Actinic Keratosis in Dallas

By routine skin exam screening, a pre-cancer, also known as an actinic keratosis, can be fairly easy for a trained dermatologist to diagnose and treat. Often times, patients report “patches of dry or scaly skin” when the reality can be discreet scaly growths that are the result of an accumulation of UV exposure over many years, even in patients who currently do not get any sun exposure at all.

Common areas where an actinic keratosis tends to appear are the scalp, face, ears, neck, upper chest, arms, and the top of the hands. These are all areas that receive the most sun exposure.

It is very important and necessary to wear sun protection and sunscreen daily! A time when most people receive exposure without necessarily realizing it is when they are driving in the car. Check with a dermatologist such as Dr. Ellen Turner in order to determine whether you may have an actinic keratosis, or pre-cancerous lesions.

Actinic keratosis is a precursor for the squamous cell cancer variant of nonmelanoma skin cancer. Typically, if left untreated, approximately 25 percent of these lesions can develop into squamous cell cancer. By treating an actinic keratosis early, it can be cleared using a variety of treatments, thus preventing actual skin cancer from occurring.

There a variety of possible treatments available for actinic keratosis. Many times, liquid nitrogen can be used to pinpoint these lesions and cause destruction of the abnormal cells. When the treatment is performed properly by a trained dermatologist, scarring can be minimized or avoided. This procedure utilizing liquid nitrogen for its non-scarring destruction is called cryotherapy.

There are additional destructive treatments that can be used similarly, but to treat a higher number of lesions, in sun-damaged areas. Chemical peels are instantaneous, and cause a “frosting” or white appearance to the skin when applied. After the first one or two days of application, the skin in the treated area begins to scale and peel, leaving behind new, undamaged skin cells.

Another topical modality used for the treatment of broader areas of actinic keratosis and damage is photodynamic therapy (PDT). Photodynamic therapy involves the use of a chemical called aminolevulenic acid (ALA), which is applied to the surface to be treated. This chemical requires incubation of at least one hour, followed by activation by a particular light source: either a blue light or broadband or pulsed light. When activated by light, ALA causes a mild tingling in the treatment site. The activation allows treatment of sun-damaged skin cells by targeting and destroying those with abnormal DNA, forcing new cellular turnover. A period of redness, swelling, and resulting scaling and peeling typically occur over one to three weeks after a PDT treatment, depending on the location of the treatment—such as the face versus the arms.

Additionally, there are topical creams that can be applied to the sun-damaged areas. The initial topical, which is still used in practice today, is a chemotherapy agent known as 5-fluorouracil (5-FU). This chemical induces a reaction that causes redness and resultant scaling and peeling to occur over one to three weeks of use. Once the treated area is inflamed and crusting, the treatment may be terminated and the area allowed to heal back to normal. There are also newer topical creams classified as immunomodulators. Imiquimod is a good example of an immunomodulatory that can be used to treat both pre-cancer and an actinic keratosis, as well as some superficial skin cancers, such as basal cell carcinoma. There are many variations as to how one can use imiquimod for the treatment of actinic keratosis, but it is typically applied to an area for two weeks, then stopped for two weeks, the re-initiated for two final weeks before completion at the end of a six-week period.

All treatments discussed in this section on actinic keratosis are non-scarring with variations as to the level of discomfort that occurs with each treatment.