INTRODUCTION

Actinic keratoses (AK), also known as solar keratoses, are common cutaneous lesions resulting from a localized proliferation of atypical epidermal keratinocytes, which have been damaged by ultraviolet radiation. AK occur most frequently on sun-exposed sites, such as the upper limbs, face, ears and neck. In immunocompetent patients, a small proportion of actinic keratoses are thought to undergo malignant transformation to squamous cell carcinoma (SCC). The transformation rate in organ transplant recipients is almost certainly higher, although there is no data on the exact rate. Actinic keratoses in organ transplant recipients can cause significant morbidity and also are a biomarker of prior excessive sun damage, thus acting as a clinically useful predictor for development of skin malignancy.

PATHOGENESIS

Cumulative ultraviolet (UV) radiation is the most significant etiological factor in the development of AK. Ultraviolet B radiation is absorbed by the germinal basal keratinocytes, and causes a signature mutation of the deoxyribonucleic acid (DNA), predominantly in the p53 tumor suppressor gene. These mutations lead to defective DNA repair and a reduced initiation of apoptosis in damaged cells, thus allowing propagation and accumulation of further genetic damage. The same genetic mutations are observed in both AK and squamous cell carcinoma (SCC), thus supporting similar pathogenesis.

Immunosuppressed solid organ transplant recipients are at high risk of AK and SCC. The pathogenesis is yet to be fully understood although UV-radiation-induced genetic damage remains a major etiological factor.