Answer: B

Actinic Keratosis

First described at the end of the 19th century,8 actinic keratoses (AKs) are common epidermal keratinocytic lesions that arise in sun-exposed areas of the skin, such as the face and backs of hands. AKs have the propensity to progress into cutaneous squamous cell carcinoma, although most lesions do not become malignant. Increased exposure to UV radiation from the sun or from artificial light sources (eg, tanning beds) is associated with higher numbers of AKs and a greater propensity for development of carcinoma.9

Because increased exposure to UV radiation is an important risk factor for AK, middle-aged and elderly patients are more likely to present with lesions, and the number of lesions will increase with age.10 Studies have shown that AK is more prevalent in men than in women, with baldness being the greatest risk factor in men.11 Individuals with light skin, blonde hair, and blue eyes are at higher risk for the development of AK. However, with sufficient UV exposure, AK will appear in a person with dark skin as well.9

Many AKs spontaneously regress without treatment, and studies typically show a regression rate of 20% to 30% within 1 year.8 However, when lesions do not regress, AK is associated with the development of skin cancer, with 0.1% to 10% of lesions progressing to invasive cutaneous squamous cell carcinoma.8,9,12 This is rare in individuals with 1 or few lesions of AK and more common in patients who have many lesions and signs of chronic actinic damage.13 In fact, studies estimate that if an individual has 7 to 8 lesions, there is a 10% chance of malignant transformation of at least 1 lesion within 1 year.10

UV-induced nonmelanoma skin cancer progresses in 3 stages: initiation, promotion, and malignant conversion. During initiation, the genome of the keratinocyte is mutated in a key proto-oncogene or tumor suppressor gene (eg, p53). This is followed by promotion, whereby the transformed cell is continuously exposed to proinflammatory agents, or promoters, and develops into an AK. Sunlight can act as both a promoter and an initiator. Finally, exposure to additional UV radiation will cause the benign AK to convert into a malignant neoplasm (eg, squamous cell carcinoma).9 In healthy patients, the immune system should recognize cellular mutations and prevent the progression to malignancy. Immunosuppression is therefore an important risk factor for the development of AK and nonmelanoma skin cancer, and patients who are chronically immunosuppressed (eg, transplant recipients) are at higher risk for AK and malignant transformation.10 AKs that progress to squamous cell carcinoma metastasize in 2% to 6% of cases.9

Clinically, AK presents as circumscribed, scaly, epidermal plaques that measure 2 mm to 5 mm in diameter.12 Because AKs feel rough to the touch, clinicians often palpate lesions during diagnosis. The plaques may be skin-colored, dark, or erythematous. The thickness of an AK depends on location; lesions on the neck and head are flat, while lesions on the hands and forearms may be thick.9 There may not be a visible difference between a benign AK and a squamous cell carcinoma, although bleeding, irritation, and hypertrophy of the plaque may suggest malignant transformation and warrants biopsy.12

Histologically, AK shows characteristic epithelial dysplasia, with unusual organization and maturation of epithelial cells. This can span the full thickness of the skin or exist only in the basal layer. Although all AKs display epithelial dysplasia, histologic variants exist and include Bowenoid, pigmented, hypertrophic, lichenoid, and acantholytic.10 In a process called field cancerization, AKs are often surrounded by clinically normal-appearing tissue that is histologically and genetically abnormal.13

The diagnosis of AK can be done in the clinic based on the appearance and location of the plaque, as well as the patient’s history of UV exposure. However, because the presentation of AK is common but nonspecific, clinical diagnosis is not always correct and confirmation with biopsy may be performed to rule out skin cancer. The differential diagnosis of AK includes DSAP, seborrheic keratosis, discoid lupus erythematosus, psoriasis, basal cell carcinoma, squamous cell carcinoma, and Bowen disease. Biopsy and histologic findings are the most reliable ways to differentiate AK from another skin disorder, especially in patients with a history of skin cancer.12

A variety of treatment options are available for AK, including topical creams, systemic retinoids, liquid nitrogen cryosurgery, and dermabrasion. Sunblock cream and avoidance of sunlight are also important for management, especially when patients are concerned about new lesions or the malignant transformation of current ones. Topical therapies include salicylic acid, 5-fluorouracil, imiquimod cream, diclofenac gel, and tretinoin cream. 5-fluorouracil is used most commonly and reduces AKs by 70%. Systemic retinoids may cause morbidity and should only be used in high-risk patients. Dermabrasion has been used with variable efficacy.10 Cryosurgery is very effective when it is used in combination with a topical agent.13 Because there is a chance of malignant transformation of AK in many patients, it is wise to treat the lesions as they appear.9

After recognizing the risk of malignant transformation of these lesions and discussing the different treatment options, the patient decided to use liquid nitrogen cryosurgery at his office visit and to follow up every 6 months for full-body skin checks. He also will begin using sunscreen on his face every day.

Ariella Noorily, BA, is a medical student at NYU School of Medicine in New York City.

Related Articles


1. Rouhani P, Fischer M, Meehan S, Pomeranz MK. Disseminated superficial actinic porokeratosis. Dermatol Online J. 2012;18(12):24.

2. Shumack SP, Commens CA. Disseminated superficial actinic porokeratosis: a clinical study. J Am Acad Dermatol. 1989;20(6):1015-1022.

3. Sertznig P, von Felbert V, Megahed M. Porokeratosis: present concepts. J Eur Acad Dermatol Venereol JEADV. 2012;26(4):404-412.

4. Xia K, Deng H, Xia JH, et al. A novel locus (DSAP2) for disseminated superficial actinic porokeratosis maps to chromosome 15q25.1–26.1. Br J Dermatol. 2002;147(4):650-654.

5. Maubec E, Duvillard P, Margulis A, Bachollet B, Degois G, Avril M-F. Common skin cancers in porokeratosis. Br J Dermatol. 2005;152(6):1389-1391.

6. Bandyopadhyay D, Saha A, Das D, Das A. Porokeratotic eccrine ostial and dermal duct nevus. Indian Dermatol Online J. 2015;6(2):117-119.

7. Lolis MS, Marmur ES. Treatment of disseminated superficial actinic porokeratosis (DSAP) with the Q‐switched ruby laser. J Cosmet Laser Ther. 2008;10(2):124-127.

8. Werner RN, Sammain A, Erdmann R, Hartmann V, Stockfleth E, Nast A. The natural history of actinic keratosis: a systematic review. Br J Dermatol. 2013;169(3):502-518.

9. Callen JP, Bickers DR, Moy RL. Actinic keratoses. J Am Acad Dermatol. 1997;36(4):650-653.

10. Berker DD, McGregor JM, Hughes BR. Guidelines for the management of actinic keratoses. Br J Dermatol. 2007;156(2):222-230.

11. Flohil SC, van der Leest RJT, Dowlatshahi EA, Hofman A, de Vries E, Nijsten T. Prevalence of actinic keratosis and its risk factors in the general population: The Rotterdam Study. J Invest Dermatol. 2013;133(8):1971-1978.

12. Venna SS, Lee D, Stadecker MJ, Rogers GS. Clinical Recognition of actinic keratoses in a high-risk population: how good are we? Arch Dermatol. 2005;141(4):507-509.

13. Heppt MV, Steeb T, Ruzicka T, Berking C. Cryosurgery combined with topical interventions for actinic keratosis: a systematic review and meta-analysis [published online November 17, 2018]. Br J Dermatol. doi:10.1111/bjd.17435