Studies that have analyzed effects of oral NSAIDs on melanoma skin cancer development, (both melanoma and NMSC), suggest that NSAIDs are chemopreventive agents. Future studies may better delineate the impact of NSAIDs.
The combination of 3% diclofenac in 2.5% hyaluronic acid gel has been shown to be an efficacious treatment in the clinical clearance of AKs.
The combination of piroxicam (PXM) in SPF 50 + has been regarded as a long-term curative and preventative treatment for nonmelanoma skin cancers.
PATIENT EDUCATION POINTS
Providers should inform patients that AKs are precursors to squamous cell carcinoma (SCC) of the skin. AKs express similar genetic alterations to SCC in the tumor suppressor gene p53. Thus, it is hypothesized that the treatment of AKs will prevent the development of SCC.
It would behoove patients to know that the treatment of AKs serves a dual purpose: as a treatment for the cosmetically displeasing, at times pruritic and painful lesion that is an AK, and as a potentially preventative treatment for the development of SCC. NSAIDs are strongly associated with a decreased risk of SCC, especially when used long-term and at high-intensities.
For many decades, nonsteroidal anti-inflammatory drugs (NSAIDs) have been widely used for their analgesic and anti-inflammatory properties and, most recently, for their anti-platelet aggregation properties. In addition, NSAIDs have been studied and utilized for their chemotherapeutic and chemopreventive properties. With regard to skin neoplasia, the first study on the efficacy of an NSAID for the treatment of actinic keratosis (AK) was published in 1997.1 Since then, over the subsequent decades, a number of studies using topical or oral NSAIDs for nonmelanoma skin cancer (NMSC) and melanoma have been conducted in vivo and in vitro models. A 1991 to 2009 population-based case-control study demonstrated that NSAIDs are strongly associated with a decreased risk of SCC, especially when used long term and at high intensities.2
BOX 49-1 OVERVIEW
The mechanism of action of nonsteroidal anti-inflammatory drugs (NSAIDs) in the prevention or treatment of skin carcinogenesis is not fully understood. However, the mechanism likely includes the inhibition of cyclooxygenase 2 and the arachidonic acid pathway.
Topical diclofenac 3% gel has been approved by the U.S. Food and Drug Administration (FDA) for the treatment of actinic keratosis (AK). Topical diclofenac is a safe and effective treatment option for AK, especially in patients with multiple lesions for which destructive therapies are less desired. The recommended dosage is a twice-daily application for 60 to 90 days.
The role of oral NSAIDs in skin cancer chemoprevention is under investigation. Animal and human studies suggest that these drugs may ...