eMedicine Specialties > Dermatology > Malignant Neoplasms

Actinic Keratosis

Author: James M Spencer, MD, Professor of Clinical Dermatology, Mount Sinai School of Medicine, New York; Private Practice, Spencer Dermatology, St Petersburg, Florida
Coauthor(s): Amy Lynn Basile, DO, MPH, Sun Coast Hospital/Largo Medical Center, Largo, Florida
Contributor Information and Disclosures

Updated: Feb 18, 2009

Introduction

Background

Actinic keratosis (AK) is a UV light–induced lesion of the skin that may progress to invasive squamous cell carcinoma.1,2,3 It is by far the most common lesion with malignant potential to arise on the skin. Actinic keratosis is seen in fair-skinned persons on skin areas that have had long-term sun exposure.4 In Australia, the country with the highest skin cancer rate in the world, the prevalence of actinic keratosis among adults older than 40 years has been reported to range from 40-60%.5

The premalignant nature of actinic keratosis was recognized almost 100 years ago, and the name literally means thickened scaly growth (keratosis) caused by sunlight (actinic). In the United States, actinic keratosis represents the second most frequent reason for patients to visit a dermatologist.6

An actinic keratosis may follow 1 of 3 paths; it may regress, it may persist unchanged, or it may progress to invasive squamous cell carcinoma. The actual percentage that progress to invasive squamous cell carcinoma remains unknown, and estimates have varied from as low as 0.1% to as high as 10%.1,7 Furthermore, predicting which course each individual lesion will follow is impossible.

Early data suggest that actinic keratoses may also progress to basal cell carcinoma, a paradigm originally not considered in the actinic keratosis risk profile; further research is necessary to confirm this potential relationship.8 Overall, actinic keratoses can be safely and effectively eradicated; therefore, therapy is warranted.

Pathophysiology

Actinic keratoses arise on fair-skinned people in areas of long-term sun exposure, such as the face, ears, bald scalp, forearms, and backs of the hands.4 However, they may occur on any area that is repeatedly exposed to the sun, such as the back, the chest, and the legs. Long-term UV light exposure is implicated as the cause from both epidemiologic observations and molecular analysis of tumor cells.2,4 Actinic keratosis frequency correlates with cumulative UV exposure.4 Therefore, the frequency of actinic keratosis increases with each decade of life, is greater in residents of sunny countries closer to the equator, and is greater in persons with outdoor occupations.4,9 DNA analysis of the cells within actinic keratoses shows characteristic UV-induced mutations in key genes, including TP53 and deletion of the gene coding for p16 tumor suppressor protein.2,10,11

Clinically, actinic keratoses range from barely perceptible rough spots of skin to elevated, hyperkeratotic plaques several centimeters in diameter.12 Most often, they appear as multiple discrete, flat or elevated, keratotic lesions. Lesions typically have an erythematous base covered by scale (hyperkeratosis).12 They are usually 3-10 mm in diameter and gradually enlarge into broader, more elevated lesions.

Over time, actinic keratoses may develop into invasive squamous cell carcinoma; according to one study of almost 7000 patients, among the small percentage of actinic keratoses that progress into squamous cell carcinoma, the length of time for this transformation to occur was approximately 2 years.13 Development of actinic keratoses may occur as early as the third or fourth decade of life in patients who live in areas of high solar radiation, are fair-skinned, and do not use sunscreen for photoprotection.4 Usually, patients demonstrate a background of solar-damaged skin with telangiectasias, elastosis, and pigmented lentigines.14

In both histologic and molecular parameters, actinic keratoses share features with squamous cell carcinoma.15 Actinic keratosis is an epidermal lesion characterized by aggregates of atypical, pleomorphic keratinocytes at the basal layer that may extend upwards to involve the granular and cornified layers.15 The epidermis itself shows an abnormal architecture, with acanthosis, parakeratosis, and dyskeratosis. Cellular atypia is present, and the keratinocytes vary in size and shape; mitotic figures are present.15 This presentation may resemble Bowen disease or carcinoma in situ, and the distinction between the 2 is a matter of degree (extent of the lesion) rather than differences in individual cells.15

Often, marked hyperkeratosis and areas of parakeratosis with loss of the granular layer are present. A dense inflammatory infiltrate is usually present. The case has been made that actinic keratosis is the earliest manifestation of squamous cell carcinoma and should be regarded as such rather than as a precancerous lesion.15,16 Others have argued that calling actinic keratosis a carcinoma unduly alarms patients. Cockerell has proposed renaming the lesion keratinocytic intraepidermal neoplasia, using a nomenclature analogous to cervical and vulvar intraepithelial neoplasia.15

Frequency

United States

Actinic keratosis occurs primarily in whites, the frequency of which correlates with cumulative UV exposure.4 Therefore, frequency increases with age, proximity to the equator, and outdoor occupation. Actinic keratoses are seen more in men than in women and have also been correlated with a high-fat diet.9,17 Overall, the rate in the United States is estimated to range from 11-26%.5

International

The prevalence is highest in Australia, where a light-skinned population is common and outdoor sports are very popular activities.18 Overall, actinic keratosis is estimated to be present in 40-60% of the Australian population older than 40 years.5

