The frequency of actinic keratoses increases with age and cumulative lifetime sun exposure. They are also more common in immunosuppressed individuals (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 actinic keratoses.
Patients with actinic keratoses are at higher risk for developing non-melanoma skin cancer. Actinic keratoses have the potential to evolve into . It is estimated that the likelihood that a given actinic keratosis will evolve into an invasive squamous cell carcinoma is approximately 0.075%-0.096% per lesion.
The term "field cancerization" is used to describe areas of skin at risk for both actinic keratosis and squamous cell carcinoma. 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 phototype, older age, underlying immunosuppression, and the degree of prior exposure to ultraviolet 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 actinic keratosis.
- 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)