Real-world approach to actinic keratosis management: practical treatment algorithm for office-based dermatology

Abstract

Actinic keratosis (AK) is a chronic skin disease in which multiple clinical and subclinical lesions co-exist across large areas of sun-exposed skin, resulting in field cancerisation. Lesions require treatment because of their potential to transform into invasive squamous cell carcinoma. This article aims to provide office-based dermatologists and general practitioners with simple guidance on AK treatment in daily clinical practice to supplement existing evidence-based guidelines. Novel aspects of the proposed treatment algorithm include differentiating patients according to whether they have isolated scattered lesions, lesions clustered in small areas or large affected fields without reference to specific absolute numbers of lesions. Recognising that complete lesion clearance is rarely achieved in real-life practice and that AK is a chronic disease, the suggested treatment goals are to reduce the number of lesions, to achieve long-term disease control and to prevent disease progression to invasive squamous cell carcinoma. In the clinical setting, physicians should select AK treatments based on local availability, and the presentation and needs of their patients. The proposed AK treatment algorithm is easy-to-use and has high practical relevance for real-life, office-based dermatology.

Keywords:

• Diclofenac
• field cancerisation
• 5-fluorouracil
• imiquimod
• ingenol mebutate
• photodynamic therapy

Acknowledgements

We thank Dr Ágota Bartha (CentroDerm GmbH, Wuppertal) for assistance with the preparation of figures in this manuscript.

Disclosure statement

TD: Speaker?s fees from Almirall, Biofrontera, Galderma, Leo, Meda, GSK, Janssen; advisory board member for Almirall, Biofrontera, Galderma, Leo, Meda; unrestricted grant from Meda.

GG: Received honoraria for presentations and for attending conferences from Almirall, Leo, Meda, Novartis; advisory board member for Leo and Meda.

GM: None.

ES: Consultant contract with Meda, Almirall, Leo, Novartis.

NBS: Consultant and investigator for Leo and Galderma.

VDM: Advisory board member for Galderma and Abbvie.

RD: Consultant contract with Meda. Research support for the institution from Galderma.

GJ: Advisory board member for AbbVie, MSD, Pfizer; Investigator for Abbvie, Actelion, Janssen-Cilag, Leo, Novartis, Regeneron; Speaker?s fees from AbbVie, Galderma, Leo, MSD; Unrestricted research grants from AbbVie and Leo.

JM: Speaker?s fees from ISDIN, Almirall, Leo, Meda, La Roche Posay, Roche, Bristol-Myers Squibb, Amgen; Advisory board member for Almirall, Leo, Meda, Amgen; Research grants from Almirall, Cantabria, GSK Biological, ISDIN, La Roche Posay, Leo.

KP: Advisory board for Abbvie, Leo, Meda, Roche; Speaker’s fees from Leo, Meda, Roche.

SP: Advisory board member for Bristol-Myers Squibb, GSK, Leo, Roche; Consultant for Almirall; Research grants from Almirall, Cantabria, GSK Biological, ISDIN, La Roche Posay, Leo; Speaker?s fees from Almirall, ISDIN, Leo, La Roche Posay, Roche, Bristol-Myers Squibb.

AS: Speaker?s fees from Meda and Leo; Research support and advisory board member for Roche and Novartis.

IZ: Speaker?s fees from Almirall, Leo, Meda, La Roche Posay, Roche, Bristol-Myers Squibb, Amgen; advisory board member for Almirall, Leo, Meda, Amgen.

GP: Research grant from Meda and Leo; advisory board member for Roche, Galderma.

Medical writing assistance in the preparation of this manuscript was provided by David Harrison, Medscript Ltd, funded by Meda.

Funding

This article was funded by Meda.