Actinic keratoses (AK) are small rough spots that develop on the skin. The clinical appearance of AK ranges from barely perceptible rough, scaly patches on the skin to increased hyperkeratoses several centimeters across. Most often, AK lesions appear as multiple demarcated, flat, or elevated keratotic lesions, but as a rule, they gradually enlarge into broad, raised lesions.1,41,4
Actinic keratoses are caused by frequent and / or intense UV radiation over many years and usually occur on skin exposed to the sun. Actinic keratoses therefore develop in areas of long-term sun exposure such as the face, ears, hairless scalp, forearms and back of the hand. The incidence of AK correlates with the cumulative UV exposure and therefore increases with each decade of life.1,4 Epidemiological studies show that the following factors increase the individual risk of AK development:1,4
- Caucasians (blue eyes and fair skin, skin type I or II according to Fitzpatrick, who burns in the sun and does not turn brown)
- Close to the equator
- Occupation practiced outdoors
- Gender Male
- Advanced age (due to cumulative exposure)
- Immunosuppression (eg after organ transplantation)
Actinic keratoses are a very common skin disease; Millions of people worldwide are affected. Rates have reportedly increased in recent decades.1,4
In the UK, 15% of men and 6% of women have AK, with incidence increasing with age. Actinic keratoses account for up to 34% in males and 18% in females over the age of 70.2 The incidence in the US is between 11% and 26%, but the highest prevalence rates are in countries near the equator and a large one fair-skinned population have. The rates in Australia (Queensland) are over 55% in men and 37% in women aged 30 to 70.3
An AK lesion begins in the epidermis after damage from frequent or intense UV irradiation. This damage leads to changes in the texture and colour of the skin, causing the characteristic mottling and increased areas or lesions.1
It is important that actinic keratosis (AK) lesions are treated because the development of any one AK lesion is impossible to predict. Untreated, an AK lesion may follow 1 of 3 paths:5
- it may spontaneously regress;
- it may persist unchanged for many years;
- or it may progress into invasive squamous cell carcinoma (SCC).
Estimates of the proportion that progress to invasive SCC range from 0.1% to 10%. This transformation is thought to take approximately 2 years5 and most invasive SCC have evidence of a pre-existing AK lesion.6 Invasive SCC can cause significant morbidity by direct extension into facial structures. In less than 10% of cases, invasive SCC may metastasize, with a low 5-year survival rate.7
Treatment options for actinic keratosis include destructive therapies, topical medications, and field ablation treatments. In general, lesion-directed treatments are the primary approach for isolated lesions. Field-directed therapies are particularly useful for treating areas with multiple AKs.
- International League of Dermatological Societies; European Dermatology Forum. Evidence- and consensus-based (S3) Guidelines for the Treatment of Actinic Keratosis – International League of Dermatological Societies
in cooperation with the European Dermatology Forum – Short version. J Eur Acad Dermatol Venereol. 2015 Nov;29(11):2069-79
- Memon AA et al. Prevalence of solar damage and actinic keratosis in a Merseyside population. Br J Dermatol 2000; 142: 1154-1159.
- Frost C, Williams G, Green A. High incidence and regression rates of solar keratoses in a Queensland community. J Invest Dermatol 2000; 115: 273-277.
- Leitlinie zur Behandlung der aktinischen Keratosen C44.X. Deutsche Dermatologische Gesellschaft 2011.
- Glogau RG. The risk of progression to invasive disease. J Am Acad Dermatol 2000; 42(1 Pt 2): 23-24.
- Salasche SJ. Epidemiology of actinic keratoses and squamous cell carcinoma. J Am Acad Dermatol 2000; 42(1 Pt 2): 4-7.
- Rowe DE et al. Prognostic factors for local recurrence, metastasis, and survival rates in squamous cell carcinoma of the skin, ear, and lip. Implications for treatment modality selection. J Am Acad Dermatol 1992; 26(6): 976-990.