A 69-year-old woman presents for evaluation of a sizeable growth on her nose. She states that the lesion was first noted several months ago and has rapidly increased in size over the last 4 weeks. She has fair skin and admits to decades-long sun exposure and cigarette smoking. The patient denies a history of skin cancer but has had several precancerous lesions removed from her arms with liquid nitrogen and topical fluorouracil cream. