摘要

Objectives: During photodynamic therapy (PDT) of actinic keratosis, either aminolevulinic acid (5-ALA) or methyl aminolevulinate (MAL) is utilized as precursor that preferentially accumulates in dysplastic cells. The precursor then converts to Protoporphyrin IX (PpIX) via the heme pathway and causes apoptosis of the cells when illuminated. Introduction: The major drawback of PDT is the pain experienced during the illumination. In fact, though ALA or MAL are not taken up into the nerve endings, reactive oxygen species produced during light exposure may cause cell degranulation of mast cells leading to release of inflammatory mediators. Among them, bradykinin and histamine are known to directly stimulate sensory nerve endings. Materials / method: When using ALA or MAL, it is important to avoid the confusion between incubation time and Drug Light Interval (DLI). When performing ALA-PDT or MAL-PDT, DLI is the period of time between first PpIX production by dysplastic cell and its activation by light. Studies of intracellular PpIX formation kinetics have demonstrated that PpIX formation by dysplastic cells is quasi-instantaneous after 5-ALA administration. Since ALA or MAL is not removed, formation of PpIX will continue as long as the dysplastic cell is alive. Results: Short DLI are associated with reduced PpIX buildup in target tissue due to absence of PpIX diffusion into surrounding tissues containing intact sensory nerve fibers. Consequently, short DLI should be used since it is a very simple way to reduce pain. Several clinical studies have confirmed the advantage of using short DLI. Conclusion: Mordon S. Painless and efficient ALA-PDT and MAL-PDT of actinic keratosis can be achieved by drastically reducing the drug-light interval. Dermatol Ther. 2020 May;33(3):e13423. Gandy J, Labadie B, Bierman D, Zachary C. Photodynamic Therapy Effectively Treats Actinic Kera