Actinic Keratoses Guidelines Overview

Study Notes

This guideline provides interdisciplinary recommendations for the diagnosis, treatment, and prevention of actinic keratoses (AKs), epithelial UV-induced dysplasia, and field cancerization.
It's based on expert consensus and current literature.
AKs are potential precursors to cutaneous squamous cell carcinoma (cSCC)
AKs have histopathological and immunohistochemical features of cSCC in an early stage.
Progression to cSCC is not predictable, and treatment is usually recommended.
Diagnosis is typically made through clinical examination. Dermatoscopy, confocal microscopy, optical coherence tomography, or line-field confocal optical coherence tomography can aid in diagnosis.
Biopsy is indicated for clinically or dermatoscopically suspicious and/or treatment-refractory lesions.

Guidelines address epithelial dysplasia (including AKs).
Increased incidence of keratinocyte cancers is notable.
Different classification schemes exist (e.g. for epithelial dysplasia and AKs) to guide treatments.
New insights into treatments are crucial for preventing invasive cutaneous squamous cell carcinoma.

Actinic keratosis (AK) is a common cutaneous keratinocyte dysplasia.
It involves abnormal proliferation of atypical epidermal keratinocytes.
AK is a carcinoma precursor.
The term "in situ SCC" can be used to define AKs.
Current literature defines field cancerization as the area around a visible AK with genetic changes similar to AKs' (e.g. telangiectasia, atrophy, pigmentation abnormalities, or a sandpaper-like texture). A visible AK lesion isn't always required for field cancerization.

Prevalence varies widely, depending on study location characteristics, UV radiation levels, and study settings.
Higher prevalence in older individuals.
Usually, higher rates in males.
Risk factors include age, fair skin type, light hair/eye color, freckles, chronic sun exposure, sunburn history.
Lower risk in sun-protective measures users and individuals with atopic history.

AKs manifest as rough, scaly patches, papules, or plaques in chronically sun-exposed areas.
Colour ranges from red, light, or dark brown.
Dermatoscopy (evaluation with a dermatoscope) is valuable for improving AK diagnosis.
RCM (reflectance confocal microscopy) and OCT (optical coherence tomography) aid in AK and SCC differentiation.

Histological confirmation is crucial for equivocal lesions or for differentiating AKs from BCC or cSCC (cutaneous squamous cell carcinoma).
In order to evaluate the possibility of iSCC (invasive squamous cell carcinoma) or other skin cancers, a biopsy is recommended in case of infiltration, induration, pain, ulceration, increase in thickness, and rapid growing.
Classifications exist to predict the likelihood of progression to cSCC.

Goal is to prevent progression to cSCC.
Risk of progression is significantly higher in immunocompromised patients.
Treatment strategies can be lesion-directed (individual AKs) or field-directed (multiple AKs).
Field-directed treatments are often more convenient for widespread, subclinical AKs in sun-damaged fields.
Lesion-directed treatments utilize destructive methods (surgery, cryotherapy, laser therapy).
Topical treatments (5-FU, imiquimod, PDT) are employed for lesion-directed and/or field-directed therapy.

Combining interventions may have synergistic effects, leading to better clearance rates.
Field-directed treatment can be complemented with lesion-directed treatments.

Chronic immunosuppression significantly increases cSCC risk.
Management strategies include reducing immunosuppressive regimens (azathioprine elimination, mTOR inhibitor regimens), photoprotection, and chemoprevention (retinoids).

Sun protection measures (sunscreen, clothing, avoiding midday sun exposure) are essential for preventing AK development.
Regular follow-up visits are crucial for skin evaluation, especially in high-risk patients or those with a history of cSCC, to detect recurrence or new lesions. Follow-up frequency depends on existing AK numbers and evolution, and immune status and medication.