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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%

Treatment of actinic keratosis through inhibition of cyclooxygenase-2: potential mechanism of action of diclofenac sodium 3% in hyaluronic acid 2.5%
Treatment of actinic keratosis through inhibition of cyclooxygenase-2: potential mechanism of action of diclofenac sodium 3% in hyaluronic acid 2.5%

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.

actinic keratosis, cyclooxygenase-2 inhibitors, diclofenac
1396-0296
1-7
Thomas, Gareth J.
2ff54aa9-a766-416b-91ee-cf1c5be74106
Herranz, Pedro
df4396c3-2f56-4f47-a6ab-9f47c57d815f
Cruz, Susana Balta
bb901a4d-a605-4f32-b455-76165fc799d5
Parodi, Aurora
4944906e-e8bc-40ec-bacb-8dcf6245aca1
Thomas, Gareth J.
2ff54aa9-a766-416b-91ee-cf1c5be74106
Herranz, Pedro
df4396c3-2f56-4f47-a6ab-9f47c57d815f
Cruz, Susana Balta
bb901a4d-a605-4f32-b455-76165fc799d5
Parodi, Aurora
4944906e-e8bc-40ec-bacb-8dcf6245aca1

Thomas, Gareth J., Herranz, Pedro, Cruz, Susana Balta and Parodi, Aurora (2018) Treatment of actinic keratosis through inhibition of cyclooxygenase-2: potential mechanism of action of diclofenac sodium 3% in hyaluronic acid 2.5%. Dermatologic Therapy, 1-7, [e12800]. (doi:10.1111/dth.12800).

Record type: Review

Abstract

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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Thomas et al 2019 Dermatologic Therapy - Version of Record
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More information

Accepted/In Press date: 3 December 2018
e-pub ahead of print date: 6 December 2018
Keywords: actinic keratosis, cyclooxygenase-2 inhibitors, diclofenac

Identifiers

Local EPrints ID: 431264
URI: http://eprints.soton.ac.uk/id/eprint/431264
ISSN: 1396-0296
PURE UUID: 77df03ae-6282-4335-8134-d4550e6dd35c

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Date deposited: 29 May 2019 16:30
Last modified: 07 Oct 2020 00:53

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