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A 65-year-old retired mailman with a history of squamous cell carcinoma presents to the dermatology clinic for his routine total body skin examination. He reports finding 2 gritty, red spots on his scalp. On examination, 2 rough, scaly, red plaques are noted on the scalp, as well as multiple telangiectasias on the cheeks and nose, areas of depigmentation, and excessive wrinkles with leathery-appearing skin.
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Actinic keratoses (AKs), also known as solar or senile keratosis, are cutaneous neoplasms caused by exposure to ultraviolet (UV) radiation that induces the development of abnormal epidermal keratinocytes.1 AKs are precancerous lesions that have the potential to develop into squamous cell carcinoma (SCC).2 Conceptually presented first in the late 1800s by Dubreuilh, these lesions were later characterized and termed actinic keratosis by Pinkus in 1958.1,3
AKs are the second most common reason for a dermatology consultation after acne, with almost universal occurrence in adults aged >80 years.1,4,5 The estimated cost of treating AKs in the United States reaches >$1 billion annually.4 The greatest risk factors for AKs are exposure to UV radiation and increasing cumulative sun exposure, the latter of which is evidenced by the increased incidence of AKs from 10% in white adults aged 20 to 29 years to 80% in white adults aged 60 to 69 years.6 Other risk factors include older age, male gender, lighter-colored hair and eyes, and fair skin that easily burns and develops freckles.1,6 Rarer risk factors include immunosuppression and certain genetic syndromes such as albinism and xeroderma pigmentosum.1,6 It is important to note that cumulative exposure to UV radiation results not only from sunlight but also from tanning bed use, and many variables can affect the amount of exposure to UV light, such as a patient’s occupation or place of residence. The greater the cumulative exposure to UV rays, the greater the prevalence of AKs.1,6
AKs arise from UV radiation that damages and induces mutations in the DNA of keratinocytes, which can lead to hyperproliferation and tumor formation. UV radiation can also damage DNA in a way that prevents the immune system from recognizing the tumor, thereby allowing it to progress to SCC. The tumor suppressor gene p53 has been implicated in the initiation of AKs, and mutated p53 can lead to unrestricted growth of skin cells.7,8 With increasing UV radiation-induced DNA damage, a progression from AKs to SCC can occur.7,8
Patients with AKs are often older, lighter-skinned, and have had significant exposure to the sun that results in burns and freckles.1 Most often found on sun-exposed body sites, AKs can present with bleeding, crusting, pruritus, burning, or stinging pain.1,6 Erythematous AKs are the most common subtype, presenting as 3- to 6-mm erythematous, flat, gritty, rough, scaly papules or plaques.1 Other clinical subtypes of AKs include hypertrophic, inflamed, pigmented, proliferative, conjunctival, spreading pigmented, actinic cheilitis, and cutaneous horn.1,6
Histologic findings reveal AKs to be confined to the epidermis with atypical, pleomorphic keratinocytes in the basal cell layer of the skin and protrusions that bud into the papillary dermis.1,8 Several histologic findings near these abnormal keratinocytes include irregular acanthosis (hyperproliferation of skin cells), hyperkeratosis (increasing skin thickness due to excess keratin production), and parakeratosis (retention of nuclei in the stratum corneum layer of the epidermis).1,8 Variations in the histology of AKs mimic the aforementioned clinical subtypes, including large amounts of hyperkeratosis for hypertrophic AKs and increased melanin production in pigmented AKs.
