What is Actinic Keratosis

Actinic keratoses are common, sun-induced, premalignant lesions that increase with age. Light-complected individuals are more susceptible than those with dark complexions. Years of sun exposure are required to induce sufficient damage to cause lesions. Actinic keratoses may undergo spontaneous remission if sunlight exposure is reduced, but new lesions may appear. Patients often present with lesions that were first noticed during the summer, suggesting that the lesions may become more active after sunlight exposure.
What are the symptoms and signs of Actinic Keratosis?
Actinic keratoses begin as an area of increased vascularity, with the skin surface becoming slightly rough. Texture is the key to diagnosing early lesions. They are better recognized by palpation than by inspection. Very gradually, an adherent yellow crust forms, the removal of which may cause bleeding . Individual lesions vary in size from 3 to 6 mm. The extent of disease varies from a single lesion to involvement of the entire forehead, balding scalp, or temples. Induration, inflammation, and oozing suggest degeneration into malignancy. Keratin may accumulate and form a cutaneous horn, particularly on the superior aspects of the pinna.
What are the changes of Actinic Keratosis at cellular level?
Histologically, an actinic keratosis consists of atypical squamous cells confined to the epidermis. The follicles are not involved, so there is no follicular plugging. Penetration through the dermoepidermal junction and into the dermis indicates the development of a squamous cell carcinoma.
How is Actinic Keratosis related to squamous cell carcinoma?
After several years, a small percentage of lesions may degenerate into squamous cell carcinomas. A very low yearly transformation rate for single lesions can translate into a substantial lifetime risk of transformation for patients with several actinic keratoses. Up to 60% of squamous cell carcinomas develop from actinic keratosis. Squamous cell carcinomas that evolve from actinic keratosis are not aggressive, but may eventually metastasize. All patients with actinic keratosis should be examined carefully for basal cell carcinomas.
What about Actinic Keratosis treatment?
Because actinic keratoses sometimes undergo spontaneous remission, definitive treatment may be delayed for patients with a few superficial lesions. Small lesions should be reexamined at a later date for spontaneous remission. Patients should make every effort to prevent further sun damage. This does not mean that patients must hibernate for a lifetime, but they should understand techniques to reduce sunlight exposure.
Cryotherapy.
Cryotherapy is the treatment of choice for most isolated, superficial, actinic keratoses. Actinic keratosis resides in the epithelium. Cryotherapy with liquid nitrogen causes the separation of the epidermis and dermis, resulting in a highly specific, nonscarring method of therapy for superficial lesions. Patients with darker complexions may develop hypopigmented areas after freezing, and treating multiple lesions on the faces of such patients may result in white-spotted faces. 5-FU is the best alternative.
Surgical removal.
Individual indurated lesions or those with thick crusts should be removed with minor surgical procedures. It is unnecessary to biopsy lesions less than 0.5 cm. Larger lesions or those occurring about or on the vermilion border of the lips should be examined. Electrodesiccation and curettage easily remove small, thicker lesions. The CO2 laser may be superior to vermilionectomy for actinic cheilitis too extensive to be treated with topical 5-FU.
Tretinoin.
Experience is accumulating that tretinoin (Retin-A) used alone or in combination with topical 5-FU is an effective treatment for certain actinic keratoses. Patients with mild actinic damage who show only erythema and scaling may be treated with tretinoin 0.05% to 0.1% cream applied once a day. If a few focal areas of scale do not respond after 2 to 4 months, they can be treated with cryotherapy. Tretinoin slightly enhances the effectiveness of 5-FU, thereby shortening treatment time, but intensifying tissue reaction and discomfort. Combination therapy is probably not worth the trouble.
Sunscreens.
Regular use of sunscreens prevents the development of solar keratoses. Sunscreens that contain a combination of ingredients to block both the UVA and UVB spectrum of ultraviolet light are most effective. Shade UVA Guard and DuraScreen 30 are examples of commercially available, broad spectrum sunscreens. Sunscreens are best applied in the morning on days when sun exposure is anticipated. Sunscreens should be applied to the face, lower lip, ears, back of the neck, and backs of the hands and forearms. Hats should cover bald heads. The physician should explain that although sunscreens are used, additional lesions may occur, but that many superficial areas of involvement may actually improve.
Acid peels.
Glycolic acid is an alpha hydroxy acid that is useful as a chemical peeling agent. Actinic keratoses involve epidermal hyperplasia and retention of stratum corneum. Alpha hydroxy acids applied topically in high concentrations (30% to 70% glycolic acid) cause epidermolysis and elimination of keratosis. Fluorouracil cream may be used for 5 to 7 days prior to the peel to "light up" and identify the lesions. Glycolic acid is applied with a cotton swab to the keratoses, is left on for 5 to 10 minutes, and is then removed with alcohol. Trichloroacetic acid (35%) and Jessner's solution (14 g of resorcinol, 14 g of lactic acid, and 14 g of salicylic acid dissolved in ethanol to make a final solution of 100 ml) induce a medium-depth peel and equal fluorouracil in efficacy.
Topical chemotherapy with 5-fluorouracil.
5-FU is an effective topical treatment for superficial actinic keratosis. Thicker lesions, especially those on the scalp, may evolve into squamous cell carcinomas and should be treated with more aggressive techniques. The agent is incorporated into rapidly dividing cells, resulting in cell death. Normal cells are less affected and clinically appear to be unaffected. Inflammation is induced during this process. Thick, indurated lesions become most inflamed and may best be managed by surgically removing them before instituting topical chemotherapy. discomfort may be experienced for 1 week or more during periods of intense inflammation. Pain can be minimized if only small areas are treated at one time; however, many patients wish to treat the full face instead of prolonging the unsightly erythema and crusting for weeks. Lesions on the back of the hands and arms require longer periods of treatment than those on the face. Patients with a small number of lesions may be treated during the summer or winter. Patients with a large number of lesions who work outdoors are best treated in the winter. Pharmaceutical companies that manufacture 5-FU supply patient information sheets with color photographs of the various stages of inflammation.
Topical chemotherapy with masoprocol.
Masoprocol (Actinex), a new topical antineoplastic agent, has been approved for treatment of actinic keratoses. A 71.4% reduction in the number of lesions occurs in 1 month when the cream is applied twice a day. Irritation is moderate. Topical 5-FU is more effective.

