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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