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Keratosis, Actinic

Author: Zoltan Trizna, MD, PhD

BASICS

DESCRIPTION

  • Common, often multiple, premalignant lesions of sun-exposed skin
  • Many resolve spontaneously; some may progress to squamous cell carcinoma (SCC)
  • Caused by cumulative ultraviolet (UV) light exposure
  • Synonym: Solar keratosis

Geriatric: Frequent
Pediatric: Rare; suggest xeroderma pigmentosum if present

EPIDEMIOLOGY

  • Age: ≥ 40 years, increasing with age
  • Sex: Male > Female
  • Common in light skin types (blonde/red hair)
  • Prevalence:
  • 6.5% in U.S. Caucasians
  • 55% in high-sun males (65–74 yrs) vs. 18% in low-sun

ETIOLOGY & PATHOPHYSIOLOGY

  • Atypical keratinocytes at basal epidermis; may extend upward
  • Resembles SCC in situ or SCC
  • Genetic: p53 mutation in AKs and SCCs
  • Similar gene expression in AK and SCC

RISK FACTORS

  • Chronic UV exposure (occupational or recreational)
  • Photosensitive skin (burns easily, doesn’t tan)
  • Immunosuppression, especially post-transplant

PREVENTION

  • Sun protection and avoidance

ASSOCIATED CONDITIONS

  • SCC
  • Chronic sun damage signs: lentigines, elastosis, telangiectasia

DIAGNOSIS

HISTORY

  • Often asymptomatic
  • May cause pruritus, burning, or hyperesthesia
  • May enlarge, thicken, scale, regress, or remain unchanged
  • Common on sun-exposed areas: head, neck, forearms, hands

PHYSICAL EXAM

  • <1 cm, red/pink/brown macules, papules, or plaques
  • Rough to touch, sometimes easier felt than seen
  • Adherent scale common
  • Variants:
  • Atrophic: dry, scaly, indistinct borders
  • Hypertrophic: may resemble SCC
  • Pigmented: tan/brown plaques
  • Bowenoid: red, scaly plaques with sharp borders
  • Actinic cheilitis: lower lip inflammation

DIFFERENTIAL DIAGNOSIS

  • SCC, Keratoacanthoma, Bowen disease, BCC
  • Verruca vulgaris, seborrheic keratoses
  • Porokeratoses, discoid lupus, psoriasis, others

DIAGNOSTIC TESTS & INTERPRETATION

  • Clinical diagnosis usually
  • Biopsy for:
  • Large, ulcerated, indurated, or bleeding lesions
  • Treatment-resistant lesions

Histology: - Dysplastic keratinocytes in lower epidermis - Cytologically identical to SCC cells - Malignant cells sparse, except in bowenoid types

TREATMENT

GENERAL MEASURES

  • Sun protection: sunscreen, clothing, avoid peak UV

FIRST-LINE

  • Cryotherapy (liquid nitrogen)
  • Topical therapies for multiple/extensive AKs (field therapy)

MEDICATIONS

Topical 5-FU (Efudex, Carac)
- BID × 3–6 weeks
- Most effective, but irritating

Imiquimod 5% (Aldara)
- 2x/week HS × up to 16 weeks
- Area-limited, irritating

Imiquimod 3.75% (Zyclara)
- Daily × 2 weeks → break → repeat 2 weeks
- Less area restriction

Diclofenac 3% gel
- BID × 60–90 days
- Least irritating, better compliance

Second-line: - Topical retinoids: enhance 5-FU efficacy
- Systemic retinoids (rare) - Photodynamic therapy (laser + delta/methyl aminolevulinate)

ADDITIONAL THERAPIES

  • Observation for mild lesions
  • Photodynamic therapy: >90% clearance, less scarring
  • Curettage + ED&C
  • Medium-depth peels
  • CO₂ laser
  • Dermabrasion
  • Surgical excision if concern for SCC

FOLLOW-UP & MONITORING

  • Depends on malignancy risk and new lesion frequency
  • Patient education:
  • UV protection: broad-spectrum SPF >30, hats, clothing
  • Avoid sun: 10 AM–4 PM
  • Self-skin exams: look for melanoma, SCC, BCC

Resources: - DermNet NZ – Solar Keratoses

PROGNOSIS

  • Very good
  • 20–30% annual regression rate per lesion
  • Risk of progression to SCC: 0.1%–few % per lesion/year
  • 60% of SCCs arise from an AK precursor

CODES

  • ICD-10: L57.0 – Actinic keratosis

CLINICAL PEARLS

  • Premalignant, but most do not progress
  • Often more easily felt than seen
  • Resistant lesions or facial involvement = biopsy