Kurokawa Ichiro, Layton Alison M, Ogawa Rei
Department of Dermatology, Meiwa Hospital, 4-31, Agenaruo-cho, Nishinomiya, Hyogo, 663-8186, Japan.
Department of Dermatology, Harrogate and District Foundation Trust, Lancaster Park Road, Harrogate, HG2 7SX, UK.
Dermatol Ther (Heidelb). 2021 Aug;11(4):1129-1139. doi: 10.1007/s13555-021-00552-6. Epub 2021 Jun 11.
Previous approaches to acne management have focused on the four main factors implicated in acne, namely, androgen-mediated sebogenesis (considered integral to acne), hyperkeratinization, colonization with Cutibacterium acnes, and inflammation related to both innate and adaptive mechanisms. Recent advances have facilitated potential novel approaches to acne management, as the pathophysiology and the immunological aspects related to acne and wound healing have evolved. Particular targets that have been shown to be closely involved in acne pathophysiology and wound healing include interleukin (IL)-1β, IL-17, IL-23, and tumor necrosis factor alpha (TNFα). Biological antibodies targeting IL-1β, IL-17, IL-23, and TNFα could provide novel approaches for treating severe acne and related disorders. Acne is primarily a disease associated with sebogenesis. Monosaturated free acids are important components. Insulin growth factor 1 (IGF-1) promotes the proliferation and differentiation of sebocytes and IL-1β. Research into the microbiome may also provide insights into potential future therapeutic options for acne. Scars, both atrophic and hypertrophic, are common sequelae to acne. Risk factors associated with the development of acne scars include genetic, systemic, local, and lifestyle factors. Pro-inflammatory cytokines have been shown to play a crucial role in the development of acne-induced hypertrophic scars. Treatment for extensive inflammatory keloid scarring is limited. Surgery and postoperative radiotherapy are two possible options. Transforming growth factor-β (TGFβ), IL-6, matrix metalloproteinase (MMP), IGF-1, and B cells are found in keloid or hypertrophic scar tissues. Biological antibodies targeting these cytokines may be a potential strategy for the prevention and treatment of this type of scar in the future. Future treatment for acne should embrace approaches that target the main etiological factors of acne. In particular, specific emphasis on aggressive treatment in the acute inflammatory phase to reduce the likelihood of scarring and other clinical sequelae, such as pigmentary changes would be highly desirable. Treatment for established acne-induced sequelae should also be considered.
以往的痤疮治疗方法主要集中在痤疮涉及的四个主要因素上，即雄激素介导的皮脂生成（被认为是痤疮的一个主要因素）、过度角化、痤疮丙酸杆菌定植以及与先天性和适应性机制相关的炎症。随着痤疮病理生理学以及与痤疮和伤口愈合相关的免疫学方面的发展，最近的进展为痤疮治疗带来了潜在的新方法。已证明与痤疮病理生理学和伤口愈合密切相关的特定靶点包括白细胞介素（IL）-1β、IL-17、IL-23和肿瘤坏死因子α（TNFα）。靶向IL-1β、IL-17、IL-23和TNFα的生物抗体可为治疗重度痤疮及相关疾病提供新方法。痤疮主要是一种与皮脂生成相关的疾病。单不饱和游离酸是重要组成部分。胰岛素生长因子1（IGF-1）促进皮脂腺细胞和IL-1β的增殖与分化。对微生物群的研究也可能为痤疮未来潜在的治疗选择提供思路。萎缩性和增生性瘢痕都是痤疮常见的后遗症。与痤疮瘢痕形成相关的危险因素包括遗传、全身、局部和生活方式因素。促炎细胞因子已被证明在痤疮诱导的增生性瘢痕形成中起关键作用。广泛的炎性瘢痕疙瘩瘢痕的治疗方法有限。手术和术后放疗是两种可能的选择。在瘢痕疙瘩或增生性瘢痕组织中发现了转化生长因子-β（TGFβ）、IL-6、基质金属蛋白酶（MMP）、IGF-1和B细胞。靶向这些细胞因子的生物抗体可能是未来预防和治疗这类瘢痕的潜在策略。未来的痤疮治疗应采用针对痤疮主要病因的方法。特别是，应特别强调在急性炎症期进行积极治疗，以降低瘢痕形成和其他临床后遗症（如色素沉着改变）发生的可能性。对于已形成的痤疮后遗症也应予以治疗。
