Efficacy of a photolyase-based device in the treatment of cancerization field in patients with actinic keratosis and non-melanoma skin cancer

G Ital Dermatol Venereol. 2013 Dec;148(6):693-8.

Abstract

Eryfotona AK-NMSC (ISDIN Spain) is a film-forming medical device in cream or fluid formulation containing the DNA-repair enzyme photolyase and high-protection UV filters in liposomes (repairsomes) indicated in the treatment of cancerization field in patients with actinic keratosis (AK) or non-melanoma skin cancer (NMSC). Photolyase is an enzyme that recognizes and directly repairs UV-induced DNA damage. The most common UV-induced DNA damage is the formation of cyclobutane pyrimidine dimers (CPD). Clinical studies evaluating the histological and cellular effects of Eryfotona AK-NMSC have shown a potential benefit in the treatment of the cancerization field in AK patients. In particular the use of Eryfotona AK-NMSC improves the confocal microscopic appearance of skin at the cancerization field level. In addition, Eryfotona AK-NMSC improves the p53 gene expression at keratinocyte level. In this study we reported a series of 6 cases of patients with AK or NMSC lesions treated with Eryfotona AK-NMSC fluid, both as coadjuvant and as single treatment, applied twice daily in the affected area with photograph documentation. Clinical photographs of the skin lesions at baseline and after Eryfotona AK-NMSC treatment were taken in all cases using a high-definition digital camera. Six patients with multiple AK lesions of the scalp or face with or without NMSC were treated for a mean of 1-3 months with Eryfotona AK-NMSC fluid formulation. Image documentations before and after treatment of this clinical series show a great improvement in AK lesions count and of cancerization field. This clinical series supports the clinical efficacy of the use of photolyase and high-protection UV filters in the treatment of cancerization field and AK lesions in patients with actinic damage.

Publication types

  • Case Reports

MeSH terms

  • Aged
  • Anticarcinogenic Agents / administration & dosage
  • Anticarcinogenic Agents / therapeutic use*
  • Carcinoma, Squamous Cell / drug therapy*
  • Carcinoma, Squamous Cell / enzymology
  • Carcinoma, Squamous Cell / genetics
  • Carcinoma, Squamous Cell / pathology
  • Cell Transformation, Neoplastic / drug effects*
  • Deoxyribodipyrimidine Photo-Lyase / administration & dosage
  • Deoxyribodipyrimidine Photo-Lyase / metabolism
  • Deoxyribodipyrimidine Photo-Lyase / therapeutic use*
  • Ear / pathology
  • Face / pathology
  • Follow-Up Studies
  • Genes, p53 / drug effects
  • Humans
  • Keratinocytes / drug effects
  • Keratinocytes / metabolism
  • Keratosis, Actinic / drug therapy*
  • Keratosis, Actinic / enzymology
  • Keratosis, Actinic / genetics
  • Keratosis, Actinic / pathology
  • Liposomes
  • Male
  • Middle Aged
  • Scalp / drug effects*
  • Scalp / pathology
  • Skin Neoplasms / drug therapy*
  • Skin Neoplasms / enzymology
  • Skin Neoplasms / genetics
  • Skin Neoplasms / pathology
  • Sunscreening Agents / administration & dosage
  • Sunscreening Agents / metabolism
  • Sunscreening Agents / therapeutic use*
  • Time Factors
  • Treatment Outcome
  • Tumor Suppressor Protein p53 / drug effects
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • Anticarcinogenic Agents
  • Liposomes
  • Sunscreening Agents
  • Tumor Suppressor Protein p53
  • Deoxyribodipyrimidine Photo-Lyase