Clinically, AKs are diagnosed by visual inspection; however, the accuracy of such a diagnosis is not well known since most AKs are not confirmed with histologic examination.1,2,6 Differential diagnoses of AKs include, but are not limited to, psoriasis, seborrheic dermatitis, verruca vulgaris, benign lichenoid keratosis, and lentigo maligna. The most important differential that must be distinguished from AKs is SCC. Signs that indicate SCC include larger size, pain, induration, bleeding, fast growth, and recurrence after treatment.1,5,7
Because of the risk of AKs transforming to SCC, most dermatologists recommend either field treatment or targeted destruction of individual lesions, the latter of which is the most commonly used method.2,6 Liquid nitrogen cryotherapy is the most common type of targeted destruction due to its ease and efficiency; hand-held cryostats can be carried easily between patient rooms, and the ideal freeze time is only 10 to15 seconds.9 Side effects of cryotherapy include pain, blisters, hypopigmentation, scarring, and alopecia in treated areas.9 Other therapies for individual lesions of AKs include curettage and shave excision.1
Field therapies are used to treat large areas of skin that contain numerous AK lesions and are categorized into medical and procedural modalities. Medical therapies for generalized AKs include topical 5-fluorouracil (5-FU), imiquimod, and diclofenac.1 Of these, 5-FU is the most common treatment and is available in a variety of formulations and strengths, with an effectiveness of up to 75%.1,5,10 Side effects of 5-FU include discomfort, crusting, pruritus, scabbing, and erythema.1,10 Counseling patients on dosage, proper application, and side effects is essential when treatment with 5-FU is initiated to improve adherence and maximize efficacy. Procedural field therapies include cryopeeling, dermabrasion, and chemical peels.1
It is important to remember that AKs are caused by UV damage and have the potential to develop into malignant lesions. Recently, an effort has been made to reclassify AKs as malignant neoplasms since they represent an essential initial stage in the evolution to SCC.1,6 AKs also represent an important clinical lesion since their presence is a strong predictor for the development of either melanoma or nonmelanomatous skin cancers. Thus, patients with AKs should undergo long-term monitoring for cutaneous malignancies and implementation of early interventions.1,6
The patient in this case was treated with liquid nitrogen cryotherapy to destroy the 2 AKs on his scalp. He was counseled on the importance of undergoing routine skin examinations every 6 to12 months and to follow up sooner if he noticed a concerning lesion during a skin self-examination.
Jay M. Patel, BS, and McKenna E. Boyd, BS, are medical students at Baylor College of Medicine, in Houston, Texas. Christopher Rizk, MD, is a dermatologist with Elite Dermatology, in Houston, Texas.
1. Duncan KO, Geisse JK, Leffell DJ. Chapter 113. Epithelial precancerous lesions. In: Fitzpatrick’s Dermatology in General Medicine. 8th ed. New York, NY: The McGraw-Hill Companies; 2012.
2. Criscione VD, Weinstock MA, Naylor MF, Luque C, Eide MJ, Bingham SF; for the Department of Veteran Affairs Topical Tretinoin Chemoprevention Trial. Actinic keratoses: natural history and risk of malignant transformation in the Veterans Affairs Topical Tretinoin Chemoprevention Trial. Cancer. 2009;115(11):2523-2530.
3. Pinkus H. Keratosis senilis; a biologic concept of its pathogenesis and diagnosis based on the study of normal epidermis and 1730 seborrheic and senile keratoses. Am J Clin Pathol. 1958;29(3):193-207.
4. Bickers DR, Lim HW, Margolis D, et al; American Academy of Dermatology Association; Society for Investigative Dermatology. The burden of skin diseases: 2004 a joint project of the American Academy of Dermatology Association and the Society for Investigative Dermatology. J Am Acad Dermatol. 2006;55(3):490-500.
5. Siegel JA, Korgavkar K, Weinstock MA. Current perspective on actinic keratosis: a review. Br J Dermatol. 2017;177(2):350-358.
6. Frost CA, Green AC. Epidemiology of solar keratoses. Br J Dermatol. 1994;131(4):455-464.
7. Grossman D, Leffell DJ. The molecular basis of nonmelanoma skin cancer: new understanding. Arch Dermatol. 1997;133(10):1263-1270.
8. Pillon A, Gomes B, Vandenberghe I, et al. Actinic keratosis modelling in mice: a translational study. PloS One. 2017;12(6):e0179991.
9. Thai K-E, Fergin P, Freeman M, et al. A prospective study of the use of cryosurgery for the treatment of actinic keratoses. Int J Dermatol. 2004;43(9):687-692.
10. Segatto MM, Dornelles SIT, Silveira VB, Frantz G de O. Comparative study of actinic keratosis treatment with 3% diclofenac sodium and 5% 5-fluorouracil. An Bras Dermatol. 2013;88(5):732-738.