> Table of Contents > Keratosis, Actinic
Keratosis, Actinic
Zoltan Trizna, MD, PhD
image BASICS
DESCRIPTION
  • Common, usually multiple, premalignant lesions of sun-exposed areas of the skin. Many resolve spontaneously, and a small proportion progress to squamous cell carcinoma
  • Common consequence of excessive cumulative ultraviolet (UV) light exposure
  • Synonym(s): solar keratosis
Geriatric Considerations
Frequent problem
Pediatric Considerations
Rare (if child, look for freckling and other stigmata of xeroderma pigmentosum)
EPIDEMIOLOGY
Incidence
  • Rates vary with age group and exposure to sun.
  • Predominant age: ≥40 years; progressively increases with age
  • Predominant sex: male > female
  • Common in those with blonde and red hair; rare in darker skin types
Prevalence
  • Age-adjusted prevalence rate for actinic keratoses (AKs) in U.S. Caucasians is 6.5%.
  • For 65- to 74-year-old males with high sun exposure: ˜55%; low sun exposure, ˜18%
ETIOLOGY AND PATHOPHYSIOLOGY
  • The epidermal lesions are characterized by atypical keratinocytes at the basal layer with occasional extension upward. Mitoses are present. The histopathologic features resemble those of squamous cell carcinoma (SCC) in situ or SCC, and the distinction depends on the extent of epidermal involvement.
  • Cumulative UV exposure
Genetics
The p53 chromosomal mutation has been shown consistently in both AKs and SCCs. Many new genes have been shown recently to have similar expression profiles in AKs and SCCs.
RISK FACTORS
  • Exposure to UV light (especially long-term and/or repeated exposure due to outdoor occupation or recreational activities, indoor or outdoor tanning)
  • Skin type: burns easily, does not tan
  • Immunosuppression, especially organ transplantation
GENERAL PREVENTION
Sun avoidance and protective techniques are helpful.
COMMONLY ASSOCIATED CONDITIONS
  • SCC
  • Other features of chronic solar damage: lentigines, elastosis, and telangiectasias
image DIAGNOSIS
PHYSICAL EXAM
  • Usually small (<1 cm), often multiple red, pink, or brown macules, papules, or plaques that are rough to palpation
  • Yellow or brown adherent scale is often present on top of the lesion.
  • Several clinical variants exist.
    • Atrophic: dry, scaly macules with indistinct borders and an erythematous base
    • Hypertrophic: Overlying hyperkeratosis (in an extreme form, cutaneous horn) may be impossible to differentiate from SCC clinically.
    • Pigmented: smooth tan/brown plaque, spreading centrifugally
    • Bowenoid: red scaly plaques with distinct borders
    • Actinic cheilitis: inflammatory lesion involving usually the lower lip
DIFFERENTIAL DIAGNOSIS
  • SCC (hypertrophic type)
  • Keratoacanthoma
  • Bowen disease
  • Basal cell carcinoma
  • Verruca vulgaris
  • Less likely: verrucous nevi, warty dyskeratoma, lichenoid keratoses, seborrheic keratoses, porokeratoses, seborrheic dermatitis or psoriasis (near hairline), lentigo maligna, solar lentigo, discoid lupus erythematosus
DIAGNOSTIC TESTS & INTERPRETATION
Diagnostic Procedures/Other
  • The diagnosis is usually made clinically, except where there is a suspicion of carcinoma.
  • Skin biopsy is especially recommended if large, ulcerated, indurated, or bleeding; or if the lesions are nonresponsive to treatment.
Test Interpretation
  • Dysplastic keratinocytes in lower levels of epidermis with a dermal lymphocytic infiltrate
  • Neoplastic cells, mostly found in the lower epidermal layers, are cytologically identical to those of SCCs.
  • If neoplastic cells extend throughout entire epidermis or into the dermis, the lesions will qualify as an SCC in situ or invasive SCC, respectively.
  • Malignant cells are sparse except of the bowenoid variety.
  • Hypertrophic, atrophic, bowenoid, acantholytic, and pigmented varieties show the corresponding epidermal findings.
image TREATMENT
First-line treatment is cryotherapy (technically, this is considered surgery, especially by insurance companies) (1,2)[A]. Medical therapy is usually reserved for extensive AKs (“field therapy”).
GENERAL MEASURES
  • Sun-protective techniques
  • Sunscreens and physical sun protection recommended.
MEDICATION
First Line
  • Topical treatments target both visible and subclinical lesions.
  • With the exception of generic 5-fluorouracil, medication cost is high ($600 to $1,200 per course).
