The adverse skin reaction after radiotherapy, also known as radiodermatit (radiodermatitis). On the one hand, ionizing rays can destroy cell chromosomes and kill cancer cells while affecting cell division in the basal layer of the skin; on the other hand, local ionizing effects of radiotherapy can form oxidized free radicals and cause local inflammation in the skin, manifesting as exudation, dermatitis, peeling and ulceration, and even fibrosis, necrosis and secondary tumors can be formed by long-term treatment. Although skin adverse reactions to radiotherapy are very common, there is still no unified evaluation standard and control strategy for skin adverse reactions after radiotherapy. Different care strategies are widely used in various radiotherapy centers at home and abroad. Now, we review the evaluation and treatment strategies of post-radiotherapy skin adverse reactions in order to summarize the best treatment measures to improve patients’ skin appearance, reduce patients’ pain and increase the safety of radiotherapy. The time of appearance and determinants of skin adverse reactions after radiotherapy Generally, acute skin adverse reactions start to appear 1-4 weeks after radiotherapy and last until 2-4 weeks, while subacute skin adverse reactions appear after 16 weeks, and chronic adverse reactions appear later. The time and duration of different adverse reactions are related to the energy, penetration rate, radiation source, dose and dose rate, irradiation time, dose distribution, area size, etc. The skin adverse reactions are especially obvious due to the superficial dose distribution of electron beam therapy. The evaluation index of skin adverse reactions after radiotherapy The skin adverse reactions after radiotherapy are mainly evaluated according to the Radiation Therapy Oncology Group (RTOG) scoring system and various modified versions of the RTOG scoring system, which are generally divided into 4 to 6 levels. Previous scoring criteria considered only single-principle scores, which were relatively simple and generally included the following objective symptoms: erythema, dry desquamation, wet desquamation, and exudation, and did not consider subjective reactions of radiotherapy patients, such as burning, itching, tenderness, and pulling sensations. Subsequently, it was found that the severity of objective and subjective symptoms was consistent in most cases, but for skin erythema, the subjective sensations varied widely from patient to patient, while the severity of pruritus and pulling sensations did not necessarily correspond to the objective responses. For this reason, new rating criteria were derived by integrating the subjective skin sensations and objective reactions after radiotherapy. Third, the treatment measures of skin adverse reactions after radiotherapy 1, the treatment measures of acute skin adverse reactions after radiotherapy: the observation of skin adverse reactions after radiotherapy should be after 2 weeks, but the care of the skin needs to be operated from the beginning of the treatment, and the treatment should not be started until the appearance of skin adverse reactions. In addition to the conventional principles of care such as maintaining cleanliness, wearing soft and clean clothing, and reducing friction, the main treatment measures for skin adverse reactions include the following 4 aspects: (1) maintaining water content in the skin: application of aloe vera oil and vitamin E complex can reduce subjective adverse reactions; aluminum thioglycollate ointment and moisturizing cream containing hyaluronidase, and hormonal ointment can reduce water loss and reduce erythema and dry peeling. (2) Reduction of subjective sensation and suppression of inflammation: antihistamines, panthenol and corticosteroids can reduce pruritus, and methyl violet can be used to reduce the pain of wet exfoliation and reduce the size of wounds. (3) Reduce the accumulation of free radicals: Reduce the accumulation of free radicals in the local skin of radiotherapy through antioxidant reduction reactions, thus reducing the adverse skin reactions of radiotherapy: such as vitamin A, vitamin C, vitamin E, superoxide dismutase. Dr. Noel developed a gel called Raygel specifically for adverse skin reactions after radiotherapy, and observed the combined scores of 9 sites after radiotherapy and found that Raygel reduced post-radiation skin reactions from 123 to 93.7, an improvement of 24%. Raygel is an aqueous matrix complex containing appropriate amounts of glutathione and anthocyanins, which are endogenous low molecular non-protein sulfhydryl compounds that are key intracellular antioxidants and inhibit the formation of oxygen radicals. The literature demonstrates that sulfhydryl compounds are generally highly permeable and can be absorbed through the skin. Glutamine has a protective effect on cells only when reduced, and reduced glutamine stimulates the onset of immune responses and acts as an antitumor agent. Anthocyanins are members of the bioflavonoid family and are commonly found within red or