Actinic keratoses (AK) are very commonly presenting skin lesions that develop after chronic exposure to UV light. They are becoming increasingly common, with numbers likely to rise even further in the near future. Although they are not malignant and a significant number will resolve spontaneously, a small percentage will transform into squamous cell carcinoma, so it is worthwhile diagnosing and treating them to reduce the chance of malignant transformation. They can usually be treated by the GP and patients need to be educated about sun protection.
Actinic keratosis, skin lesions, sun damage
Also known as solar keratoses or senile keratoses, AK are very common skin lesions that develop following chronic exposure to UV light, which results in the proliferation of mutated keratinocytes in the epidermis. Estimates from NICE suggest that 23% of the UK population over the age of 60 years have AK.1
They are not malignant and 15-25% are thought to resolve spontaneously over a one-year period. Malignant transformation into squamous cell carcinoma will occur in a small percentage of cases, with estimates varying from 0.1% to 10%. The risk of malignant change increases with the number of AK and how long they have been present, with the presence of 10 AK giving a 14% risk of developing squamous cell carcinoma over the following five years.2
One study has suggested that there may be potential for transformation into the more common basal cell carcinoma.3 For this reason, the treatment of AK is considered worthwhile, with the goal of reducing malignant transformation by early and accurate diagnosis and treatment.
Taking the history
The first step when presented with a patient who you think might have AK is to take a detailed history. AK are generally asymptomatic and slow to develop.
With the relationship between UV light and the development of AK, skin type is a good place to start. AK are most commonly seen in patients with Fitzpatrick skin types I and II and almost exclusively in white-skinned individuals. The presence of melanin in the skin protects the keratinocytes from UV damage.
The incidence also increases with age, so AK are more likely to be seen in elderly patients. The exceptions to this are people with xeroderma pigmentosum and albinism, who may develop AK at a very young age.
AK occur as a result of UV light damaging the skin, with the cumulative dose and the intensity of UV light being important. A careful history of light exposure should therefore be the next step. Occupation can be important, with those working outside being at greater risk, as can the country of residency, with Australia having a high incidence of AK, at 40-60% in the over-40 age group.4
Sunbed use (including therapeutic UV light treatment) will also increase the risk of developing AK, which may develop in less common areas of the body and at a younger age, especially if there has been excessive use at a young age. AK are generally more common in men than in women.
AK, as with other types of skin cancer, are also more common in those patients who are immunosuppressed, such as those who have undergone organ transplantation, so a careful drug and medical history is important. Transplant recipients are usually also under surveillance by a dermatologist and will have any early AK treated by them.
Appearance of lesions
After taking a thorough history, the next step in the diagnosis is to look at the skin and the location of the lesions. AK generally develop in the areas of highest sun exposure and those affected will usually have evidence of sun-damaged skin, such as solar lentigines, telangiectasia, collagenosis and erythema.
In men, the areas affected are more commonly the head, especially in those with male pattern baldness, the face, the ears, the dorsal forearms and the hands, while in women, the areas affected are primarily the face and hands.
AK are usually multiple in a single anatomical area and may be more easily felt than seen, so it is helpful to palpate the skin as well as look at it.
Early AK vary in size from 3mm to 10mm, but with time, tend to increase in size and may coalesce into confluent AK covering a large area. Lesions will usually have a similar appearance. On palpation, the skin will be rough and dry, with a sandpaper feeling and a surface scale or thicker crust. Initially, they may be skin or grey coloured, progressing to pink and more red and inflamed in older lesions.
Although most AK fit this description, variants can occur:
- Pigmented AK are a rare variant presenting as macules or plaques with a brown appearance; they may be difficult to differentiate from lentigo maligna or solar lentigines.
- Hyperkeratotic AK have a more exaggerated keratin surface, which is more adherent to an erythematous base. These may project beyond the skin, causing a horny growth (40% of horns are caused by underlying AK). Where this is the case, the important differential is squamous cell carcinoma, so the horn and adjacent epidermis should be removed for histology.
- Bowenoid AK are more likely to be solitary lesions with defined margins. These are differentiated from Bowen's disease by the degree of epithelial change on histology.