  • Topical fluorouracil (Efudex, Carac, Fluoroplex cream, Fluoroplex solution)
    • Every day—BID for 3 to 6 weeks, depending on the brand, concentration, and formulation
    • Can be very irritating
    • May be most effective of the topical treatments (3)[A] listed in this section.
  • P.579

  • Topical imiquimod (Aldara) 5% cream
    • Apply 2 days per week at HS for up to 16 weeks to an area not larger than the forehead or one cheek.
    • Can be irritating
  • Topical imiquimod (Zyclara) 3.75% cream
    • Apply once a day for 2 weeks, followed by no treatment for the next 2 weeks; then apply once a day for another 2 weeks.
    • Can be irritating
  • Topical ingenol mebutate (Picato) 0.015% and 0.05% gel
    • Apply to the face and scalp once a day for 3 consecutive days.
    • Apply to the trunk and extremities once a day for 2 consecutive days.
      • It should only be used on one contiguous skin area of not more than 25 cm2.
      • Cases of severe allergic reactions (including anaphylaxis) and herpes zoster reactivation unrelated to application errors have been reported.
  • Diclofenac (Solaraze) 3% gel
    • Apply BID for 60 to 90 days.
Second Line
  • Topical tretinoin (Retin-A) or tazarotene (Tazorac): may be used to enhance the efficacy of topical fluorouracil
  • Systemic retinoids: used infrequently
ADDITIONAL THERAPIES
Close monitoring with no treatment is an appropriate option for mild lesions.
SURGERY/OTHER PROCEDURES
  • Cryosurgery (“freezing,” liquid nitrogen)
    • Most common method for treating AK
    • Cure rate: 75-98.8%
    • May leave scars
    • May be superior to photodynamic therapy for thicker lesions
  • Photodynamic therapy with a photosensitizer (e.g., aminolevulinic acid) and “blue light”
    • May clear >90% of AKs
    • Less scarring than cryotherapy
    • May be superior to cryotherapy, especially in the case of more extensive skin involvement
  • Curettage and electrocautery (electrodesiccation and curettage [ED&C]; “scraping and burning”)
  • Medium-depth peels, especially for the treatment of extensive areas
  • CO2 laser therapy
  • Dermabrasion
  • Surgical excision (excisional biopsy)
image ONGOING CARE
FOLLOW-UP RECOMMENDATIONS
Patient Monitoring
Depends on associated malignancy and frequency with which new AKs appear
PATIENT EDUCATION
  • Teach sun-protective techniques.
    • Limit outdoor activities between 10 AM and 4 PM.
    • Wear protective clothing and wide-brimmed hat.
    • Proper use (including reapplication) of sunscreens with SPF >30, preferably a preparation with broad-spectrum (UV-A and UV-B) protection
  • Teach self-examination of skin (melanoma, squamous cell, basal cell).
  • Patient education materials
    • http://dermnetnz.org/lesions/solar-keratoses.html
    • www.skincarephysicians.com/actinickeratosesnet/index.html
    • www.skincancer.org/Actinic-Keratosis-and-Other-Precancers.htm
PROGNOSIS
Very good. A significant proportion of the lesions may resolve spontaneously (4), with regression rates of 20-30% per lesion per year.
REFERENCES
1. Helfand M, Gorman AK, Mahon S, et al. Actinic Keratoses. Rockville, MD: Agency for Healthcare Research and Quality; 2001.
2. de Berker D, McGregor JM, Hughes BR. Guidelines for the management of actinic keratoses. Br J Dermatol. 2007;156(2):222-230.
3. Gupta AK, Paquet M. Network meta-analysis of the outcome “participant complete clearance” in nonimmunosuppressed participants of eight interventions for actinic keratosis: a follow-up on a Cochrane review. Br J Dermatol. 2013;169(2):250-259.
4. Criscione VD, Weinstock MA, Naylor MF, et al. Actinic keratoses: natural history and risk of malignant transformation in the Veterans Affairs Topical Tretinoin Chemoprevention Trial. Cancer. 2009;115(11):2523-2530.
Additional Reading
&NA;
  • Kanellou P, Zaravinos A, Zioga M, et al. Genomic instability, mutations and expression analysis of the tumour suppressor genes p14(ARF), p15(INK4b), p16(INK4a) and p53 in actinic keratosis. Cancer Lett. 2008;264(1):145-161.
  • Rossi R, Mori M, Lotti T. Actinic keratosis. Int J Dermatol. 2007;46(9):895-904.
Codes
&NA;
ICD10
L57.0 Actinic keratosis
Clinical Pearls
&NA;
  • AKs are premalignant lesions.
  • Often more easily felt than seen
  • Therapy-resistant lesions should be biopsied, especially on the face.