Journal of Clinical and Aesthetic Dermatology

OCT 2017

An evidence-based, peer-reviewed journal for practicing clinicians in the field of dermatology

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28 JCAD JOURNAL OF CLINICAL AND AESTHETIC DERMATOLOGY October 2017 • Volume 10 • Number 10 O R I G I N A L R E S E A R C H A Actinic keratosis (AK) is a product of cumulative exposure to ultraviolet (UV) light and is considered the most common precursor of invasive squamous cell carcinoma (SCC) of the skin. 1,2 The relative risk of progression from AK to SCC depends on patient-related factors, such as immune status and Fitzpatrick skin category, as well as on the presence of AK- associated features, such as lesional thickness, inflammatory changes, and the extent of photodamage to perilesional skin. 3 Studies assessing the rate of progression to SCC have found considerable variability, but averaging and extrapolation of the data suggest a 10-year risk of dermal invasion of at least one lesion to be about eight percent, 2 thus making AK an excellent target for preventive strategies. Visible AKs are well-accepted candidates for treatment, before these lesions have the opportunity to become more aggressive. The skin surrounding a visible AK lesion is subject to the same UV radiation-induced damage that promotes the AK and can harbor dysplastic subclinical lesions that are genetically similar to AK but not clinically apparent. 4,5 For this reason, field cancerization, which is defined as the damaging effects of chronic UV exposure on large areas of skin, increases the likelihood of the development of AKs and their potential progression into SCC. 4 Field-directed therapy rather than lesion-directed therapy is warranted for multiple visible (clinical) AKs on contiguous areas, and also for suspected subclinical lesions or contiguous sun-damaged areas at risk for subclinical lesions. 6 Identifying and treating field cancerization might prevent the development A B S T R A C T OBJECTIVE: To determine whether actinic keratosis and photodamaged perilesional areas (field cancerization) treated successfully with topical ingenol mebutate gel 0.015% remained clear one year later, and to treat actinic keratosis and perilesional skin not treated one year earlier. DESIGN: Single-center, single-arm, open-label extension of an original clinical study completed one year earlier. SETTING: An outpatient clinic. PARTICIPANTS: Fifteen of the original 28 study patients enrolled in and who completed the extension phase. MEASUREMENTS: All treated and untreated lesions in the original study were evaluated clinically, dermoscopically, and with optical coherence tomography at Day 0 of the extension study. Previously untreated lesions were then treated with ingenol mebutate gel 0.015% for three days and reevaluated at Day 60. RESULTS: There was no significant increase in actinic keratoses over one year. The majority of actinic keratoses not treated in the original study were still present at the beginning of the extension study. Following treatment, 69 percent of these lesions cleared by Day 60 of the extension study, which was not significantly different from the 79 percent clearance observed in the original study. CONCLUSION: Ingenol mebutate 0.015% maintained clearance of lesions treated one year earlier. Optical coherence therapy demonstrated its reliability as a noninvasive mode of diagnosis for actinic keratosis as well as actinic damage in the surrounding areas of field cancerization. Optical coherence therapy also showed that previously untreated lesions exhibited similar clearance rates once treated with the medication. KEYWORDS: Actinic keratosis, ingenol mebutate, perilesional, field cancerization, photodamage, optical coherence tomography Noninvasive Long-term Monitoring of Actinic Keratosis and Field Cancerization Following Treatment with Ingenol Mebutate Gel 0.015% by ORIT MARKOWITZ, MD; KATIE WANG, DO; AMANDA LEVINE, MD; MICHELLE SCHWARTZ, BA; SUMEET MINHAS, BA; ELEANOR FELDMAN, BA; and DANIEL M. SIEGEL, MD Drs. Markowitz, Wang, Levine; Ms. Minhas; and Ms. Schwartz and Ms. Feldman are associated with the Department of Dermatology, SUNY Downstate Medical Center, New York, New York; the Department of Dermatology, Brooklyn VA Harbor Healthcare System, Brooklyn, New York; and the Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, New York. Dr. Siegel is associated with the Department of Dermatology, SUNY Downstate Medical Center, New York, New York and the Department of Dermatology, Brooklyn VA Harbor Healthcare System, Brooklyn, New York. J Clin Aesthet Dermatol. 2017;10(10):28–33 FUNDING: This study was sponsored and funded by LEO Pharma. This material is the result of work supported with resources and the use of facilities at the VA New York Harbor Healthcare System. The contents do not represent the views of the United States Department of Veterans Affairs or the United States Government. DISCLOSURES: Dr. Siegel is on the board of directors for Caliber Imaging and Diagnostics Inc. and is a consultant and on the advisory board for Leo Pharmaceuticals. He is also a principle investigator for Michelson diagnostics. Dr. Markowitz is a consultant for Leo Pharmaceuticals and is a principle investigator for Michelson Diagnostics. Drs. Wang, Dr. Levine, Ms. Schwartz, Ms. Minhas, and Ms. Feldman report no financial conflicts relevant to the content of this article. CORRESPONDENCE: Orit Markowitz, MD; Email:

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