Answer to Dermacase continued from page 985
4. Keratoacanthoma
Keratoacanthoma (KA) is a neoplasm of epithelial cells, and typically affects fair-skinned, middle-aged to older individuals; it has a slightly higher predominance in males.1–3 It usually appears as a solitary, nontender, flesh-coloured or pink nodule with a central-crusted, keratotic plug on hair-bearing, sun-exposed areas, primarily the face, neck, and hands.1–3 The lesion is characterized by rapid growth and achieves an average diameter of 2.5 cm within 6 to 10 weeks.1,3 In approximately 50% of cases, spontaneous resolution of the tumour occurs within 4 to 9 months of achieving maximal size, although an atrophic and pigmented scar usually remains.1,3,4
The etiology of KA is unknown, but it is thought to derive from hair follicles.1–3 Additionally, several factors have been postulated to be involved in its development: Poor immunocompetence, UV radiation, mineral oil, cigarettes, and chemical carcinogens, such as tar and pitch, all might play an etiologic role.1,2 Not uncommonly, KA forms in areas of trauma, such as surgical sites or areas subject to laser resurfacing.1–3 Certain types of human papillomavirus have also been implicated1 and DNA related to the virus has been found in some KA tumours.2
Keratoacanthoma might present with clinical and pathological findings similar to those of squamous cell carcinoma (SCC), and many SCC lesions resemble KA lesions.2,3 Classification of KA is therefore a source of controversy; it could be a distinct entity, but also has been proposed as a variant of cutaneous SCC.1–3,5 Because spontaneous involution of the tumour has been described, some consider KA lesions to be benign; however, their potential for evolution into invasive SCC lesions that might metastasize, as well as their potential for recurrence following excision, could suggest otherwise.1–5
Diagnosis and management
Upon presentation of the lesion, KA can usually be diagnosed based on its distinctive clinical history; however, because of a lack of features distinguishing KA from SCC in appearance, it is suggested that KA be considered as potential SCC and handled accordingly.1,2,5 A biopsy is typically performed to rule out SCC and a sample of sufficient depth is required.1–3,5 Recent studies have suggested chromosomal differences in the 2 conditions, which can be detected using comparative genomic hybridization1,2; however, cytogenetics is not currently a standard investigation for KA.
A variety of treatment modalities are available for KA. Intralesional 5-fluorouracil, topical imiquimod, cryosurgery, electrodessication and curettage, wide local excision, radiation therapy, and laser therapy have all been successfully employed to treat small, solitary lesions.1–4 In areas of cosmetic importance, or if the lesions are large or invasive, referral for Mohs micrographic surgery is preferred.1,2 Should a patient or physician seek a nontreatment approach, regular follow-up sessions with a dermatologist who can observe and photograph the lesion from presentation to complete resolution is recommended.1,4 Even in cases where the KA is expected to regress on its own, treatment is a reasonable option for anxiety reduction and cosmetic purposes.1–4
It is also important to reinforce conservative measures, such as minimizing contact with those aforementioned factors that might play a role in the development of KA (chemical carcinogens, cigarettes, etc). Excessive sun exposure should be avoided and sunscreen should be applied regularly to reduce scarring and prevent recurrence.1
Footnotes
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Competing interests
None declared
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