Actinic Keratosis and Bowen Disease



Patient Story





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.)







Introduction





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.






Synonyms





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.)







Epidemiology






  • 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






Etiology and Pathophysiology





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 than 6% per AK over a 10-year period.3






In a large prospective cohort study, the risk of progression of AK to primary SCC (invasive or in situ) was 0.60% at 1 year and 2.57% at 4 years. Approximately 65% of all primary SCCs and 36% of all primary BCCs diagnosed in the study arose in lesions that previously were diagnosed clinically as AKs. Many AKs did resolve spontaneously, 55% AKs that were followed clinically were not present at 1 year and the 70% were not present at the 5-year follow-up.4






On a spectrum of malignant transformation, BD is SCC in situ before the SCC becomes invasive.






Risk Factors






  • Total lifetime dose of UV radiation (natural sunlight, UV from tanning beds and radiation).1
  • Fair skin.1
  • Site-specific risk factors include tobacco for actinic cheilitis and human papilloma virus for genital and anal lesions.1
  • Exposure to immunosuppressive drugs, especially organ transplant recipients.
  • Personal or family history of skin cancers.






Diagnosis





Clinical Features



AKs are rough scaly spots seen on sun-exposed areas (Figure 166-1, 166-2, 166-3, 166-4, 166-5, and 166-6). They may be found by touch, as well as close visual inspection of the patient’s skin. BD appears similar to an AK, but tends to be larger in size and thicker with a well-demarcated border (Figure 166-7 and 166-8).




Figure 166-4



Large actinic keratoses over the eyebrow of an older adult. A biopsy was performed to make sure this was not already Bowen disease or squamous cell carcinoma. (Courtesy of Richard P. Usatine, MD.)





Figure 166-5



Actinic keratoses on the balding head of an older man. Hair loss results in less natural sun protection and is a risk factor for skin cancers on the scalp. The visible and palpable actinic keratoses were treated with cryotherapy. (Courtesy of Richard P. Usatine, MD.)





Figure 166-6



Actinic keratoses on the dorsum of the hand with some lesions suspicious for Bowen disease (squamous cell carcinoma in situ). (With permission from Usatine RP, Moy RL, Tobinick EL, Siegel DM. Skin Surgery: A Practical Guide. St. Louis, MO: Mosby; 1998,.)





Figure 166-7



Lesions on the arm of an older man with Bowen disease in the central lesion and actinic keratosis on the upper lesion. (Courtesy of Richard P. Usatine, MD.)





Figure 166-8



Bowen disease on the leg of an older woman. (Courtesy of Richard P. Usatine, MD.)







Typical Distribution



Both lesions are seen in areas with greatest sun exposure such as the face, forearms, dorsum of hands, lower legs of women, and the balding scalp (Figure 166-5) and tops of the ears in men.






Laboratory Studies



AKs that appear premalignant may be diagnosed by observation only and treated with destructive methods (e.g., excision, electrosurgery, or cryosurgery) without biopsy. BD requires a biopsy for diagnosis. BD or SCC should be biopsied prior to treatment. A shave biopsy should produce enough tissue for histopathology.




Tags:
Jun 5, 2016 | Posted by in GENERAL & FAMILY MEDICINE | Comments Off on Actinic Keratosis and Bowen Disease

Full access? Get Clinical Tree
Get Clinical Tree app for offline access