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A 57-year-old woman presented with red and scaling skin on both arms (Figure 166-1) with a request for a prescription for 5-fluorouracil (5-FU). The patient had blue eyes and white hair and was found to have 2 basal cell carcinomas (BCCs) on her face and shoulder. The patient stated that 5-FU had helped her arms in the past, but that the scaly lesions had returned. She avoids sun exposure now, but acknowledges receiving too much sun exposure while growing up. Another course of 5-FU was prescribed for her arms to prevent new skin cancers from forming.

Figure 166-1

Actinic keratoses covering both arms and the dorsum of both hands in a fair-skinned woman who had significant sun exposure. Note that her left arm and hand are worse from driving a car and receiving more sun on the left arm. (Courtesy of Richard P. Usatine, MD.)

Actinic keratoses (AKs) are precursors on the continuum of carcinogenesis toward squamous cell carcinomas (SCCs). However, each AK has a low risk of progression to malignancy and a high probability of spontaneous regression.1 Bowen disease (BD) is SCC in situ confined to the epidermis.

AK is also known as solar keratosis. AK on the lips is known as actinic cheilitis (Figure 166-2). BD is also known as SCC in situ of the skin. SCC in situ involving the penis is known as erythroplasia of Queyrat (Figure 166-3).

Figure 166-2

Actinic cheilitis involving lower lips. Note the erythema and scale caused by the sun damage. (Courtesy of Richard P. Usatine, MD.)

Figure 166-3

Bowen disease of the penis also known as erythroplasia of Queyrat. Human papillomavirus is a risk factor in this location. (Courtesy of Richard P. Usatine, MD.)

  • AKs and BD are seen frequently in light-skinned individuals who have had significant sun exposure.
  • The prevalence of AK is estimated at 11% to 25% in adults older than age 40 years in the northern hemisphere, and increases with age.1 AKs are so common that they account for more than 10% of visits to dermatologists.
  • The prevalence of BD is unknown.1

AKs and BD are both caused by cumulative UV exposure, most commonly from sunlight.

UV rays induce mutation of the tumor-suppressor gene P53. Subsequent proliferation of mutated atypical epidermal keratinocytes give rise to the clinical lesion of AK.2 Multiple clinical and subclinical lesions may exist in an area of sun-damaged skin, a concept known as “field cancerization.”

AKs have the potential to become SCCs. The rate of malignant transformation has been variably estimated, but is probably no greater ...

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