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Treatment of actinic keratosis through inhibition of cyclooxygenase‐2: Potential mechanism of action of diclofenac sodium 3% in hyaluronic acid 2.5%
Author(s) -
Thomas Gareth J.,
Herranz Pedro,
Cruz Susana Balta,
Parodi Aurora
Publication year - 2019
Publication title -
dermatologic therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.595
H-Index - 68
eISSN - 1529-8019
pISSN - 1396-0296
DOI - 10.1111/dth.12800
Subject(s) - medicine , actinic keratosis , cyclooxygenase , diclofenac sodium , prostaglandin e2 , skin cancer , carcinogenesis , hyaluronic acid , cancer research , pharmacology , prostaglandin , mechanism of action , diclofenac , cancer , enzyme , biochemistry , basal cell , in vitro , chemistry , anatomy
Cyclooxygenase‐2 (COX‐2) and its metabolic product prostaglandin E 2 (PGE 2 ) are induced in response to growth factors, inflammatory cytokines, tumor promoters, activated oncogenes, and, in the skin, ultraviolet (UV) radiation. Accumulating evidence suggests a role for the COX‐2/PGE 2 pathway in tumorigenesis in various tissue types including cutaneous squamous cell carcinoma. There is also strong evidence for a role in the development of actinic keratoses (AKs) — common dysplastic lesions of the skin associated with UV radiation overexposure — considered as part of a continuum with skin cancer. Non‐steroidal anti‐inflammatory drugs (NSAIDs) exert their anti‐inflammatory, analgesic, and antipyretic effects by reversibly or irreversibly acetylating COX isoforms, inhibiting downstream prostaglandins, and may have a chemopreventive role in malignancies, including skin cancer. Topical treatment of AK lesions with the NSAID diclofenac sodium 3% in combination with hyaluronic acid 2.5% has been shown to be effective and well tolerated, although the mechanism of action remains to be elucidated.

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