Costa Claudia, Scalvenzi Massimiliano, Ayala Fabio, Fabbrocini Gabriella, Monfrecola Giuseppe
Department of Dermatology, Federico II University, Naples, Italy.
J Dermatol Case Rep. 2015 Jun 30;9(2):29-35. doi: 10.3315/jdcr.2015.1199.
Actinic keratosis (AKs) is one of the most common skin lesions leading to an increased risk of developing squamous cell carcinoma and other skin malignancies. The lesions principally arise as a result of excessive ultraviolet (UV) exposure. AKs may regress spontaneously, remain stable or evolve to invasive squamous cell carcinoma. The risk of squamous cell carcinoma is significantly increased patients with more than 5 AKs. The main mechanisms involved in the formation of AK are inflammation, mutagenesis, oxidative stress, impaired apoptosis, immunosuppression, disregulation of cell growth and proliferation, and tissue remodeling. Human papilloma virus has also been correlated with the formation of some AKs. As an individual ages, his skin is exposed to increasing cumulative amounts of UV light and other environmental insults. This is especially true for the head, neck and forearms. These insults do not target only the skin where individual lesions develop, but also the surrounding area. In this area undetectable preclinical AK lesions or dysplastic cells may be present. The whole affected area is known as the 'field'. Therefore, management is divided into lesion-directed and field-directed therapies. Currently, the therapies in use are lesion-directed cryotherapy and/or excision, and field-directed topical agents: 5-fluorouracil, diclofenac, photodynamic therapy, imiquimod, and ingenol mebutate. Combining lesion- and field-directed therapies showed good results and several novel therapies are under investigation. Treatment is variable and personalized, what makes a gold standard management algorithm difficult to design. This review aims to describe the rationale behind the available treatment options for AKs based on current understanding of pathophysiology and epidemiology.
光化性角化病（AKs）是最常见的皮肤病变之一，会增加患鳞状细胞癌和其他皮肤恶性肿瘤的风险。这些病变主要是由于过度暴露于紫外线（UV）而产生的。AKs可能会自发消退、保持稳定或演变成浸润性鳞状细胞癌。患有5个以上AKs的患者患鳞状细胞癌的风险会显著增加。AK形成的主要机制包括炎症、诱变、氧化应激、细胞凋亡受损、免疫抑制、细胞生长和增殖失调以及组织重塑。人乳头瘤病毒也与某些AKs的形成有关。随着个体年龄的增长，其皮肤会受到越来越多累积的紫外线和其他环境损伤。头部、颈部和前臂尤其如此。这些损伤不仅针对单个病变发生的皮肤部位，还针对周围区域。在这个区域可能存在无法检测到的临床前AK病变或发育异常细胞。整个受影响的区域被称为“场”。因此，治疗分为针对病变的治疗和针对场的治疗。目前使用的治疗方法是针对病变的冷冻疗法和/或切除术，以及针对场的局部用药：5-氟尿嘧啶、双氯芬酸、光动力疗法、咪喹莫特和鬼臼毒素酯。联合针对病变和场的治疗显示出良好的效果，并且有几种新的治疗方法正在研究中。治疗方法因人而异且需要个性化，这使得难以设计出一个金标准的管理算法。这篇综述旨在根据目前对病理生理学和流行病学的理解，描述AKs现有治疗选择背后的基本原理。
