Skin Disorders Guide

Diagnostic Hallmarks

1. Sun-exposed surfaces of the face, ears, bald scalp, hands, and arms
2. Lesions occur on visibly sun-damaged skin
3. Lesions occur primarily in fair-skinned people who tan poorly

Clinical Presentation

Clinically, actinc keratoses consist of little more than bits of scale adherent to sun-damaged skin, there is little in the way of underlying substance on palpation. Small lesions are barely elevated and simply feel like slightly roughened spots of skin. More advanced keratoses appear as small flecks of gray, white, or slightly yellow scale that seems to be “stuck on” the underlying skin. Early lesions may be as little as 2-4 mm in diameter; older lesions are usually 5-15 mm in diameter; and both are wider than they are tall.

Actinic keratoses occur against a background of freckled, atrophic, reddened, telangiectatic, sun-damaged skin. Thus they are found primarily on the face, ears, bald scalp, and dorsal surface of the hands and arms. Occasionally, the shoulders and back are involved. The development of squamous cell carcinoma in an advanced actinic keratosis is recognized by the presence of an underlying firm papule or a shallow erosion with roughened, scaling edges.

The diagnosis of an actinic keratosis is generally made on a clinical basis. Confirmation, if desired, can easily be obtained by shave biopsy. Lesions that have a papular or an eroded base require biopsy so that the presence of any carcinomatous change can be recognized.

Course and Prognosis

Most clinicians believe that actinic keratoses left untreated will eventually transform into squamous cell carcinomas. That potential no doubt exists, but it often remains unexpressed. Small actinic keratoses can be left untreated for years without exposing the patient to undue risk. Nevertheless, their premalignant nature should be appreciated by both clinician and patient lest a cavalier attitude lead to the development of an otherwise easily preventable, serious problem.

Recurrences at the margins of treated actinic keratoses are frequently seen. These are not unexpected and simply reflect the fact that surrounding skin has shared in significant sun damage. Such lesions should be evaluated on their own merits, the recurrence itself carries no particular implication in terms of malignancy.

Pathogenesis

Actinic keratoses consist of localized areas of epithelial cells that are undergoing dysplastic change. These changes are induced by long-term exposure to sunlight. The wavelengths of sunlight responsible for carcinogenesis appear to be in the 280- to 320-nm ultraviolet light (sunburn) spectrum (UVB). Longer wavelengths in the 320- to 400-nm ultraviolet light spectrum (UVA) may play a synergistic role through the process of photoaugmentation.

Oncogenic damage to the skin is not instantaneous. It requires both years of cumulative exposure and a long latent period. Thus patients, often to their considerable surprise, develop their first lesions years after their most intense outdoor exposure. In addition to the quantity of sunlight received, oncogenic risk factors include the quality of the sunlight and the person’s ability to mount a protective, tanning response. Thus, sunlight exposure at equatorial latitudes and at high elevations contains a higher proportion of UVB wavelengths and is proportionally more carcinogenic than exposure at other latitudes and at lower elevations. Light-skinned people, particularly those of Celtic origin, who tan poorly are at additional risk. Results of animal studies show that other environmental effects, such as heat, humidity, and wind, augment the carcinogenic effect of sunlight.

Therapy

Individual keratoses that are sharply demarcated are best treated with liquid nitrogen cryotherapy . Patients with more diffusely damaged skin can be treated with topically applied fluorouracil or masoprocol if they are willing to accept the unsightly appearance and considerable discomfort that accompanies the use of this agent. Unfortunately, fluorouracil treatment of the hands and arms is considerably less effective than that carried out for the face and bald scalp.

Biopsy is not necessary prior to treating actinic keratoses with either cryotherapy, masoprocol, or fluorouracil, unless there is clinical evidence of carcinomatous change . All treated patients should be reexamined at regular intervals, however, so that new lesions (whether keratoses or carcinomas) can be recognized in their earliest stages.

Patients with actinic keratoses should be taught sun protective techniques. Outdoor activities should be transferred to the early morning or late afternoon, and protective clothing and hats should be worn. Most important of all, patients should be instructed in the daily use of topically applied sunscreens . Even if all of these measures are taken, however, patients will continue to develop new lesions for many additional years, based on the latent damage of previous exposure. Patients should be forewarned of this eventuality so that they do not become discouraged over what appears to be a lack of efficacy of their sun protective efforts.