Actinic Keratoses Guidelines Overview

European Consensus-Based Guideline for Actinic Keratoses

• 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.

Introduction

• 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.

Definition, Epidemiology, Etiology, and Diagnosis

• 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.

Pathophysiology

• AKs arise from chronic sun exposure.
• Locations are typically chronically sun-damaged areas.
• UVB radiation may induce mutations.
• UV radiation and HPV infection may influence AK development.
• Immunosuppression is a major risk factor.

Epidemiology

• 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.

Clinical and Non-Invasive Diagnosis

• 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.

Histopathological Confirmation

• 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.

Treatment of Actinic Keratoses

• 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.

Combination Treatments

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

Treatment in Immunocompromised Patients

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

Prevention and Follow-up

• 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.