UV-induced erythema and thymine dimer mutations contribute to photocarcinogenesis. In addition, UV-induced reactive oxygen species induce mutations on the p53 gene, which affects the repair of damaged DNA and induces a process of programmed cell death (apoptosis) 35 . In laboratory studies, application of 10% topical vitamin C has been shown to reduce UVB-induced erythema by 52% and apoptotic sunburn cell formation by 40–60% 36 . In clinical studies, vitamin C containing solutions have been shown to be particularly effective at reducing UV-induced thymine dimers, thereby potentially reducing the risk of photocarcinogenesis 37 .
The obvious priority is immediate discontinuation of any further topical corticosteroid use. Protection and support of the impaired skin barrier is another priority. Eliminating harsh skin regimens or products will be necessary to minimize potential for further purpura or trauma, skin sensitivity, and potential infection. Steroid Atrophy   is often permanent, though if caught soon enough and the topical corticosteroid discontinued in time, the degree of damage may be arrested or slightly improve. However, while the accompanying Telangectasias may improve marginally, the Striae is permanent and irreversible.