Evidence for field cancerisation treatment of actinic keratoses with topical diclofenac in hyaluronic acid.
Actinic keratosis (AK) is a common skin disease seen in daily practice. It is associated with a risk of progression to invasive squamous cell carcinoma and can be regarded as a marker of increased risk for non-melanoma skin cancer. The use of a field-directed treatment approach reflects the need to initiate early treatment over an affected area to prevent tumour development and local recurrence. Candidate field-directed treatments require a mechanism of action compatible with an effect on field cancerisation, immediate and long-term efficacy against visible lesions and efficacy against subclinical AK. Applicability to large treatment areas, tolerability compatible with long-term use, utility in organ transplant patients and, ideally, evidence of extended long-term activity may also be desirable. We review the evidence of a role for topical diclofenac sodium 3% administered in a 2.5% hyaluronic acid gel (diclofenac/HA) as field-directed treatment. Diclofenac/HA directly targets AK pathophysiology through multiple mechanisms, including induction of apoptosis, inhibition of angiogenesis and reduced inflammation. Clearance of visible field cancerisation is safely and rapidly achieved with a 90-day treatment course in patients with affected areas of up to 50 cm(2) and is associated with a ≥75% reduction in target lesion number score in 85% and 91% of patients, respectively, at 30 days and 1 year post-treatment. Following treatment of AK in high-risk transplant patients, 45% remained free of lesions in the treatment area at 2 years post-treatment. We conclude that diclofenac/HA fulfils most criteria necessary to be considered an appropriate candidate for a field-directed treatment in AK.
Dermatologie am Regierungsviertel, Luisenstr. 54/55, 10117 Berlin, Germany.
Martina
M
Ulrich
Department of Dermatology, University of Modena and Reggio Emilia, via del Pozzo 71, 41100 Modena, Italy.
Giovanni
G
Pellacani
Servicio de Dermatología, Hospital Universitario Germans Trias i Pujol, Badalona, Universidad Autónoma de Barcelona, Spain.
Carlos
C
Ferrandiz
Dermatology Department and Manchester Academic Health Science Centre, Manchester Royal Infirmary, Oxford Road, Manchester, M13 9WL, United Kingdom.
John T
JT
Lear
D000279:Administration, Cutaneous; D002294:Carcinoma, Squamous Cell / Q000209:etiology / Q000517:prevention & control*; D016861:Cyclooxygenase Inhibitors / Q000008:administration & dosage*; D004008:Diclofenac / Q000008:administration & dosage*; D018450:Disease Progression; D005782:Gels; D006801:Humans; D006820:Hyaluronic Acid / Q000008:administration & dosage*; D055623:Keratosis, Actinic / Q000188:drug therapy* / Q000473:pathology; D012878:Skin Neoplasms / Q000209:etiology / Q000517:prevention & control*
D016861:Cyclooxygenase Inhibitors; D005782:Gels; D004008:Diclofenac; D006820:Hyaluronic Acid
actinic keratoses; diclofenac sodium; field cancerisation; hyaluronic acid; subclinical lesions