Actinic Keratosis, Basal Cell Carcinoma, and Squamous Cell Carcinoma

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Actinic Keratosis, Basal Cell Carcinoma, and Squamous Cell Carcinoma





Actinic Keratoses (AKs)



• Also referred to as solar keratoses, AKs are considered “precancerous” lesions that have the potential to progress into invasive SCC; estimates of progression vary from a rate of 0.075–0.1% per lesion per year to ~10% over 10 years.


• The atypical keratinocytes are confined to the lower portion of the epidermis (Fig. 88.1).



• AKs are one of the most frequently encountered lesions in clinical practice.


• Occur primarily in sites that have received the greatest amount of cumulative sun exposure (e.g. scalp in bald individuals, face, ears, neck, dorsal forearms and hands, shins); seen primarily in middle-aged to older, fair-skinned individuals.


• Classic presentation is a gritty papule with an erythematous base; the associated scale is usually white to yellow in color and feels rough (Fig. 88.2).



• Common clinical variants: hypertrophic (referred to as HAK [Fig. 88.2C,D]), pigmented, lichenoid, and atrophic (Fig. 88.2B); in actinic cheilitis, there is scaling and roughness of the lower vermilion lip (see Fig. 13.5).


• Dx: usually made by visual inspection and palpation; because of the rough texture, it is sometimes easier to detect lesions via touch.


• AKs have the potential to persist, spontaneously regress, or progress to SCC, but clinically it is difficult to predict which course a given AK will take.


• Clinical clues to progression to invasive SCC and need for biopsy: tenderness, volume (particularly thickness), inflammation, and failure to respond to appropriate therapy.


• DDx: SCC in situ, BCC, lichen planus-like keratosis (LPLK; see Chapter 89), irritated seborrheic keratosis (SK) or verruca vulgaris, and amelanotic melanoma; for thicker lesions (e.g. HAK), invasive SCC; for lesions on extensor extremities, actinic porokeratosis; occasionally, isolated lesions of psoriasis or seborrheic dermatitis may resemble an AK.


• Rx: localized or lesion-targeted treatments are best for an isolated or limited number of lesions; field treatments are best for more numerous or larger lesions (Table 88.2).



• Prevention is possible with broad-spectrum sunscreens and sun avoidance measures.



SCC In Situ (Bowen’s Disease)



• May arise de novo or from a pre-existing AK; sometimes caused by oncogenic strains of human papillomavirus (HPV, e.g. periungual [see Chapter 66]).


• Keratinocyte atypia is seen throughout the entire epidermis (full-thickness) (see Fig. 88.1) and has the potential to progress to invasive SCC, with an estimated risk of ~3–5% if untreated.


• With the exception of HPV- or arsenic-related SCC in situ, the risk factors for and the locations of SCC in situ are similar to those for AKs (see above and Table 88.1).


• Clinically presents as an erythematous patch or thin plaque with scale (Fig. 88.3); occasionally, the lesions are pigmented.



• Less common sites (may be related to HPV infection): beard area, periungual (see Figs. 88.3B and 58.7) and subungual, anogenital (now referred to as intraepithelial neoplasia, further qualified by anatomic site [see Chapter 60 and Fig. 88.4]); SCC in situ in non-sun-exposed sites may also be related to arsenic exposure.


Apr 22, 2016 | Posted by in Dermatology | Comments Off on Actinic Keratosis, Basal Cell Carcinoma, and Squamous Cell Carcinoma

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