Mortality/Morbidity

Lesions begin as barely perceivable rough spots of skin, better felt than seen.14,19 Early lesions feel like sandpaper; later lesions become erythematous, scaly plaques that may enlarge to several centimeters.4,14 Lesions may remain unchanged for years, may spontaneously regress, or may progress to invasive squamous cell carcinoma.7 Most actinic keratoses do not progress to invasive squamous cell carcinoma; however, most invasive squamous cell carcinomas have evidence of a preexisting actinic keratosis.4,7 Invasive squamous cell carcinoma may produce significant morbidity by direct extension into facial structures. In less than 10% of cases, invasive squamous cell carcinoma may metastasize, with a low 5-year survival rate.20,21

Race

The prevalence of actinic keratosis is much higher in individuals with fair skin and blue eyes and is lower in individuals with darker skin types.9 Actinic keratosis is relatively nonexistent in black skin.22 Patients with actinic keratoses tend to have Fitzpatrick type I or II skin, which burns and does not tan.4 The prevalence is reduced precipitously in persons with Fitzpatrick types III, IV, and V skin and is nonexistent in those with Fitzpatrick type VI skin.22 Although the incidence of cutaneous malignancies in darker-skinned individuals is much lower than in white persons, UV exposure may still play a role in the etiology of squamous and basal cell carcinoma; screening and sun safety education should still be promoted because cutaneous malignancies in darker-skinned individuals can be very aggressive.22

Sex

The prevalence of actinic keratosis is higher in men than in women.4 This is theorized to result from a greater likelihood that men have an outdoor occupation and thus have greater cumulative UV exposure.9

Age

One of the most important determinants of actinic keratosis risk is age, particularly when evaluated with other strong predictors, including cumulative sun exposure, place of birth, occupation, and skin type.4,9 Actinic keratoses can occur in patients aged 20-30 years, but they are more common in patients aged 50 years and older.4

Clinical

History

Actinic keratoses are seen almost exclusively in whites, especially those with skin phototypes I and II.9 The incidence increases with each decade of life, and men have a slightly increased frequency of actinic keratosis.5,9 Actinic keratosis is correlated with long-term UV exposure, such as occurs in persons with outdoor occupations.9

Patient who are immunosuppressed following organ transplantation are at markedly increased risk of developing actinic keratoses.23 The lesions still arise in areas of long-term exposure,13,24,25 and they are thought to be actinically induced.

Physical

The typical patient with actinic keratoses is an elderly, fair-skinned, sun-sensitive person.9 The lesions arise in areas of long-term sun exposure, including the face, ears, bald scalp in men, and the dorsal forearms and hands.4,24 Actinic keratoses begin as small rough spots that are easier felt than seen, often described as being similar to rubbing sandpaper.14 With time, the lesions enlarge, usually becoming red and scaly; most are only 3-10 mm, but they may enlarge to several centimeters.14,26,27

Courtesy of Hon Pak, MD, and reviewed by Ross Lev...

Courtesy of Hon Pak, MD, and reviewed by Ross Levy, MD.

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Courtesy of Hon Pak, MD, and reviewed by Ross Lev...

Courtesy of Hon Pak, MD, and reviewed by Ross Levy, MD.



Erythematous, scaly lesions on the temple area, t...

Erythematous, scaly lesions on the temple area, typical of actinic keratosis.

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Erythematous, scaly lesions on the temple area, t...

Erythematous, 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.28

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.2,11 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 keratoses23 ; however, actinic keratoses do not occur without sun exposure.

Additional studies have shown an association between cutaneous human papillomavirus and actinic keratosis.29,30,31 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 .30 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.30 The exact mechanism by which this family of viruses contributes to tumor growth remains unknown.

More on Actinic Keratosis

Overview: Actinic Keratosis
Differential Diagnoses & Workup: Actinic Keratosis
Treatment & Medication: Actinic Keratosis
Follow-up: Actinic Keratosis
Multimedia: Actinic Keratosis
References
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Further Reading

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Keywords

actinic keratosis, solar keratosis, carcinoma in situ, carcinoma in-situ, premalignant skin lesions, sun-related growth, hyperkeratosis, skin cancers, telangiectasias, elastosis, pigmented lentigines, acanthosis, parakeratosis, dyskeratoses, Fitzpatrick type I and II skin, multiple erythematous keratoses

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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

Coauthor(s)

Amy Lynn Basile, DO, MPH, Sun Coast Hospital/Largo Medical Center, Largo, Florida
Amy Lynn Basile, DO, MPH is a member of the following medical societies: American Medical Association, American Osteopathic Association, and American Osteopathic College of Dermatology
Disclosure: Nothing to disclose.

Medical Editor

Kelly M Cordoro, MD, Fellow and Clinical Instructor, Department of Pediatric Dermatology, University of California at San Francisco; Assistant Professor (On Educational Leave), Assistant Program Director for Resident Medical Education, Department of Dermatology, University of Virginia 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.

Pharmacy Editor

Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center
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.

Managing Editor

Mary Farley, MD, Dermatologic Surgeon/Mohs Surgeon, Anne Arundel Surgery Center
Disclosure: Nothing to disclose.

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine 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, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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