eczema (Figure 1). The topographical diversity of the skin results in differing regional environments and therefore the organisms that can reside in the regions. The face and the body are exposed to differing levels of aeroallergens, UV radiation, and personal hygiene and cosmetic products.
Although it is important to recognize the conditions that trigger AD, and how these conditions differ based on location, it is also important to focus attention on preserving the skin microbiome and skin barrier despite such exposures. With increased evidence of the importance of commensal organisms in maintaining structural integrity of the skin, future research should investigate the role of probiotics, both topical and oral, in treatment for both facial and body eczema. In addition to supporting the development of a robust microbiome at the site of AD, further research is needed on maintaining the integrity of the skin barrier through the use of products to replenish NMF levels. Understanding differences in structure and environmental exposures can be used in the management of facial vs body eczema, as well as for the development of new AD treatments.
DISCLOSURES
The authors report no conflicts of interest.
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5. Furue M, Iida K, Imaji M, et al. Microbiome analysis of forehead skin in patients with atopic dermatitis and healthy subjects: implication of Staphylococcus and Corynebacterium. J Dermatol. 2018;45(7):876-877. doi: 10.1111/1346-8138.14486. PMID: 29971837.
6. Clausen ML, Agner T, Lilje B, et al. Association of disease severity with skin microbiome and filaggrin gene mutations in adult atopic dermatitis. JAMA Dermatol. 2018;154(3):293-300. doi: 10.1001/jamadermatol.2017.5440. PMID: 29344612; PMCID: PMC5885821.
7. Reiger M, Schwierzeck V, Traidl-Hoffmann C. Atopisches ekzem und mikrobiom [atopic eczema and microbiome]. Hautarzt. 2019;70(6):407-415. German. doi: 10.1007/s00105-019-4424-6. PMID: 31111169.
8. Kaesler S, Volz T, Skabytska Y, et al. Toll-like receptor 2 ligands promote chronic atopic dermatitis through IL-4-mediated suppression of IL-10. J Allergy Clin Immunol. 2014;134(1):92-9. doi: 10.1016/j.jaci.2014.02.017. Epub 2014 Apr 1. PMID: 24698321.
9. Francuzik W, Franke K, Schumann RR, et al. Propionibacterium acnes abundance correlates inversely with Staphylococcus aureus: data from atopic dermatitis skin microbiome. Acta Derm Venereol. 2018;27;98(5):490- 495. doi: 10.2340/00015555-2896. PMID: 29379979.
10. Zeng J, Dou J, Gao L, et al. Topical ozone therapy restores microbiome diversity in atopic dermatitis. Int Immunopharmacol. 2020;80:106191. doi: 10.1016/j.intimp.2020.106191. Epub 2020 Jan 24. PMID: 31986325.
11. Mukherjee S, Mitra R, Maitra A, et al. Sebum and hydration levels in specific regions of human face significantly predict the nature and diversity of facial skin microbiome. Sci Rep. 2016;6:36062. doi: 10.1038/srep36062. PMID: 27786295; PMCID: PMC5081537.
12. Paller AS, Kong HH, Seed P, et al. The microbiome in patients with atopic dermatitis [published correction appears in J Allergy Clin Immunol. 2019;143(4):1660]. J Allergy Clin Immunol. 2019;143(1):26-35. doi:10.1016/j. jaci.2018.11.015
13. Grice EA, Segre JA. The skin microbiome. Nat Rev Microbiol. 2011;9(4):244- 53. doi: 10.1038/nrmicro2537. Erratum in: Nat Rev Microbiol. 2011;9(8):626. PMID: 21407241; PMCID: PMC3535073.
14. Groscurth P. Anatomy of sweat glands. Curr Probl Dermatol. 2002; 30:1-9. doi: 10.1159/000060678. PMID: 12471693.
15. Akaza N, Akamatsu H, Takeoka S, et al. Malassezia globosa tends to grow actively in summer conditions more than other cutaneous Malassezia species. J Dermatol. 2012;39(7):613-6. doi: 10.1111/j.1346-8138.2011.01477.x. Epub 2012 Jan 10. PMID: 22229642.
