Actinic keratosis is a scaly, cutaneous lesion that is often seen in elderly patients. It develops on areas such as the face, ears and dorsa of the hands with chronic sun exposure. Actinic keratosis is a premalignant lesion, since histologic changes in the epidermis may progress to squamous cell carcinoma if left untreated.
Actinic Keratosis (Solar Keratosis)
Actinic keratosis appears as an adherent keratotic lesion that often has a hyperemic base (Figures 1 and 2). Many patients have multiple lesions measuring approximately 0.5 to 1.5 cm in diameter. Patients may also have elastotic degeneration of the skin related to chronic sun exposure.
Other clinical types include pigmented, hypertrophic and lichenoid actinic keratoses.[1(pp4-10)] Spreading pigmented actinic keratosis can resemble seborrheic keratosis, senile lentigo, melanocytic nevus and early malignant melanoma. The hypertrophic variant is hyperkeratotic and sometimes develops as a cutaneous horn. The lichenoid type may suggest the diagnosis of lichen planus, lichenoid drug eruption, lichenoid polymorphous fight eruption or lichenoid contact dermatitis.
Two special types of actinic keratosis are actinic cheilitis, which occurs on the lower lip, and actinic conjunctivitis. Actinic cheilitis has a high potential for transformation into squamous cell carcinoma and possible metastatic spread. Actinic conjunctivitis can also progress to squamous cell carcinoma.
Induration, erythema or erosion of actinic keratoses may be indicative of progression to squamous cell carcinoma. It is believed that several years can elapse before this transformation occurs. Up to 1 percent of patients with untreated actinic keratosis have been reported to develop squamous cell carcinoma.[2,3] However, the tumor that develops is usually slow-growing, with little tendency to metastasize.[1(pp4-10),4,5]
Histologically, actinic keratosis is a cutaneous dysplasia of the epidermis showing changes in cellular polarity and nuclear atypia (Figure 3). Five different types may occur: hypertrophic, atrophic, bowenoid, acantholytic or pigmented.[6] In contrast to malignant skin lesions, the basal cell lamina remains intact as the epidermis proliferates downward.
Since actinic keratosis is a superficial lesion, conservative, cosmetically acceptable treatment is appropriate. Cryosurgery is die treatment of choice, with a cure rate of 98.8 percent.[7] Treatment is simple, using liquid nitrogen applied with a cotton-tipped swab or with the openspray technique, and cosmetic results are excellent.
Actinic keratoses may also be removed by curettage followed by electrodessication. This method permits histologic examination of the curetted specimen. The application of 5-fluorouracil cream is also effective treatment but may be uncomfortable if a large area is affected. In cases of widespread involvement, either dermabrasion or chemical peeling can be useful. Multiple injections of [alpha.sub.2]-interferon have also been shown to induce complete regression.[8]
Large-scale educational campaigns have alerted the public to the dangers of sun exposure and emphasized the importance of prevention and protection.
Squamous Cell Carcinoma
Squamous cell carcinoma is the second most common type of skin cancer among white persons, following only basal cell carcinoma. Approximately 20 percent of all nonmelanoma skin cancers are due to squamous cell carcinoma.[9] The incidence of squamous cell carcinoma increases with age and is most common between the ages of 40 and 60 years. Squamous cell carcinoma often appears on sun-exposed areas of the body.[1(pp36-47)] Fair-skinned individuals and those who work outdoors are at greatest risk.
In addition to ultraviolet fight, other etiologic factors such as bums, chemical carcinogenesis, chronic immunosuppression, ionizing radiation and viral oncogenesis (human papillomavirus types 16, 18 and 31) may be involved in the development of squamous cell carcinoma. These lesions may also arise from benign dermatoses, such as porokeratosis, or from preexisting squamous cell carcinoma. However, they may also redevelop in a more aggressive form than that seen in actimc lesions.
Clinically, an early squamous cell carcinoma may be a small, erythematous, nodular or keratotic lesion. The lesion may become ulcerated (Figure 4), crusted, plaque-like, verrucous (Figure 5), or exophytic as it enlarges. The metastatic potential of the lesion varies with the type and location of the cancer. Actinic lesions and verrucous carcinoma have less potential for metastasis,[2,3] while lesions that develop on the lips, ears, vulva or penis have a greater tendency to metastasize.
