Babilas P, Landthaler M, Szeimies R-M
Klinik und Poliklinik für Dermatologie, Klinikum der Universität Regensburg.
Hautarzt. 2003 Jun;54(6):551-60; quiz 561-2. doi: 10.1007/s00105-003-0543-0.
Actinic keratoses are defined as proliferation of cytologically atypical keratinocytes in the zone of epidermal-dermal junction in photodamaged skin. In the northern hemisphere the prevalence of actinic keratoses ranges depending on different epidemiological studies from 11% to 25% for people aged 40 or older. The main cause of actinic keratoses is exposure to UVB radiation in sunlight UVB radiation induces mutations in the telomerase gene and in the tumor suppressor gene P53, which can also be detected in invasive squamous cell carcinoma. The only histological parameter to distinguish between actinic keratoses and SCC is the level of invasiveness. The risk for actinic keratoses to develop into SCC is about 16% over lo years. For this reason and because of the high prevalence of actinic keratoses, it has been suggested to replace the term,, actinic keratosis K with intraepidermal squamous cell carcinoma' to better characterize the lesion. In the following review recent aspects of pathogenesis and therapy of actinic keratoses are discussed.
光化性角化病被定义为光损伤皮肤中表皮-真皮交界处细胞学上非典型角质形成细胞的增殖。在北半球,根据不同的流行病学研究,40岁及以上人群光化性角化病的患病率在11%至25%之间。光化性角化病的主要原因是阳光中的紫外线B辐射。紫外线B辐射会导致端粒酶基因和肿瘤抑制基因P53发生突变,在浸润性鳞状细胞癌中也能检测到这些突变。区分光化性角化病和鳞状细胞癌的唯一组织学参数是浸润程度。光化性角化病发展为鳞状细胞癌的风险在10年内约为16%。出于这个原因,也由于光化性角化病的高患病率,有人建议用“表皮内鳞状细胞癌”取代“光化性角化病”这一术语,以便更好地描述这种病变。在以下综述中,将讨论光化性角化病发病机制和治疗的最新进展。