Actinic keratosis: Skin Cancers and their precursors

Non melanoma skin cancer ---> squamous cell carcinoma ---> Early skin cancer ---> Actinic keratosis

Actinic keratosis (solar keratosis) are lesions that result from cumulative damage to keratinocytes by ultraviolet radiation. They are common lesions, particularly in individuals with skin phototypes I and II who are over the age of 40 and give a history of chronic sun exposure. On examination, they appear as multiple red, scaly plaques on sun-exposed skin. All patients should be strongly advised to minimize their sun exposure. Cryotherapy is effective in most cases; otherwise topical 5-fluorouracil cream or retinoids can be used. The presence of actinic keratosis is an indicator of increased risk of non-melanoma skin cancers. They occasionally disappear spontaneously but in general remain for many years.

Bowen's disease

Non melanoma skin cancer ---> squamous cell carcinoma ---> Early skin cancer ---> Bowen's disease

Bowen's disease (squamous cell carcinoma in situ) presents as a fixed red plaque and represents an intra epidermal squamous cell carcinoma.
Epidemiology
Bowen's disease may occur at any age but is rare before the age of 30; most patients are aged over 60 at presentation. In the UK, it occurs predominantly in women (85% of cases).
Pathology
A number of different factors have been implicated in the aetiology of Bowen's disease. The age group and body sites affected are suggestive of a relationship with chronic exposure to ultraviolet radiation.
Histologically, keratinocytes show loss of polarity, atypia and increased mitotic rate with involvement of the entire thickness of the epidermis from basal layer to stratum corneum. The basement membrane remains intact.
Clinical features
Bowen's disease presents as solitary or multiple, gradually enlarging, well-demarcated erythematous macules, papules or plaques. The lesions usually have an irregular border with surface crusting or scaling. Approximately 75% of lesions are on the lower legs. They are most often asymptomatic, but may bleed. In the uncircumcised male, the lesions can present as smooth, red, velvety plaques on the glans penis (erythroplasia of Queyrat).
Investigations
The diagnosis is suggested on the basis of clinical features.
Skin biopsy
Histology is required to confirm the diagnosis.
Management
Ablation of the lesion
Treatment options for Bowen's disease include cryotherapy, curettage and cautery, excision, laser (CO2, argon and Nd:YAG) and topical 5-fluorouracil (applied once or twice daily as 5% cream for up to 2 months). All have recurrence rates of up to 10% and no treatment modality appears to be superior.
Prognosis
If Bowen's disease is untreated, most studies suggest a 3% risk of progression to invasive squamous cell carcinoma. Up to 50% of patients have other previous or subsequent skin malignancies, most commonly basal cell carcinoma. Genital Bowen's disease carries a higher risk of invasive cancer.