Actinic (Solar) Keratosis

Synonyms: Actinic keratosis

The term actinic keratosis (AK) was coined in 1958 and means literally thickened scaly growth (keratosis) caused by sunlight (actinic). Solar or actinic (AK) are ultraviolet light–induced lesions of the skin and are by far the most common lesions with malignant potential to arise on the skin (they can progress to invasive squamous cell carcinoma). AK is seen in fair-skinned persons in areas of long-term sun exposure, like Australia where about half of the population over age 40 years are affected. Although the condition is very similar to Bowen's disease or carcinoma-in-situ, most lesions do not progress to malignant change. However, recognition and simple treatment helps to prevent progression.

• Cells within AKs shows characteristic UV-induced gene mutations.
• Histologically AKs share features with squamous cell carcinoma. AK is an epidermal lesion characterised by:
  • Collections of atypical, pleomorphic keratinocytes in the basal layer which can extend to the upper granular and cornified layers.
  • The epidermis is abnormal in architecture, with acanthosis, parakeratosis, and dyskeratoses. Cellular atypia is present with keratinocytes varying in size and shape.
  • Mitotic figures are present.
• It has features of Bowen's disease or carcinoma in situ:
  • They can be distinguished more by the degree of cellular change and the extent of the lesions rather than differences in the features of individual cells.
  • Often, marked hyperkeratosis and areas of parakeratosis with loss of the granular layer are present.
  • A dense inflammatory infiltrate is usually present.
  • AK is considered by some to be the the earliest manifestation of squamous cell carcinoma (SCC) and should be regarded as such rather than as a precancerous lesion.

• AK occurs most often in whites at a rate according to cumulative UV exposure.
• Frequency increases according to a number of risk factors:
  • Increasing age, as the dose of UV is cumulative.
  • Proximity to the equator as this affects UV dosage and cumulative exposure.
  • Lifestyle and time spent outdoors. Outdoor lifestyles whether with work or recreation and sport will increase risk.
  • Other specific practices such as use of tanning booths. Artificial sunlight from is a risk factor and may produce lesions in unusual places.
  • How fair the individual's skin is. Skin is graded from Fitzpatrick type I to VI according to sensitivity to sunlight as displayed by a tendency to burn or to tan. These lesions are almost entirely confined to fair skin types I and II.
  • Patients who are immunosuppressed following organ transplantation have a markedly increased risk of developing AKs and developing malignant change in the AKs.
• AKs are more common in men than in women. Traditionally men are more likely with work and recreational activities to spend time outdoors.
• AK has also been associated with a high-fat diet.
• Overall, the rate in Australia is highest with a prevalence around 50%.
• In the United States the rate is estimated to be between 11 and 26%.
• Elsewhere they are very common in fair skinned people in countries like South Africa, New Zealand.
• They tend to present between 30 and 60 years of age but can present earlier or later.

• Lesions occur in fair-skinned people in parts of the body exposed to long-term sun exposure, such as the head area (face, ears, scalp), forearms, and backs of the hands. Other areas repeatedly exposed to the sun include the back, the chest, and the legs.
• There may be other features of solar damage such as telangiectasiae, elastosis, and pigmented lentigines.
• The first lesion is usually a single plaque on the face in the 20s or 30s but with time and further exposure to strong sunlight they tend to progress on the nose, forehead and cheeks.
• AKs begin as small rough spots that are easier felt than seen (like rubbing sandpaper). Over several years lesions enlarge, often becoming red and scaly. From small 3-10 mm lesions they can enlarge to several centimeters.
• Patients may develop a multiplicity of such lesions within a sun exposed area. Lesions collide and produce confluent AK over a relatively large area.
• Variations on this theme include brown (pigmented AK), lichen planus–like areas, and exaggerated hyperkeratosis (the hornlike projection known as a cutaneous horn for example).
• They flare and become more erythematous when immunity is suppressed. This may be with systemic disease or its treatment, such as chemotherapy for malignancy but it can also be the result of much ultraviolet light.
• As the years progress and especially with continued exposure to strong sunlight, about 10% will undergo malignant change.¹ This is more likely in those that are erythematous, elevated and indurated. It may be necessary to remove the layer of keratin to see this.

This is according to clinical features. Skin biopsy is used where there are features which are high risk for malignant change.

• The roughness is more easily felt than seen, and occurs on sites which have had considerable exposure to the sun such as bald scalp, face, dorsum of hands and lower legs.
• There must be signs of solar damage such as solar elastosis shown by yellow thickening of the skin with increased wrinkles.
• Seborrhoeic warts are not so rough and the keratin is more easily picked off.
• SCCs may arise from solar keratoses but under the surface keratin there is a feel that the dermis has been infiltrated.

