Actinic Keratosis Clinical Presentation

  • Author: James M Spencer, MD; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Mar 19, 2012
 

History

Actinic keratoses are seen almost exclusively in whites, especially those with skin phototypes I and II.[10] The incidence increases with each decade of life, and men have a slightly increased frequency of actinic keratosis.[5, 10] Actinic keratosis is correlated with long-term UV exposure, such as occurs in persons with outdoor occupations.[10]

Patient who are immunosuppressed following organ transplantation are at markedly increased risk of developing actinic keratoses.[24] The lesions still arise in areas of long-term exposure,[14, 25, 26] and they are thought to be actinically induced.

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Physical

The typical patient with actinic keratoses is an elderly, fair-skinned, sun-sensitive person.[10] The lesions arise in areas of long-term sun exposure, including the face, ears, bald scalp in men, and the dorsal forearms and hands.[4, 25] Actinic keratoses begin as small rough spots that are easier felt than seen, often described as being similar to rubbing sandpaper.[15] With time, the lesions enlarge, usually becoming red and scaly; most are only 3-10 mm, but they may enlarge to several centimeters.[15, 27, 28] Note the images below.

Courtesy of Hon Pak, MD, and reviewed by Ross LevyCourtesy of Hon Pak, MD, and reviewed by Ross Levy, MD. Erythematous, scaly lesions on the temple area, tyErythematous, scaly lesions on the temple area, typical of actinic keratosis.

Patients may develop multiple lesions within a single anatomic area, to the extent that the lesions collide and produce confluent actinic keratosis over a relatively large area. Variants may be brown (pigmented actinic keratosis), atrophic, bowenoid, lichen planus–like, or have exaggerated hyperkeratosis, producing a hornlike projection above the skin surface known as a cutaneous horn.[29]

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Causes

Actinic keratoses are induced by UV light. Both epidemiologic observations and molecular biologic characteristics of the tumor cells suggest UV light is sufficient by itself to induce actinic keratosis.[2, 12] Sensitivity to UV light is inherited; actinic keratoses occur more frequently in fair, redheaded, or blonde patients who burn frequently and tan poorly.[4] Increased sun exposure and higher-intensity exposure increase the chance of actinic keratosis development. Immunosuppression following organ transplantation dramatically increases the risk of developing actinic keratoses[24] ; however, actinic keratoses do not occur without sun exposure.

Additional studies have shown an association between cutaneous human papillomavirus and actinic keratosis.[30, 31, 32] The role of human papillomavirus in skin tumorigenesis was discovered the 1950s, and the group of known human papillomavirus types associated with skin tumorigenesis has been classified as beta-papillomavirus .[31] Beta-papillomavirus DNA has been identified in healthy skin and in squamous cell carcinoma, basal cell carcinoma, and actinic keratosis. A 2007 study suggests that only a small association exists between beta-papillomavirus and actinic keratosis; however, when evaluated in combination with other risk factors including age, sun damage, and skin color, the risk for actinic keratosis increased as much as 13-fold.[31] The exact mechanism by which this family of viruses contributes to tumor growth remains unknown.

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Contributor Information and Disclosures
Author

James M Spencer, MD  Professor of Clinical Dermatology, Mount Sinai School of Medicine, New York; Private Practice, Spencer Dermatology, St Petersburg, Florida

James M Spencer, MD is a member of the following medical societies: American Academy of Cosmetic Surgery, American Academy of Dermatology, American College of Mohs Micrographic Surgery and Cutaneous Oncology, American Dermatological Association, American Medical Association, American Society for Dermatologic Surgery, American Society for Laser Medicine and Surgery, and International Society for Dermatologic Surgery

Disclosure: Graceway Pharmaceutical Honoraria Speaking and teaching; Sanofi Aventis Honoraria Consulting; Medicis Grant/research funds Independent contractor; Peplin Grant/research funds Independent contractor

Coauthor(s)

Michelle Henry, MD  Resident Physician, Department of Dermatology, Mount Sinai School of Medicine of New York University

Disclosure: Nothing to disclose.

Specialty Editor Board

Kelly M Cordoro, MD  Assistant Professor of Clinical Dermatology and Pediatrics, Department of Dermatology, University of California, San Francisco School of Medicine

Kelly M Cordoro, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Association of Professors of Dermatology, Dermatology Foundation, Medical Society of Virginia, National Psoriasis Foundation, Society for Pediatric Dermatology, and Women's Dermatologic Society

Disclosure: Nothing to disclose.

Michael J Wells, MD  Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association

Disclosure: Nothing to disclose.

Mary Farley, MD  Dermatologic Surgeon/Mohs Surgeon, Anne Arundel Surgery Center

Disclosure: Nothing to disclose.

Catherine M Quirk, MD  Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania

Catherine M Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors, James Fulton Jr, MD, PhD, and Amy Lynn Basile, DO, MPH, to the development and writing of this article. The authors and editors of eMedicine also gratefully acknowledge the contributions of previous Chief Editor, William D. James, MD, to the development and writing of this article.

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Courtesy of Hon Pak, MD, and reviewed by Ross Levy, MD.
Actinic keratosis during treatment with topical 5-fluorouracil. Courtesy of Hon Pak, MD, and reviewed by Ross Levy, MD.
Actinic keratosis right after treatment with topical 5-fluorouracil. Courtesy of Hon Pak, MD, and reviewed by Ross Levy, MD.
Erythematous, scaly lesions on the temple area, typical of actinic keratosis.
 
 
 
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