Actinic Keratosis Treatment & Management

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

Medical Care

Actinic keratoses may remain unchanged, spontaneously resolve, or progress to invasive squamous cell carcinoma.[15] The fate of any one actinic keratosis is impossible to predict. Although the risk of progression of any one actinic keratosis to invasive squamous cell carcinoma is small (at most approximately 10%),[1] a patient may have many lesions, and thus the risk of progression becomes significant. Additionally, actinic keratoses can be clinically indistinguishable from more serious cutaneous malignancies, including squamous cell carcinoma and lentigo maligna.[35, 36] Therapy is generally well tolerated and simple; therefore, treatment of all actinic keratoses is warranted.

The appropriate treatment is generally chosen based on the number of lesions present and the efficacy of the treatment.[37] Additional variables to consider include persistence of the lesion(s), age of the patient, history of skin cancer, and tolerability of the treatment modality.[1] Treatment consists of 2 broad categories: surgical destruction of the lesion and medical therapy. Medical management begins with educating the patient to limit sun exposure. Patients should be cautioned to avoid sun exposure from 10:00 am to 3:00 pm as much as possible. They also must wear adequate sunscreens and protective clothing daily.[38]

Medical therapy has the advantage of being able to treat large areas with many lesions. The disadvantages of medical therapies include lengthy courses of treatment with irritation and discomfort. The US Food and Drug Administration (FDA) has approved 4 medications for the treatment of actinic keratoses. These are topical 5-fluorouracil (5-FU), 5% and 3.75% imiquimod cream, topical diclofenac gel, and PDT with topical delta-aminolevulinic acid.[39, 40, 41]

5-Fluorouracil

The most experience in topical therapy for actinic keratoses is with 5-FU, known to inhibit thymidylate synthetase and cause cell death in actively proliferating cells.[42] Several formulations are available, including a 5% cream or solution, a 2% solution, a 1% cream or solution, and, most recently, a micronized 0.5% cream.[39] Although not well studied, efficacy among the various formulations does not seem to differ significantly.[43, 44]

The most popular formulation is the 5% cream, which is applied twice daily for 1 month. During the treatment phase, the lesions become increasingly erythematous and cause discomfort; small subclinical lesions become visible. This treatment can be temporarily disfiguring, with erythematous ulcerations and crust formation. However, if the patient completes the treatment, the lesions usually heal within 2 weeks of stopping treatment, the complexion is smooth, and the actinic keratoses are improved.

The 0.5% micronized cream was developed to increase tolerability because inflammation and discomfort can be a limiting factor in the use of topical 5-FU. The 0.5% micronized cream is applied once daily for 1 month.

Usage of the 0.5% micronized cream 1 week prior to cryosurgery has also been shown to produce complete lesion clearance in a higher number of patients compared with cryosurgery alone (32.4% and 15%, respectively).[45] Note the images below.

Actinic keratosis during treatment with topical 5-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 topicActinic keratosis right after treatment with topical 5-fluorouracil. Courtesy of Hon Pak, MD, and reviewed by Ross Levy, MD.

Imiquimod

Imiquimod is a topical medication that up-regulates a variety of cytokines, which, in turn, invoke a nonspecific immune response (interferons, natural killer cells) and a specific immune response (T cells). It is applied 2-3 times a week for up to 4 months, although generally 1 month is sufficient.[46] Reaction to the drug is idiosyncratic, with some patients barely reacting and others developing marked inflammation. Subclinical lesions previously not appreciated may become inflamed during therapy. In patients with a brisk inflammatory response, dosing is reduced to twice or even once a week, with preservation of therapeutic efficacy but increased tolerability.

Two new formulations of imiquimod (2.5% and 3.75%) were studied and found to be efficacious in clearing actinic keratoses (25% and 34% clearance, respectively), with a more intuitive daily dosing schedule. Although not as efficacious as 5% imiquimod, the new formulations cause less irritation, promoting better compliance.[47] Experimental evidence suggests patients may develop T-cell memory after treatment with this drug and thus may be less likely to develop new actinic keratoses in the future. Imiquimod 5% cream has also been shown to be safe and effective in transplantation patients.[48, 49]

Ingenol mebutate topical

Ingenol mebutate gel (Picato) was approved by the FDA for actinic keratosis in January 2012 as a 2-3 day course of therapy. The dosage for actinic keratosis differs depending on the application site. The 0.015% gel is used for application to the face or scalp for 3 consecutive days, whereas the 0.05% gel is used for application to the trunk or extremities for 2 consecutive days.

