Ingenol mebutate treatment in keloids

BACKGROUND: Ingenol-mebutate has been used for the treatment of actinic keratosis. It has been shown that ingenol-mebutate inhibits the growth of cancer cells or induces tumor cell death through pro-apoptotic effects. Keloids are benign skin tumours and are the effect of a deregulated wound-healing process in genetically predisposed patients. Increased cell proliferation, which accounts for the progressive and hypertrophic nature of keloids, correlates with the failure of apoptosis and plays a role in the process of pathological scarring. Keloid cells show a mutated p53 gene resulting in functionally inactive p53 protein which cannot control genomic integrity. They tend to escape from apoptosis which leads to keloid development by means of accumulation of continuously proliferating cells. Currently, the treatment of keloids remains a challenge for high recurrence rates. However, the design and the development of pro-apoptotic therapeutic strategies would be beneficial to keloids treatment. CASE PRESENTATION: A 55-year-old caucasian woman presented recurrent keloids on a presternal scar. Standard surgical intervention was used to treat the scar. However, this was unsuccessful and a year later the patient sought treatment again, but only by alternative means as the patient refused further surgical intervention. Consequently, based on past research and experience, the authors attempted to treat these lesions with ingenol mebutate gel, due to the pro-apoptotic effects. CONCLUSION: After 1 month, there was a clinical resolution of lesions, with a slightly squamous, post-inflammatory erythema. A cutaneous biopsy proved the absence of residual keloids and deregulated expression of molecular markers. The last follow-up of the patient, 1 year after treatment, showed that the patient was still free of keloids recurrence. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13104-015-1429-9) contains supplementary material, which is available to authorized users.