AK: Stopping the Progression

transcript

Jerome R. Obed, DO, FAOCD

Broward Dermatology &Cosmetic Specialists

Objectives

• Pathophysiology of cutaneous malignancy

• Recognition of suspicious lesions

• Prognosis & long-term risks

• Treatment options

Types of Actinic keratosis

• Classic

• Hyperplastic

• Pigmented

• Lichenoid

• Atrophic

• Actinic Cheilitis

• Bowenoid

Sun Damage (Solar Elastosis)

68 y/o female with extensive sun damage, as well as a history of cutaneous malignancy

More Dermatoheliosis(37 y/o male)

More Dermatoheliosis(48 y/o female)

More Dermatoheliosis(60 y/o male)

Extensive solar elastosis

More Dermatoheliosis(89 y/o female)

26 y/o female with early malignancy

Normal Skin

Actinic keratosis

Normal v/s AK

Squamous cell carcinoma

Normal v/s SCC

Keratoacanthoma

AK: Stopping the Progression

• Non-melanoma skin cancers are the most common malignancy amongst Caucasians

• Risk factors include UV light exposure, ionizing radiation, arsenic, organic chemicals, HPV, immunosuppression, and genetics

Actinic keratosis

Described as precancerous/premalignant because the atypical keratinocyteswithin these lesions are confined to the epidermis

Actinic keratosis

• Risk of malignant transformation is 0.075-0.096% per lesion per year

– patient with 7.7 AK’s: SCC risk is 10.2% over

10 years

• These numbers are similar to those determined for intraepithelial neoplasms in other sites

– 15% of untreated cervical CIN lesions will progress if left untreated

AK: Clinical Features

• Well demarcated erythematous hyperkeratoticlesions on sun-exposed skin

• Overlying scale is white to yellow-brown

• Surrounding areas typically demonstrate overt evidence of long-standing actinic damage

• Usually asymptomatic but itching or tenderness may be present

AK: Differential Diagnosis

• SCC in situ

• Superficial BCC

• Bowenoid Papulosis

• Lentigo Maligna

• Spongiotic Dermatosis

What are we looking for? What are we missing?

Extensive sun damage with well-demarcated AK

Well-demarcated AK

Numerous AK

Extensive sun damage with numerous Actinic keratosis

Same patientSCC (well differentiated)

Solar elastosis with numerous AK

Solar Elastosis + AK

Hyperplastic AK

More Hyperplastic AK’s

Solar elastosis + AK

Actinic Keratosis

Solar elastosis + AK

Solar Elastosis/Actinic Keratosis

SCC in-situ

SCC (well-differentiated)

SCC (microinvasive)

Forehead: Hyperplastic AK

Temple: Squamous cell carcinoma in-situ

AK + SCC

SCC x 2

Solar elastosis + SCC

AK + SCC

AK + SCC (1 of 2)

AK + SCC (2 of 2)

A: Hyperplastic AK

B: Squamous cell carcinoma (well differentiated)

SCC in-situ

SCC (well differentiated, invasive)

Actinic Cheilitis

• Premalignant condition that predisposes to intraepidermal carcinoma and invasive SCC

• Involved skin (usually lower lip) has a mottled appearance with indistinct vermilion border

• Scaling, crusting, and erosions are seen, as well as loss of elasticity, dryness, and atrophy

Actinic Cheilitis

• DDX: contact dermatitis; plasma cell cheilitis

• Recurring cycle of crusting and healing is common, while prolonged ulceration ulceration may signify malignancy

Actinic Cheilitis

Therapeutic options

• Watchful waiting

• Cryotherapy

• Chemical Peels

• Laser resurfacing

• Photodynamic Therapy

• Topical immunotherapy

• Electrodessication & Curretage

• Nicotinamide??

Topical immunotherapy

• Imiquimod

– Aldara/Zyclara

• 5-Fluorouracil

– Effudex, Carac, Fluoroplex

• Ingenol mebutate

– Picato

Treatment benefits

• Halt disease progression

• Field cancerization

Treatment complications

• Pain/Discomfort

• Scarring

• Post-inflammatory pigmentary changes

Before and during treatment with topical Imiquimod

During and following treatment with topical Imiquimod

During treatment with IngenolMebutate

During treatment with Fluorouracil

Thank you!!

Drjobed@BrowardDerm.com

AK: Stopping the Progression

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