Basics
Description
- Common, usually multiple, premalignant lesions of sun-exposed areas of the skin
- 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
- Age-adjusted prevalence rate for actinic keratoses (AKs) in US Caucasians is 6.5%.
- For 65–74-year-old males with high sun exposure: ~55%; low sun exposure, ~18%.
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
Genetics
The p53 chromosomal mutation has been shown consistently in both AKs and squamous cell carcinomas (SCCs). Many new genes have been shown recently to have similar expression profiles in AKs and SCCs.
General Prevention
Sun avoidance and protective techniques are helpful.
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 SCC in situ or SCC, and the distinction depends on the extent of epidermal involvement.
Etiology
Cumulative UV exposure
Commonly Associated Conditions
- SCC
- Other features of chronic solar damage: Lentigines, elastosis, and telangiectasias
Diagnosis
History
- The lesions are frequently asymptomatic; symptoms may include pruritus, burning, and mild hyperesthesia.
- Lesions may enlarge, thicken, or become more scaly. They also may regress or remain unchanged.
- Most lesions occur on the sun-exposed areas (head and neck, hands, forearms).
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
Diagnostic Tests and Interpretation
Diagnostic Procedures/Surgery
- 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.
- 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.
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
Treatment
First-line treatment is cryotherapy (technically, this is considered surgery, especially by insurance companies) (1,2)[A].
Medication (Drugs)
First Line
- Topical treatments target both visible and subclinical lesions.
- Topical fluorouracil (Efudex, Carac, Fluoroplex cream, Fluoroplex solution):
- Every day–b.i.d. for 3–6 weeks, depending on the brand, concentration, and formulation
- Can be very irritating
- Topical imiquimod (Aldara) 5% cream:
- Apply every day, 2 days per week, for up to 4 months to an area not larger than the forehead or 1 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.
- 3% diclofenac (Solaraze) gel:
- Apply b.i.d. for up to 3 months.
- Topical tretinoin (Retin-A) or tazarotene (Tazorac): May be used to enhance the efficacy of topical fluorouracil
- Systemic retinoids: Used infrequently
Additional Treatment
General Measures
- Sun-protective techniques
- Sunscreens and physical sun protection recommended
Additional Therapies
Close monitoring with no treatment is an appropriate option for mild lesions.
Surgery/Other Procedures
- Cryosurgery (“freezing,” liquid nitrogen):
- Most common method
- 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 (ED&C, “scraping and burning”)
- Medium-depth peels, especially for the treatment of extensive areas
- CO2 laser therapy
- Dermabrasion
- Surgical excision (excisional biopsy)
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 . and 4 .
- 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:
Prognosis
Very good. A significant proportion of the lesions may resolve spontaneously (3).
Complications
- AKs are premalignant lesions that may progress to SCCs. The rate of malignant transformation is unclear; the reported percentages vary (3).
- Patients with AKs are at increased risk for other cutaneous malignancies.
Additional Reading
- 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;264:145–161.
- Rossi R, Mori M, Lotti T. Actinic keratosis. Int J Dermatol. 2007;46:895–904.
Codes
ICD-9
702.0 Actinic keratosis
ICD-10
- L57.0 Actinic keratosis
SNOMED
- 201101007 Actinic keratosis (disorder)
- 254667001 Hypertrophic solar keratosis
- 403200005 Atrophic actinic keratosis
- 403198004 lichenoid actinic keratosis (disorder)
- 403199007 Acantholytic actinic keratosis
Clinical Pearls
- AKs are premalignant lesions.
- Often more easily felt than seen
- Therapy-resistant lesions should be biopsied, especially on the face.
Authors
Zoltan Trizna, MD, PhD
Figures
Figure 22-1
Solar keratoses. Rough, scaly papules are present on the scalp. This is a typical finding in bald, elderly men with fair complexions who have spent much of their lives working outdoors.
Figure 22-2

Solar keratoses. This is a closer view of Figure 22.1.
Figure 22-3

Solar keratoses. This elderly woman has vitiligo. The solar keratoses occur primarily in areas of unprotected, melanocyte-poor, vitiliginous skin.
Figure 22-4

Pigmented solar keratosis. This lesion is slightly rough to the touch.
Figure 22-5

Hypertrophic solar keratosis. A shave biopsy was necessary to rule out squamous cell carcinoma.
Figure 22-6

Cutaneous horn produced by an actinic keratosis. Underlying the cutaneous horn, a biopsy revealed a solar keratosis.
Figure 22-8 A

Solar keratoses. A: Before treatment, few lesions are clinically visible. B: Two weeks after treatment with topical 5-fluorouracil, crusting and erythema are evident in areas that had lesions that were not initially apparent.
Figure 22-8 B

Solar keratoses. A: Before treatment, few lesions are clinically visible. B: Two weeks after treatment with topical 5-fluorouracil, crusting and erythema are evident in areas that had lesions that were not initially apparent.
Bibliography
- Helfand M, Gorman AK, Mahon S, et al. AHRQ evidence report from OHSU Evidence-Based Practice Center. 2001.
- de Berker D, McGregor JM, Hughes BR, et al. Guidelines for the management of actinic keratoses. Br J Dermatol. 2007;156:222–230. [PMID:17223860]
- 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;115:2523–2530. [PMID:19382202]
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