Topical prescription creams are a common, non-invasive method used by dermatologists to treat abnormal growths on the skin’s surface. These treatments target cellular changes in the superficial layers of the skin. They are typically employed when a patient has multiple affected areas requiring “field” treatment across a larger sun-damaged region. The primary target for these topical medications is Actinic Keratosis (AK). Treating this precancerous lesion is a crucial step in skin cancer prevention, aiming to destroy atypical cells and allow healthy skin to regenerate.
Understanding Actinic Keratosis
Actinic Keratosis (AK) is a common skin lesion resulting from chronic, cumulative exposure to ultraviolet (UV) radiation. This long-term sun damage causes abnormal growth and proliferation of skin cells, specifically keratinocytes, in the outermost layer of the skin. AK is considered precancerous because it can potentially progress into invasive Squamous Cell Carcinoma (SCC).
AK lesions typically present as rough, dry, or scaly patches that feel like sandpaper. They range in color from skin-colored to reddish-brown and are often easier to feel than to see. These lesions commonly develop on chronically sun-exposed areas such as the face, ears, scalp, forearms, and the back of the hands.
While an individual AK lesion has a relatively low chance of progressing to invasive SCC, the presence of multiple lesions indicates significant sun damage and a higher overall risk. AK is an indicator of a patient’s increased susceptibility to non-melanoma skin cancers. Treating these lesions is a preventive measure intended to eliminate the abnormal cells.
The Key Topical Treatment Medications
Topical creams for actinic keratosis work either by directly killing the abnormal cells or by stimulating the body’s immune system to attack them. The choice of medication depends on the lesion location, the extent of sun damage, and the patient’s tolerance for side effects.
Fluorouracil (5-FU)
Fluorouracil (5-FU) is a widely used agent that acts as an antimetabolite, targeting the cellular machinery of precancerous cells. It is a pyrimidine analog that inhibits the enzyme necessary for DNA synthesis. By interfering with DNA and RNA formation, 5-FU causes growth inhibition and death in rapidly dividing cells, such as those in AK lesions.
Imiquimod
Imiquimod is classified as an immune response modifier. This cream does not directly kill the cells but rather stimulates the innate and adaptive immune systems. Imiquimod acts as a Toll-like receptor 7 (TLR-7) agonist, triggering the release of inflammatory signaling proteins (cytokines) at the application site. This localized immune response leads to the destruction and elimination of the abnormal keratinocytes by the body’s defense mechanisms.
Diclofenac Sodium 3% Gel
Diclofenac Sodium 3% gel, a nonsteroidal anti-inflammatory drug (NSAID), offers a gentler mechanism of action. Its therapeutic effect is believed to involve the inhibition of cyclooxygenase-2 (COX-2), which can reduce inflammation and cellular proliferation associated with sun-damaged skin. The medication also promotes apoptosis, or programmed cell death, in the dysplastic keratinocytes.
Tirbanibulin
Tirbanibulin is a newer, short-course topical treatment that disrupts the internal structure of the precancerous cells. This agent is a microtubule inhibitor that prevents the formation of microtubules essential for cell division. By inhibiting tubulin polymerization, Tirbanibulin induces cell cycle arrest and apoptosis, primarily affecting fast-proliferating keratinocytes.
Navigating the Treatment Process
The effectiveness of these topical therapies is often accompanied by a temporary, predictable inflammatory reaction. This localized skin reaction is a sign that the medication is working to destroy the abnormal cells. The severity and duration of this reaction vary significantly depending on the specific agent used.
Treatment with 5-FU is typically applied once or twice daily for two to four weeks and often produces the most intense reaction. The treatment area progresses through redness, blistering, scaling, and eventual erosion before healing begins. Patients should be prepared for this discomfort, as the inflammation is an expected part of the therapeutic process.
Diclofenac sodium gel causes the least irritation but requires a longer treatment course, typically twice daily for 60 to 90 days. Imiquimod regimens vary, often requiring application two to five times per week for several weeks, and produce a moderate, immune-driven inflammatory response. Tirbanibulin is applied once daily for only five days, offering the shortest duration, though it still causes redness and flaking.
Post-treatment care is necessary to promote healing and reduce the risk of recurrence. After the inflammatory phase subsides, the treated skin is often sensitive and may appear red for a month or longer. Strict sun protection is required throughout and after treatment, as is the use of bland emollients to soothe and support the regenerating skin barrier.
Adjunctive and Alternative Therapies
While topical creams are the standard for treating large areas of sun-damaged skin, other procedures are available for single, thicker, or resistant lesions. These alternatives are chosen based on the number and thickness of lesions, and the desired speed of treatment. They provide options when a patient cannot tolerate the side effects of a cream or requires immediate removal.
Cryotherapy, or freezing with liquid nitrogen, is a common office procedure used to destroy individual AKs. The intense cold causes cell death and subsequent blistering, leading to the lesion crusting and falling off. This method is fast and highly effective for localized spots, though it can sometimes lead to temporary skin lightening or scarring.
Photodynamic Therapy (PDT) is a two-step process where a light-sensitizing topical solution is applied to the skin and then activated by a specific wavelength of light. This light-drug interaction selectively destroys the precancerous cells. PDT is useful for treating multiple lesions across a large area and often provides a good cosmetic outcome.
For lesions that are thick, highly suspicious, or resistant to field treatments, surgical removal options may be performed. These include curettage and electrodesiccation or traditional excision. Curettage involves scraping the lesion away, sometimes followed by heat application, while excision is a deeper surgical removal. These procedures are typically reserved for advanced or isolated cases where laboratory analysis of the tissue is necessary.