The frequency of AKs increases with age and cumulative lifetime sun exposure. They are also more common in individuals who are immunosuppressed (especially after solid organ transplantation) and in males. They may resolve with protection from ultraviolet (UV) light. Some medications (ie, capecitabine, sorafenib) may induce inflammation of existing AKs.
Patients with AKs are at higher risk for developing nonmelanoma skin cancer. AKs have the potential to evolve into . It is estimated that the likelihood that a given AK will evolve into an invasive SCC is approximately 0.075%-0.096% per lesion.
The term "field cancerization" is used to describe areas of skin at risk for both AK and SCC. Clinically, this manifests as numerous AKs and squamous cell carcinoma in situ (SCCis) with or without invasive SCCs in a field of chronically sun-damaged skin. Risk factors include male sex, lighter skin color, older age, underlying immunosuppression, and the degree of prior exposure to UV light.
Related topic: actinic cheilitis
L57.0 – Actinic keratosis
201101007 – Actinic keratosis
- Superficial basal cell carcinoma
- SCCis (Bowen disease)
- Flat wart
- Common wart
- Seborrheic dermatitis – Patients with significant seborrheic dermatitis will benefit from initial treatment of dermatitis before beginning treatment for AK.
- Seborrheic keratosis
- Discoid lupus erythematosus
- Disseminated superficial actinic porokeratosis
- Severe xerosis – Wiping the skin with water or an alcohol pad will minimize background xerosis. In addition, xerosis lacks the classic gritty sensation on light palpation.
- Lentigo (pigmented variant)
- Lentigo maligna (pigmented variant)