Department of Dermatology, Clínica Dermatológica Multidisciplinar Dermik, Barcelona, Spain.
Department of Dermatology, Hospital Clínic de Barcelona, Universitat de Barcelona, Barcelona, Spain.
J Cosmet Dermatol. 2023 Jun;22(6):1919-1928. doi: 10.1111/jocd.15726. Epub 2023 Mar 22.
Acne pathophysiology includes a complex interaction among inflammatory mediators, hyperseborrhea, alteration of keratinization and follicular colonization by Propionibacterium acnes.
To describe the impact of the exposome on acne and how photoprotection can improve outcomes.
A narrative review of the literature was carried out; searches with Google Scholar and Pubmed from January 1992 to November 2022 were performed. The keywords used were "acne," "sunscreens," "photoprotection," "cosmetics," "cosmeceuticals," "pathogenesis," "etiology," "exposome," "sunlight," "stress," "lack of sleep," "diet," "postinflammatory hyperpigmentation," "pollution," "exposome," "ultraviolet radiation," and "visible light."
Environmental factors such as solar radiation, air pollution, tobacco consumption, psychological stress, diverse microorganisms, nutrition, among others, can trigger or worsen acne. Solar radiation can temporarily improve lesions. However, it can induce proinflammatory and profibrotic responses, and produce post-inflammatory hyperpigmentation and/or post-inflammatory erythema. While photoprotection is widely recommended to acne patients, only four relevant studies were found. Sunscreens can significantly improve symptomatology or enhance treatment and can prevent post-inflammatory hyperpigmentation. Furthermore, they can provide camouflage and improve quality of life. Based on acne pathogenesis, optimal sunscreens should have emollient, antioxidant and sebum controlling properties.
The exposome and solar radiation can trigger or worsen acne. UV light can induce post-inflammatory hyperpigmentation/erythema, and can initiate flares. The use of specifically formulated sunscreens could enhance adherence to topical or systemic therapy, camouflage lesions (tinted sunscreens), decrease inflammation, and reduce the incidence of post-inflammatory hyperpigmentation/erythema.
痤疮的发病机制包括炎症介质、皮脂分泌过多、角蛋白角化改变以及痤疮丙酸杆菌在毛囊内定植等多种因素的复杂相互作用。
描述外显子组对痤疮的影响以及光防护如何改善痤疮的结局。
对文献进行了叙述性综述；在 Google Scholar 和 Pubmed 上进行了从 1992 年 1 月至 2022 年 11 月的检索，使用的关键词为“痤疮”、“防晒霜”、“光防护”、“化妆品”、“药妆品”、“发病机制”、“病因学”、“外显子组”、“日光”、“压力”、“睡眠不足”、“饮食”、“炎症后色素沉着”、“污染”、“外显子组”、“紫外线辐射”和“可见光”。
环境因素如太阳辐射、空气污染、烟草使用、心理压力、多种微生物、营养等都可能引发或加重痤疮。太阳辐射可以暂时改善皮损，但也会引起促炎和促纤维化反应，并导致炎症后色素沉着和/或炎症后红斑。虽然广泛建议痤疮患者进行光防护，但仅发现了四项相关研究。防晒霜可以显著改善症状或增强治疗效果，并预防炎症后色素沉着。此外，它们还可以提供伪装效果，改善生活质量。根据痤疮发病机制，理想的防晒霜应具有保湿、抗氧化和控制皮脂的特性。
外显子组和太阳辐射可以引发或加重痤疮。紫外线会引起炎症后色素沉着/红斑，并可能引发病情加重。使用特定配方的防晒霜可以增强对局部或系统治疗的依从性，伪装皮损（有色防晒霜），减轻炎症，并减少炎症后色素沉着/红斑的发生。
