Actinic keratosis (AK) is also known as solar keratosis. This is a premalignant lesion that results from the proliferation of atypical epidermal keratinocytes. The importance for identifying actinic keratosis is because they represent early lesions on a continuum with skin squamous cell carcinoma (SCC). Therefore, if untreated, they may progress to cutaneous squamous cell carcinoma.
Causes and Risk Factors
- The cause and risk factors for AK are the same for Squamous cell carcinoma, mainly UV radiation and environmental factors. UV cause AK via induction of mutations in the epidermal keratinocytes, causing increased survival and proliferation of atypical cells.
- UV can also induce DNA damage causing mutations in the p53 tumor suppressor gene (known as the master regulator of the cell cycle, apoptosis, and DNA repair). p53 mutation have been detected in up to 50% of skin samples from patients with actinic keratosis (AK) and almost all cancers.
- Fair complexion, men and elderly are also more prone to developing AK.
- Immune suppression have been linked to basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). It is no doubt that patients on organ transplant and HIV patients have a higher risk for developing AK.
- Genetic disorders that increase the consequence of UV DNA damage also increase AK risk. Examples include xeroderma pigmentosum, albinism which are both risk factors for SCC and BCC.
Symptoms and Clinical Presentation
- Since UV exposure is one of the major risk factors, AK typically present on sun exposed areas such as balding scalp, side of neck, face, distal upper and lower extremities.
- Actinic keratosis often present as erythematous and scaly maculopapular lesion often described as “sand paper” appearance.
- AK lesions are most commonly detected in adults with fair skin and skin adjacent to AKs lesions typically shows signs of photo damage, such as a yellow to pale color, hyperpigmentation spots, scattered telangiectasias (dilated vessel) and dry skin (xerosis).
- Actinic keratosis are generally asymptomatic, but some individuals may complain of local tenderness and stinging sensation.
- Actinic keratosis are usually diagnosed clinically via physical examination include touch and inspection. When there is suspicion for malignancy, a biopsy is typically done.
- Clinical differentiation between pigmented AKs and lentigo maligna can be challenging. Dermatoscopy may not be reliable for distinguishing between these lesions and histopathologic examination remains the gold standard for such cases.
Clinical Course of Actinic Keratosis
Progression to SCC
- Although occurring at a low rate, AK does progress to SCC from 0.03 to 20%. It has been shown that 60% of SCC derives from AK.
- AK lesions that do not progress to SCC can either persist or regress itself. Regression rate between 20-30% per year have been reported.
- However, lesions that regress may also later reappear.
Treatments and Managements
In general, surgery and liquid nitrogen are the most common therapy approach for AK that are isolated whereas topical treatment are for multiple AKs.
Treatment of actinic keratosis include destructive treatments such as the following
- Liquid nitrogen cryotherapy
- Liquid nitrogen therapy is the most widely utilized treatment for AK
- Surgical excision
- Surgical excision procedures are not commonly used for AKs unless there is indications for histological examination such as recurrent or aggressive lesions that are suspicious for squamous cell carcinoma (SCC).
- Shaved excision and curettage
- This approach is commonly used for AKs, especially lesions that are hyperkeratotic in nature. The lesions excised can be used for histological examination but may not be adequate in most cases.
- Dermabrasion also known as skin planning
- This approach can be used for treating large areas such as photodamaged hairless scalp or forehead where the lesion is too large to be treated effectively with topical treatment. This approach sand the skin to improve skin contour via removing the stratum corneum of the epidermis, leaving the skin red and raw like appearance.
- Photodynamic therapy (PDT)
- PDT has the added advantage of allowing the treatment of multiple AK lesions with one application. Some studies have shown superior results when compared with topical treatment. The most common side effect PDT is burning/stinging during light exposure and in some cases, pigment changes.
- Medical treatments
- Topical medication are usually used for multiple actinic keratosis.
- Topical 5-fluorouracil (5-FU)
- Have shown great success via inflammation and destruction of lesion. The treated skin go through few stages of progression from erythema on application to blistering, necrosis with erosion and eventually reepithelialization. However, patient compliance to treatment regimen is generally low, due to common side effects like skin irritation, erosions, ulcerations and the prolong 4-6 weeks long duration of treatment
- Topical Imiquimod
- Topical imiquimod have also shown good treatment response for AK via stimulating the immune system.
- Side effects include erythema and scabbing of treated skin.
- Chemical Peels (trichloroacetic acid)
- These approach is more suitable for treatment of multiple non-hypertrophic AKs and patient who can follow a close regimen and avoid sunlight exposure ro apply sunscreen religiously after treatment.
- Sunscreen application is imperative because, post chemical peel skin is very sensitive to sunlight. Chemical peel are typically applied on the face, producing a smooth, rejuvenated skin appearance via wound repair process, collagen remodeling, and skin exfoliation.
- Laser therapy
- Have been attempted with carbon dioxide but with limited results.