Dermoscopically, AK have a strawberry-like appearance with a red pseudo-network, although the presence of a lot of scale may obscure this. Careful removal of scale can therefore be helpful. The rosette sign may occasionally be present, as four white points arranged in a cloverleaf pattern around a central follicular opening, which is thought to correspond to the histological 'flag sign' of orthokeratosis and parakeratosis.5
Aids to diagnosis
Most AK are diagnosed from the history and examination, but where there is diagnostic doubt, the appearance is not typical or there has not been the expected response to treatment, a biopsy can be helpful to check histology and rule out an invasive squamous cell carcinoma. A punch or ellipse biopsy will usually be adequate.
Histologically, AK show alternating zones of hyperkeratosis and parakeratosis overlying a thickened or atrophic epidermis. Associated with this, solar elastosis will be present in the upper dermis and the normal maturation pattern of the epidermis will be absent. Atypical keratinocytes are usually also present, with hyperpigmented or pleomorphic nuclei extending to the basal layer of the epidermis. Hair follicles, apocrine, eccrine and sebaceous glands will all be unaffected.
Another much less commonly used diagnostic aid is a Wood's lamp or photodynamic therapy lamp. After the application of a sensitising drug such as those used for photodynamic therapy, AK will typically emit a pink fluorescence.6
Seborrhoeic keratoses are more common than AK, with a greasier appearance, brown or darker crusts and a more demarcated border. They typically have a stuck-on appearance, a non-erythematous base/margin and a more generalised distribution, including areas not previously exposed to UV light.
Bowen's disease plaques tend to be larger than AK and have a redder appearance with a more sharply defined edge. These are more common on the legs in women, but may occur anywhere.
Squamous cell carcinoma has a more eroded, friable or ulcerated appearance, will have grown more rapidly than AK and may be nodular, with a firmer feel. It may also be more tender on palpation.
Viral warts tend to occur more commonly in younger patients, especially on the hands and feet, and on close inspection, will have blood vessels present which appear as darker dots.
Other rarer differentials include discoid lupus erythematosus, porokeratosis and keratoacanthoma.
|IS AN AK BECOMING MALIGNANT?7|
|When trying to decide whether AK are undergoing malignant
transformation, the acronym IDRBEU can be useful
|Diameter usually >1cm|
Treatment of AK can usually be undertaken by GPs.2 This will either consist of the treatment of individual AK which are clinically evident, or field treatment, which will also include the subclinical lesions. These lesions may be extensive in very sun-damaged skin. Patients should be warned about this, as they may be surprised by the size of the area affected.
Treatment options include cryotherapy, photodynamic therapy, surgery (curettage plus cryosurgery, shave excision or dermabrasion), lasers and chemical peels. Medication includes topical anti-inflammatory preparations, such as diclofenac gel, and chemotherapy agents, such as 5-fluorouracil, imiquimod and ingenol mebutate gel, which is derived from the milkweed plant and only requires a twoor three-day application.1
Education about sun protection is important. Greater awareness of the effects of UV light should mean that in future, AK will decrease, but this is not likely for some years.
- Dr Nigel Stollery is a GP with a special interest in dermatology, in Kibworth, Leicestershire
Competing interests: None declared
1. NICE. Actinic keratosis: ingenol mebutate gel ESNM14. London, NICE, 2013.
2. Primary Care Dermatology Society. Actinic Keratosis 2014.
3. Jancin B. Study hikes risk of cancer from AKs Dermatology News 2008.
4. Frost CA, Green AC, Williams GM. The prevalence and determinants of solar keratoses at a subtropical latitude (Queensland, Australia). Br J Dermatol 1998; 139(6): 1033-9.
5. Cuellar F, Vilalta A, Puig S et al. New dermoscopic pattern in actinic keratosis and related conditions. Arch Dermatol 2009; 145(6): 732.
6. Sanmartin O, Guillen C. Images in clinical medicine. Fluorescence diagnosis of subclinical actinic keratoses. N Engl J Med 2008; 358(19): e21.
7. Quaedvlieg PJ, Tirsi E, Thissen MR et al. Actinic keratosis: how to differentiate the good from the bad ones? Eur J Dermatol 2006; 16(4): 335-9.
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Look up photographs of AK to improve your diagnostic skill
Produce a patient information leaflet on AK, explaining their cause, treatment and prevention, and outlining the risk of malignant transformation into squamous cell carcinoma
Review your knowledge of the diagnosis and management of squamous cell carcinoma and outline how that compares with that of AK
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