purple fruits, such as blueberries, purple sweet potatoes, and purple kale. Anthocyanins inhibit redox reactions and tumor formation, and can cause apoptosis of tumor cells. Anthocyanins chelate iron, which can scavenge free radicals and resist lipid peroxidation, and in combination with glutathione can promote glutathione in a reduced state, thus achieving recycling. Another benefit of Raygel is that it can be absorbed across the skin and thus enter the epidermal dermis to provide protection. (4) Increase the oxygen content in the skin: Increasing the oxygen content in the skin after local radiotherapy by hyperbaric oxygen or oxygen blowing promotes the formation of local collagen matrix and blood vessel formation, and increases the resistance to infection. At present, the drugs used to reduce the adverse skin reactions after radiotherapy improve the epidermis and dermis of the skin, which do not affect the killing effect of radiotherapy on tumor cells because they do not penetrate into the tumor. 2.Therapeutic measures for chronic skin adverse reactions after radiotherapy: Once chronic adverse reactions such as skin ulceration, fibrosis, keratosis imperfecta and necrosis occur, other therapeutic measures are needed. For example, the application of retinoids to treat keratosis imperfecta until the keratinization is complete, ulcers need to use platelet growth factor to promote the growth of local granulation, local or systemic application of antibiotics to fight infection, with acetone-cocodine, vitamin E and y interferon to inhibit local fibrosis. The use of etacrynic acid increases local microcirculation and promotes local regenerative repair. When conservative treatment is ineffective, even flap transplantation is needed to repair damaged skin, and tissue with rich blood circulation should be selected as the donor area to ensure local skin survival. Recent studies have found that human MSCs can also promote the healing of local skin reactions after radiotherapy. Multipotential stem cells in bone marrow can differentiate into mesenchymal cells, osteoblasts, chondrocytes and adipocytes, and MSCs can differentiate various tissues, including skin, under specific culture conditions. By transplanting bone marrow-derived stem cells into the skin, skin structures can be regenerated at the site of injury. Application of a murine skin injury model revealed that bone marrow-derived cells can differentiate into myofibroblasts, thereby accelerating the healing of the injury. Injection of bone marrow-derived stem cells into mice after radiotherapy regenerated functional skin tissue. It was found that transplanted MSCs were promoting healing of localized compound radiotherapy injury by promoting platelet-derived alpha growth factor and human beta defensin-2. These two factors promote mitosis and resistance to bacterial infection, respectively, and better promote granulation tissue growth, maturation and regeneration of skin attachments. In a nude mouse transplantation model, human MSCs combined with basic fibroblast growth factor promoted the differentiation of local MSCs into epithelial tissue. Radiotherapy of immunodeficient mice followed by intravenous administration of human MSCs improved the adverse skin reactions. In 2007, the first MSCs treatment was performed on radiotherapy patients and also found that MSCs improved the adverse skin burn response after radiotherapy. The underlying mechanism was found to be that β-transforming growth factor (TGF-β) promotes the growth and differentiation of stem cells and the synthesis of extracellular matrix, and that a sustained increase in local concentrations of TGF-β and fibroblast growth factor accelerates The skin exhibits better cell alignment polarity and a more organized collagen structure through sustained local increases in TGF-β and fibroblast growth factor concentrations, which accelerate the healing of skin damage. Although the therapeutic efficacy of MSCs is quite positive, based on the subsequent effects of their genetic instability after transplantation, the risk of secondary tumorigenesis needs to be excluded before they can be included within the standard strategy for the treatment of cutaneous adverse effects after radiotherapy. In conclusion, post-radiotherapy skin adverse reactions not only seriously affect the local skin aesthetics of patients, but also limit the completion of radiotherapy doses as the course of treatment progresses and various skin symptoms cause pain to patients. In recent years, with the improvement of skin protection measures, new treatment measures for post-radiotherapy skin reactions have been gradually developed, but there is still no standard treatment procedure. With the establishment of a follow-up system for patients after radiotherapy and the accumulation of treatment experience, we aim to establish a diagnosis and treatment plan based on evidence-based medicine by observing the improvement effects of different combinations of treatment measures, so as to better prepare radiotherapy patients to return to normal work and life