Invasive squamous cell carcinoma refers to the proliferation of malignant keratinocytes beyond the basement membrane into the dermis.[6] Variation in the size of cells, atypical nuclei, keratinization and mitotic figures are characteristics of malignant cells (Figures 6 and 7).
Broders' grading system correlates biologic behavior of the tumor with the degree of histologic differentiation. Grade 1 represents the highest differenfiation of cells and indicates a low metastatic potential. In addition, horn pearls are often seen. In grade 2 carcinoma, differentiated cells range from 50 to 75 percent, while grades 3 and 4 have less differentiation, with spindle cell formation.
Treatment of squamous cell carcinoma includes local destruction, excisional surgery, Mohs surgery, cryosurgery and radiotherapy. The goal of treatment is complete eradication of the tumor, but the cosmetic and functional results are also important. Curettage and electrodesiccaton are frequently used to treat early squamous cell carcinoma, with a cure rate of over 95 percent.[10]
Excision is often the treatment of chioce. A skin flap or graft may be necessary for large tumors. A sufficient margin of normal tissue surrounding the lesion should be excised to ensure success. Mohs micrographic surgery is a specialized technique that is useful for difficult, recurrent, large or aggressive tumors.[11]
Cryosurgery involves freezing the tumor with liquid nitrogen.[12] It is particularly useful for lesions on the ears, since cartilage is resistant to the effects of deep freezing. Healing is by secondary intention. Radiotherapy is effective for tumors of the head and neck. Experience and good technique are crucial in the successful use of these modalities.
REFERENCES
[1.] Schwartz RA. Skin cancer. recognition and management. New York: Springer-Verlag 1988:4-10,36-47 [2.] Marks R, Rennie G, Selwood TS. Malignant transformation of solar keratoses to squamous cell carcinoma. lancet 1988;1(8589):795-7 [3.] Dodson JM, DeSpain J, Hewett JE, Clark DP. Malignant potential of actinic keratoses and the controversy over treatment. A patient-oriented perspective. Arch Dermatol 1991;127.1029-31. [4.] Nixon RL, Dorevitch AP, Marks R. Squamous cell carcinoma of the skin. Accuracy of clinical diagnosis and outcome of follow-'up in Australia. Med J Aust 1986;144:235-9. [5.] Marks R. The role of treatment of actinic keratoses the prevention of morbidity and mortality due to squamous cell carcinoma. Arch Dermatol 1991; 127-.1031-3. [6.] Lever WF, Schaumburg-Lever G. Histopathology of the skin. 7th ed. Philadelphia: Lippincott, 1990.523-77. [7.] Lubritz RR, Smolewski SA. Cryosurgery cure rate of actinic keratoses. j Am Acad Dermatol 1982,7: 631-2. [8.] Edwards L, Levine N, Weidner M, Piepkom M, Smiles K Effect of intralesional alpha 2-interferon on actinic keratoses. Arch Dermatol 1986;122:779-82. [9.] Scotto J, Fears TR, Fraumeni JF Jr. Incidence of non-melanoma skin cancer in the United States. Md.: National Cancer Institute, 1983; NIH publication no. 83-2433. [10.] Freeman RG, Knox JM, Heaton CL. The treatment of skin cancer. A statistical study of 1341 skin tumors comparing results obtained with irradiation, surgery and curettage followed by electrodessication. Cancer 1964;17-535-8. [11.] Robins P, Dzubow LM, Rigel DS. Squamous-cell carcinoma treated by Mohs' surgery: an experience with 414 cases in a period of 15 years. J Derm Surg Oncol 1981;7:800-1. [12.] Kuflik EG, Gage AA. The five-year cure rate achieved by cryosurgery for skin cancer. J Am Acad Dermatol 1991;24(6 Pt 1):1002-4.
Avery S. Kuflik, M.D. is currently completing an internship at the North Shore University Hospital (Manhasset, N.Y.) of Cornell University Medical College, New York, N.Y., and will begin a residency in dermatology at the Virginia Commonwealth University Medical College of Virginia, Richmond. He is a graduate of the University of Health Sciences/chicago Medical School m North Chicago.
Robert A. Schwartz, M.D., M.P.H. is professor of medicine, professor of pediatrics and professor and head of dermatology at UMDNJ-NEW Jersey Medical School, Newark. He received his medical degree from New York Medical College, Valhalla, arid completed a residency in dermatology at the University of Cincinnati College of Medicine. He is a member of AFP's editorial advisory board.
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