Reduction in actinic keratoses following 9‐valent human papilloma virus vaccination

Wenande, Emily; Bech-Thomsen, Niels; Hædersdal, Merete

doi:10.1111/dth.13454

Cited by 3 publications

(3 citation statements)

References 8 publications

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“…In the literature, there are emerging reports of the vaccine's potential as an off-label treatment strategy for HPV-associated cutaneous conditions [ 5 ]. Indeed, using an identical vaccination protocol, we previously treated a patient with exceedingly high AK burden (>1,000 AKs), noting marked reduction in lesion number and improved skin texture over 1 year [ 6 ]. Interestingly, systemic and intratumoral use of HPV vaccines were recently described in the context of KC for 4 immunocompetent and 1 immunocompromised patient [ 7 , 8 , 9 , 10 ].…”

Section: Discussionmentioning

confidence: 99%

Off-Label 9-Valent Human Papillomavirus Vaccination for Actinic Keratosis: A Case Series

et al. 2021

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Background: The suspected link between human papillomavirus (HPV) and the development of premalignant and malignant skin lesions remains inadequately examined in clinical settings. This case series describes HPV vaccination as an off-label adjuvant therapy for actinic keratosis (AK). Methods: Twelve immunocompetent AK patients underwent HPV vaccination at a private dermatology clinic in Naestved, Denmark. Prior to vaccination, all patients demonstrated a high AK burden that required regular control visits. At 0, 2, and 6 months, the patients received an intramuscular injection of a commercially available 9-valent HPV vaccine. Concurrently, patients continued conventional AK therapies at 3-month intervals. Clinical response, consisting of reduction in AK number and general change in skin appearance, was assessed by a dermatologist over 12 months following first vaccination. Results: All patients (mean age 76.2 years; 10 M and 2 F) completed the vaccine schedule. Overall, an average 85% reduction in total AK burden was recorded 12 months after beginning vaccination. Median AK burden thus fell from 56 (IQR: 44–80) to 13.5 (IQR: 1–18) lesions after 12 months. Lesion reduction was observable by the second inoculation at month 2 (34 AKs; IQR 22–80), continuing steadily until month 6 (15 AKs; IQR 5–30) and plateauing between 6 and 12 months. Clinically, HPV vaccination elicited fading of lesions’ erythematous background after the first dose, often followed by sloughing of hyperkeratotic elements in subsequent weeks. Patients reported no adverse effects related to HPV vaccination. Conclusion: This case series introduces the possibility that 9-valent HPV vaccination in combination with conventional treatments may be used as a therapeutic strategy for AK.

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Section: Discussionmentioning

confidence: 99%

Off-Label 9-Valent Human Papillomavirus Vaccination for Actinic Keratosis: A Case Series

et al. 2021

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“…Additionally, chronic sun exposure is the most significant environmental factor contributing to AK ( 13 , 57 – 60 ). Individuals with HPV infection or chronic lymphocytic leukemia who have undergone solid-organ transplantation are at a greater risk of developing cSCC compared to the general population ( 61 – 66 ). In summary, AK can progress to cSCC and serves as a pre-cancerous lesion ( 49 ).…”

Section: Summary and Perspectives On Ak Studiesmentioning

confidence: 99%

Advancements in elucidating the pathogenesis of actinic keratosis: present state and future prospects

Wang,

Shi

et al. 2024

Front. Med.

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Solar keratosis, also known as actinic keratosis (AK), is becoming increasingly prevalent. It is a benign tumor that develops in the epidermis. Individuals with AK typically exhibit irregular, red, scaly bumps or patches as a result of prolonged exposure to UV rays. These growths primarily appear on sun-exposed areas of the skin such as the face, scalp, and hands. Presently, dermatologists are actively studying AK due to its rising incidence rate in the United States. However, the underlying causes of AK remain poorly understood. Previous research has indicated that the onset of AK involves various mechanisms including UV ray-induced inflammation, oxidative stress, complex mutagenesis, resulting immunosuppression, inhibited apoptosis, dysregulated cell cycle, altered cell proliferation, tissue remodeling, and human papillomavirus (HPV) infection. AK can develop in three ways: spontaneous regression, persistence, or progression into invasive cutaneous squamous cell carcinoma (cSCC). Multiple risk factors and diverse signaling pathways collectively contribute to its complex pathogenesis. To mitigate the risk of cancerous changes associated with long-term UV radiation exposure, prompt identification, management, and prevention of AK are crucial. The objective of this review is to elucidate the primary mechanisms underlying AK malignancy and identify potential treatment targets for dermatologists in clinical settings.

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“…Epidermodysplasia verruciformis-associated HPV (EV-HPVs) are possibly involved in the development of AK, as has been demonstrated in serological studies, and may play a role in the pathogenesis of SCC [ 120 , 121 ]. Interestingly, an observational report with 9-valent HPV vaccination as adjunctive, off-label management of AK showed AK regression beginning within months of the first injection, leading to the clearance of thousands of lesions before the vaccination protocol was completed [ 122 ]. Regarding the possible association with other viral infections, the literature is scarce and controversial.…”

Section: Influential Role Of Exposome Factorsmentioning

confidence: 99%

Exposome and Skin. Part 2. The Influential Role of the Exposome, Beyond UVR, in Actinic Keratosis, Bowen’s Disease and Squamous Cell Carcinoma: A Proposal

Molina-García

Malvehy

Granger

et al. 2022

Dermatol Ther (Heidelb)

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Actinic keratosis (AK) is the main risk factor for the development of cutaneous invasive squamous cell carcinoma (SCC). It represents the first sign of severe chronic ultraviolet radiation exposure, which has a clear significant effect. Nevertheless, the skin is exposed to many other exposome factors which should be thoroughly considered. Our aim was to assess the impact of exposome factors other than ultraviolet radiation (UVR) on the etiopathology of AK and Bowen's disease (BD) and progression of AK to SCC and to design tailored prevention strategies. We performed an exhaustive literature search in September 2021 through PubMed on the impact of exposome factors other than UVR on AK, BD and SCC. We conducted several parallel searches combining terms of the following topics: AK, BD, SCC and microbiome, hormones, nutrition, alcohol, tobacco, viral infections, chemical contaminants and air pollution. Notably, skin microbiome studies have shown how Staphylococcus aureus infections are associated with AK and AK-to-SCC progression by the production of chronic inflammation. Nutritional studies have demonstrated how a caloric restriction in fat intake, oral nicotinamide and moderate consumption of wine significantly reduce the number of premalignant keratoses and SCC. Regarding lifestyle factors, both alcohol and smoking are associated with the development of SCC in a dosedependent manner. Relevant environmental factors are viral infections and chemical contaminants. Human papillomavirus infections induce deregulation of cellular proliferation and are associated with AK, BD and SCC. In addition to outdoor jobs, occupations such as industrial processing and farming also increase the risk of developing keratoses and SCC. The exposome of AK will undoubtedly help the understanding of its etiopathology and possible progression to

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Reduction in actinic keratoses following 9‐valent human papilloma virus vaccination

Cited by 3 publications

References 8 publications

Off-Label 9-Valent Human Papillomavirus Vaccination for Actinic Keratosis: A Case Series

Off-Label 9-Valent Human Papillomavirus Vaccination for Actinic Keratosis: A Case Series

Advancements in elucidating the pathogenesis of actinic keratosis: present state and future prospects

Exposome and Skin. Part 2. The Influential Role of the Exposome, Beyond UVR, in Actinic Keratosis, Bowen’s Disease and Squamous Cell Carcinoma: A Proposal

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