Four multicenter, randomized, double-blind studies showed that ingenol mebutate gel applied topically for 2 to 3 days is effective for field treatment of actinic keratoses. The studies reported adverse effects that were generally mild to moderate in intensity and resolved without sequelae.[50]

Although a precise mechanism of action has not been defined, a dual mechanism of action was described by Rosen et al. This dual mechanism includes 1) rapid lesion necrosis by mitochondrial swelling and membrane disruption, and 2) specific neutrophil-mediated, antibody-dependent cellular cytotoxicity by antibodies produced from B cells that bind to antigens on dysplastic epidermal cells.[51]

Topical diclofenac sodium 3% gel

Topical diclofenac sodium 3% gel is a nonsteroidal anti-inflammatory drug approved by the FDA for the treatment of actinic keratosis. Its mechanism of action against actinic keratoses is unknown. It is effective therapy when applied twice a day for 3 months. A shorter course of therapy is dramatically less effective. Its chief advantage is that it produces little-to-no inflammation and thus is very well tolerated. Diclofenac therapy after cryosurgery has also been shown to produce complete lesion clearance in a higher number of patients compared with cryosurgery alone (64% vs 32%, respectively).[52]

Photodynamic therapy

PDT uses a light-sensitizing compound that preferentially accumulates in actinic keratosis cells, where it can be activated by the appropriate wavelength of light. Delta-aminolevulinic acid is a component of the heme biosynthetic pathway that accumulates preferentially in dysplastic cells. Once inside these cells, it is enzymatically converted to protoporphyrin IX, a potent photosensitizer. With exposure to light of an appropriate wavelength, oxygen free radicals are generated and cell death results.[53]

Patients experience pain, similar in scope to the pain resulting from topical 5-FU, in the areas treated. The treated lesions may become erythematous and crusted. One treatment with PDT appears to be as effective as topical 5-FU therapy.[54]

Immunosuppressed patients may also benefit from PDT in the prevention of nonmelanoma skin cancers.[55]

When used with light sources that have a cosmetic benefit by themselves, such as the pulsed dye laser or intense pulsed light devices, a cosmetic benefit may be seen from the use of topical PDT beyond that of actinic keratosis eradication. Compared with other destructive therapeutic options such as cryotherapy, PDT may offer better cosmetic results and higher patient preference.[55, 56]

An unknown parameter in the use of topical PDT is the optimal incubation time following application of the topical aminolevulinic acid before light exposure. A second unknown parameter is the optimal light source to use for this treatment. Ongoing studies are addressing these issues.[55, 57]

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Surgical Care

The goal of surgical therapy is complete eradication of the actinic keratoses, usually by physical destruction, with limited-to-no damage to surrounding healthy tissue. When the diagnosis is unclear and an invasive tumor is possible, biopsy is indicated. However, biopsy generally leaves a scar.

Cryosurgery refers to use of a cryogen to lower the temperature of the skin and produce cell death. The most common cryogen used is liquid nitrogen, with a temperature of -195.8°C. Keratinocytes die when exposed to approximately -40 to -50°C. Other structures in the skin, such as collagen, blood vessels, and nerves, are more resistant to the lethal effects of cold than keratinocytes. Melanocytes are more sensitive than keratinocytes; thus, cryosurgery often leaves white spots. This technique has not been studied in a scientific fashion until 2004, when it was demonstrated to produce an overall clearance rate of 67-88%.[56, 58]

Lesions suggestive of invasive cancer may be treated with curettage, shave excision, or conventional excision, all of which provide a sample for histologic evaluation. These treatments require local anesthesia, produce a wound that requires time to heal, and are likely to scar.

Cosmetic resurfacing procedures, in which the entire epidermis is removed, sometimes with some portion of the dermis, are effective for actinic keratosis eradication. Cosmetic resurfacing procedures include medium and deep chemical peels, dermabrasion, and ablative laser resurfacing.[59, 60, 61] All of these are cosmetic procedures unlikely to be covered by insurance, all carry the risk of scarring and infection, and all require experience and expertise on the part of the dermatologic surgeon. They are highly unlikely to be performed solely for actinic keratosis therapy.

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Diet

One study has suggested that a low-fat diet in humans leads to greater resolution of existent actinic keratoses and the development of fewer new ones during the study period.[18]

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Activity

Instruct patients to practice sun safety, such as the use of sunscreen and protective clothing, and to limit outdoor activity from 10:00 am to 3:00 pm.[38]

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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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