Actinic Keratosis

Peter Foley, MBBS, BMedSc, MD, FACD

What are Actinic Keratoses?

Actinic Keratoses (AK) (singular is actinic keratosis), also called solar keratosis (SK) by doctors, are commonly known as sunspots. They most commonly appear as small, reddish-pink, scaly spots on sun damaged skin. These spots (or lesions) usually measure 2-6mm in diameter; although several may join together to form larger patches. Most sunspots are flat; however, they can be slightly raised. Sunspots typically develop on sun-damaged skin in fair-skinned individuals at sites that have received large amounts of sunlight exposure; for example the face, scalp, neck, hands, and forearms. Often these spots are more easily felt than seen. Sufferers do not commonly have symptoms but itch, burn, or sting with exposure to the sun. On rare occasions the sunspots bleed, or become crusted (scabby). Variants of AK may be thickened or brown in colour or have very thick scale (horn).


What Causes Actinic Keratoses?

Actinic Keratoses are the result of sunlight (ultraviolet radiation) exposure. They can develop in early adulthood but are uncommon before the age of 40. The frequency of AK increases with age. Childhood sun exposure seems to be particularly important for setting the stage for AK development later in life. There is a lag between exposure and AK appearing; presumably because it takes time for sunlight damaged cells to multiply and form AK. Although childhood exposure is critical, even adults who protect themselves develop fewer AK than those who take no precautions. Less common factors that may contribute to AK development are arsenic, radiation exposure, and human papilloma virus infection (wart).


Genetics of Actinic Keratoses

Not everyone who is exposed to excessive sunlight will develop AK; some individuals are genetically susceptible. Although specific genes have not been isolated, individuals prone to AK development typically have physical characteristics such as pale/fair skin that burns easily and does not tan or tans poorly; light coloured eyes (typically blue), and fair hair - red or blonde.

Looking at AK at the cellular level, characteristic UVB induced mutations are seen in certain genes such as the tumor suppressor gene, p53.


Actinic Keratoses Triggers

There are no specific triggers for AK although they do become more common with age. Patients on immune suppressing medications (for example after an organ transplant) are much more likely to develop AK.


Actinic Keratoses and the Immune System

The importance of the immune system in preventing or limiting the development of AK is emphasized by the increased frequency with age and certain medications (i.e. that suppress the immune system). Presumably a healthy immune system is able to keep these spots in check but declining function with age or medication to prevent transplant rejection allows the sun damaged cells to multiply and develop into an AK.

Our first case study involves a patient named Julie. In her early years Julie, a typical red-headed freckled child of Irish-descent, spent a lot of time in the sun playing tennis. Julie would regularly be sunburnt, red with blisters sometimes, but would not really tan. At 40 Julie started to develop a few AK on her hands.

Julie underwent a kidney transplant at 42, and by 47, after 5 years on several drugs to prevent organ transplant rejection; Julie has dozens of AK on her hands, forearms, face, and ears.

Bill is a 90 year old man; a fair-skinned individual who spent 2 years as a P.O.W. in the Asia-Pacific region with very extreme sun exposure. Bill started to develop AK in his 40's. For the next 30 years he seemed to be developing more spots each year. With careful sun protection for the last two decades, Bill still develops AK but their frequency appears to have plateaued.


How Did I Get Here?

To develop AK, individuals need to have the right (or wrong) genetic makeup, fair skin, light hair, pale eyes, and have sufficient exposure to the sun. Fair-skinned individuals who take great care in the sun are less prone to develop AK, as are dark-skinned individuals who may get away with excessive sun exposure. When the immune system declines, due to age or medication, AK appears in increased numbers.


What Happens If I Don't Do Anything?

AK are at least premalignant, with a risk of developing into squamous cell carcinoma (SCC), a type of skin cancer that can spread to lymph glands and other areas of the body. Some doctors consider AK already skin cancer/SCC; although the risk of AK disappearing without treatment is greater than the risk of AK becoming squamous cell carcinoma and spreading.

No one can predict which AK will disappear and which will cause problems such as SCC; so most doctors consider it practical (and easier) to treat AK rather than waiting and dealing with SCC if they arise.


What Are My Options?

One option is to use moisturizer to reduce scale and to apply sunscreen every day to give the body's immune system (which is suppressed by UVB) a chance to fight off the AK.

The most common treatment of AK is freezing obvious spots with liquid nitrogen. This is called cryotherapy. Although sometimes referred to as 'burning spots off', the liquid nitrogen actually freezes the skin (and AK), causing frostbite. The treated area turns red, swells (may blister), becomes crusted, and heals from underneath. Usually the skin returns to a fairly normal appearance after liquid nitrogen, although a paler area of skin (or rarely darker) may result.

Occasionally, thicker, tender, or resistant AK may be surgically excised or curetted (scraped) off.

Photodynamic therapy (PDT) involves applying a cream or lotion to the affected skin that makes the area to be treated very sensitive to light. After a defined time period, intense light is shone on the prepared area. The light activates chemicals within the cells of the AK and destroys them. PDT may be used to treat an individual spot or an entire area e.g. forehead or scalp.

Several topical treatments are available, usually to treat a field of sun damage or AK. Individual spots may be targeted but usually these gels or creams are used as 'field treatment'. Options include:

  1. Diclofenac in hyaluronan gel usually applied twice daily for 90 days. Most individuals using Diclofenac have few problems although some may have severe local skin reactions.
  2. 5-fluorouracil (5-FU) cream is a form of chemotherapy that destroys the abnormal cells of an AK. It may be applied once or twice daily for 2-4 weeks. Most patients develop dusky red skin discolouration (within the treatment field) with crusting and peeling.
  3. Imiquimod is an agent that stimulates the immune system to fight off AK. Standard treatment involves cream application 2 or 3 days per week for at least 3, and up to 16, weeks. Local skin reactions may be severe and occasionally patients develop flu-like symptoms, including headache and muscle aches.

Other less commonly used treatments include retinoids (synthetic vitamin A derivatives), laser resurfacing, dermabrasion, and chemical peels.

The various treatment options for AK work in different ways and can be used complementary. Ongoing sun protection is important to help reduce risks.

Early treatment to prevent progression to squamous cell carcinoma is advocated.

Associate Professor Peter Foley has been practicing dermatology in Australia for over 10 years. At the Skin and Cancer Foundation in Victoria. Associate Professor Peter Foley and his colleagues (over 50 dermatologists and specialists) host clinics for psoriasis, eczema, vitiligo, organ transplant recipients, melanoma, and non-melanoma skin cancer, including actinic keratoses. For more information about Associate Professor Peter Foley and the Skin and Cancer Foundation please visit - Skin and Cancer Foundation.


For more information on actinic keratosis please visit:

American Academy of Dermatology: Actinic Keratosis Actinic Keratosis


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