Actinic keratosis- Causes, Symptoms, Diagnosis, Treatment and Ongoing care
- Synonym: Solar keratosis
- Common, usually multiple, premalignant skin lesions of sun-exposed areas of the skin
- Common consequence of excessive cumulative ultraviolet (UV) light exposure
Rare (if child, look for freckling and other stigmata of xeroderma pigmentosum)
- Incidence: Between 12.6% and 43.4% per year
- 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: It is 55.4%, and for those with low sun exposure, it is 18.5%.
- 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
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.
The epidermal lesions are characterized by atypical keratinocytes at the basal layer with occasional extension upwards. Mitoses are present. The histopathological features resemble those of SCC in situ or SCC, and the distinction depends on the extent of epidermal involvement.
Cumulative UV exposure
Commonly Associated Conditions
- Other features of chronic solar damage: Lentigines, elastosis, and telangiectasias
- 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).
- 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 & Interpretation
- 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 (1).
- If neoplastic cells extend throughout entire epidermis or into the dermis, the lesions will qualify as an SCC in situ or invasive SCC, respectively (2).
- Malignant cells are sparse except in the bowenoid variety.
- Hypertrophic, atrophic, bowenoid, acantholytic, and pigmented varieties show the corresponding epidermal findings.
- SCC (hypertrophic type)
- Bowen’s 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
First-line treatment is cryotherapy (technically this is considered surgery, especially by insurance companies) (2,3)[A].
- 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
- 3% diclofenac (Solaraze) gel:
- 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
- Sun-protective techniques
- Sunscreens and physical sun protection recommended
Close monitoring with no treatment is an appropriate option for mild lesions.
- 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
- Surgical excision (excisional biopsy)
Depends on associated malignancy and frequency with which new AKs appear
- Teach sun-protective techniques:
- Limit outdoor activities between 10 a.m. and 4 p.m.
- 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:
Very good. A significant proportion of the lesions may resolve spontaneously (4).
- AKs are premalignant lesions that may progress to SCCs. The rate of malignant transformation is unclear; the reported percentages vary (4).
- Patients with AKs are at increased risk for other cutaneous malignancies.
1. Rossi R, Mori M, Lotti T. Actinic keratosis. Int J Dermatol. 2007;46:895–904.
2. Helfand M, Gorman AK, Mahon S, Chan BKS, Neil Swanson N. AHRQ evidence report from OHSU Evidence-Based Practice Center 2001.
3. de Berker D, McGregor JM, Hughes BR, British Association of Dermatologists Therapy Guidelines and Audit Subcommittee et al. Guidelines for the management of actinic keratoses. Br J Dermatol.2007;156:222–30.
4. Criscione VD, Weinstock MA, Naylor MF, Luque C, Eide MJ, Bingham SF, Department of Veteran Affairs Topical Tretinoin Chemoprevention Trial Group et al. Actinic keratoses: Natural history and risk of malignant transformation in the Veterans Affairs Topical Tretinoin Chemoprevention Trial. Cancer. 2009;115:2523–30.
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. Cacner Lett.2008;264:145–61.
702.0 Actinic keratosis
201101007 actinic keratosis (disorder)
- AKs are premalignant lesions.
- Often more easily felt than seen
- Therapy-resistant lesions should be biopsied, especially on the face.