1. A rapidly growing dome-shaped papule with a central dull pebbly core (see Photo 40).
2. A rapidly growing dome-shaped nodule with a central dull pebbly core (see Photos 41,42).
The initial lesion is a papule with a central depression or dell. The peripheral epithelial lip can vary from flesh-colored to pink or orange-red depending on the degree of inflammatory reaction and the number of dilated (telangiectatic) vessels. There is no infiltration of the skin peripheral to the margins of the lesion. The central cavity develops as the KA matures, and becomes increasingly larger as the epithelial rim thins. The central keratotic material has a gray-yellow color. In the early papule/nodule stage with the dell there can be considerable resemblance to a basal cell carcinoma. Small lesions with an early keratotic core can simulate a large molluscum wart.
1. Giant lesions form a rough, pebbly central vegetation. The epithelial margin may become quite diminutive and difficult to recognize.
2. Scarring with a depression and peripheral epidermal tags are usually left after spontaneous regression (see Photo 43).
Microdistribution: Some keratoacanthomas develop from the upper epithelium of the hair follicle; however, this distribution is not clinically evident.
Macrodistribution: 90% of KAs occur on the sun-exposed skin of the face, hands, and forearms. They can also occur on covered sites and have been reported on the vermilion margin of the lip, the buccal mucosa, in the anogenital regions, and beneath nails (see Fig. 9).
Grouped in the case of multiple KAs.
Indicated Supporting Diagnostic Data
The histology of a keratoacanthoma is very similar to that of a well-differentiated squamous cell carcinoma of the skin. KAs commonly contain squamous cells with atypical mitosis, individual cell keratinization, and other histologic signs of malignancy. The microscopic differentiation is dependent on both the cellular detail and the low-power configuration of the lesion. At each margin, a narrow spur of dermal connective tissue separates the normal epidermis from the lesion at the transitional junction between the normal and proliferating cells. For this reason, marginal punch biopsy is not adequate to distinguish between the two. Excisional biopsy or an incisional biopsy that contains a cross-section of the lesion into the adjacent normal skin is needed.
Because keratoacanthomas are difficult to separate clinically and microscopically from squamous cell carcinoma, and since substantial scarring occurs after spontaneous involution, small- to moderate-sized lesions are usually removed by excisional surgery. Giant lesions, or those in locations where removal would be mutilating or require extensive reconstruction, should be referred to a dermatologic consultant for consideration of alternative treatment. Recurrences of keratoacanthoma can occur after any type of therapy, and after apparent spontaneous involution.
Other modalities used in the destruction of KAs include curettage and electrodesicca-tion, cryosurgery, intralesional injections of triamcinolone or 5-FU, highly fractionated soft X-irradiation, and the use of oral retinoids for multiple lesions.
Conditions That May Simulate Keratoacanthomas
An early KA lesion with a keratotic core may resemble a giant molluscum wart. The solitary lesion, rapid growth, and ultimate size will usually serve to distinguish the two.
Early KA lesions with a central dell, a flesh-colored margin, and prominent vessels can be confused with a BCC. Basal cells are slow-growing, however, and are distinguishable as the central keratin core of the KA develops.
Both tumors can develop rapidly and show great clinical and microscopic similarities. They must be distinguished microscopically; however, this is not always possible.
Some deep fungal diseases produce vegetating lesions that could be confused with a giant highly keratotic KA. A punch biopsy with appropriate special stains should distinguish the two.
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