INTRODUCTION Keratoacanthoma is a relatively common squamoproliferative neoplasm that occurs on sun-exposed areas of adults, the incidence increasing with advancing years. Males outnumber females by a ratio of 2:1. It resembles squamous cell carcinoma both clinically and pathologically, and in 15% to 17% of cases squamous cell carcinoma is misdiagnosed as keratoacanthoma. Some authors have argued that keratoacanthoma should be classified as a variant of well-differentiated squamous cell carcinoma. However, the two lesions have been shown to be distinct on immuno-histochemical grounds. Although multiple, aggressive and giant varieties have been described, most are solitary and self-limited. The lesion may also occur as part of Muir-Torre syndrome (skin lesion associated with an internal malignancy). The etiology is unknown but sunlight, trauma, chemical carcinogens, UVB exposure, and immunocompromised status have been implicated as etiologic factors.
CLINICAL PRESENTATION The classic lesion appears spontaneously as a small flesh-colored papule that evolves very rapidly over three to six weeks to a 0.5 to 2.5 cm dome-shaped violaceous or brownish nodule. The nodule is usually umbilicated with a distinctive central crater filled with a keratin plug. The edges of the crater may have elevated rolled margins. Lesions have a predilection for the lower eyelid where more than half are located. It typically undergoes spontaneous involution within four to six months to leave an atrophic scar. Lesions that occur on the eyelids may produce ectropion or ptosis, and occasionally may cause destructive changes.
HISTOPATHOLOGY Keratoacanthomas have a proliferation of well-differentiated, keratinizing squamous epithelium at the sides and bottom of the lesion, with a central keratin-filled crater that enlarges as the lesion matures. A key diagnostic feature is a lip of epidermis (collarette) overlapping the central crater. The lesion usually has a relatively even lower border that remains superficial to
the sweat glands. The adjacent dermis contains a mixture of lymphocytes, macrophages, plasma cells, neutrophils, and varying numbers of eosinophils. Keratoacanthomas lack marked epithelial dysplasia, abnormal mitotic figures, and a marked desmoplastic reaction in the stroma, helping to distinguish them from squamous cell carcinomas.
TREATMENT In the past treatment of keratoacanthoma has typically been conservative. However, because of its sometimes aggressive behavior and uncertain relationship to squamous cell carcinoma complete surgical excision is now considered the treatment of choice. In a recent study 16% of lesions clinically diagnosed as keratoacanthoma proved to be invasive squamous cell carcinoma on biopsy. Surgical excision, besides providing definitive treatment also confirms diagnosis, speeds recovery, and limits scarring. Complete excision is recommended under frozen section control or Mohs surgery since invasive variants exist with the potential for perineural and intramuscular spread. When surgery is not possible cryotherapy, radiotherapy, and chemotherapy have been effective. Both intralesional injections and topical 5-fluorouracil (5-FU) have been advocated. Intralesional methotrexate has also been used with complete resolution of the lesion after three weeks.
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