• Basal cell carcinoma and SCC (these are indurated nodular lesions reflecting more rapid growth and tend to be eroded or ulcerated on the surface)
• Seborrhoeic keratosis (produces greasy, brown crusts with a sharply demarcated borders and a non-erythematous base. They may occur in areas that are not exposed to sun)
• Bowen's disease (tends to be a large plaque with a sharp outline)
• Discoid lupus erythematosus (shows abnormal pigmentation, dilated follicles and atrophy)

No specific investigations are required unless there is suspicion that the lesion may be malignant when biopsy is needed. This includes:

• Lesions with pronounced hyperkeratosis, increased erythema, or induration.
• Lesions that recur.
• Lesions which are unresponsive to treatment.
• Large confluent lesions.
• Lesions in transplant recipients.
• Lesions in patients with a history of SCC.

Many options are open to patients with AKs. The natural history of individual lesions studied in the U.K. suggests that treatment is not universally required on the basis of preventing progression into squamous cell carcinoma (SCC).² However, others feel that prevention of SCC is the main reason for therapy.

• The first part of management is education of the patient about the nature of the lesion and the need to avoid excessive exposure to sunlight. Both sunscreens and protective clothing should be worn. The public's awareness of the dangers of the sun is poor.³
• Cryotherapy with liquid nitrogen is very effective, especially if lesions are few and this can be done in primary care.
• Dermabrasion and chemical peels can be used for facial and scalp lesions. Recurrence 6 months after chemical peels is quite high.²
• Topical 5 fluorouracil can be used. The 5% cream is applied twice daily for 3 to 4 weeks for facial lesions but lesions on other parts of the body need 6 to 8 weeks. The whole area should be treated rather than just the lesions. During treatment the lesions become more red and small subclinical lesions may appear. Red ulcers and crusts are a cosmetic embarrassment but the course should be completed and within 2 weeks a smooth complexion replaces the lesions. The course can be repeated and resistant lesions can be treated surgically but resistant lesions should probably be biopsied in case of malignant change.
• Systemic retinoids in very high risk patients, such as transplant patients, may be justified.²
• Photodynamic therapy is another treatment option.⁴ Topical 5-aminolevulinic acid accumulates preferentially in the dysplastic cells. Exposure to irradiation with light of an appropriate wavelength generates oxygen free radicals that kill the cells. There is pain in the areas treated, similar to that from topical 5FU. One treatment with PDT appears to be as effective as 5FU and may be considered in patients with contact sensitivity to 5FU. The cosmetic result can be better and patients prefer it.⁵

The most important complication is the progression to malignant change.

Progression to squamous cell carcinoma occurs slowly and affects about 10%.¹ The problem is to decide who is in that 10%. It is more likely to occur in the over 70s and look for the warning signs mentioned above. The cost-effectiveness of treating all solar keratoses to prevent malignant transformation is questionable.⁶ When it does undergo malignant change it tends to be of low aggression and distant metastases are rare.

It is important to educate patients that AKs can be reduced or delayed by use of sunscreens but most important, by reducing sun exposure:

• Patients should limit all sun exposure whether recreational or work related.
• It is particularly important to avoid sun in tropical areas.
• It is best to seek shade particularly when the sun is high between 11am and 3 pm.
• For patients unable to avoid sun exposure apply a sunscreen (sun protection factor (SPF) 30 or more) wear protective clothing daily (hats, long sleeves for example).

Widespread lesions and suspected malignant change require referral. Patients with multiple and confluent AKs are likely to be at higher risk of nonmelanoma skin cancer, particularly patients with organ transplants.² GPs should be aware of those at high risk of malignant change. These include:

• Organ transplant recipients
• Those with multiple large AKs or previous SCCs

Lesions in such patients of an actinic nature or unclear diagnosis should be promptly referred.²

AKs are a biological marker of sun damage and hence patients with AKs are at a greater risk of skin cancer than those with no AKs. Patients with AKs need to be educated on self-monitoring and the need to seek a medical opinion if they detect new lesions or changes in old lesions on their skin.² It is important to:

• Ensure that the patient is provided with information about AKs and sun damage. Leaflets can be downloaded from the British Association of Dermatologists (see Further reading below).
• Ensure the patient is adequately informed concerning the nature of any treatment when given.
• Ensure that as GPs we know how to evaluate and manage AKs when they develop.²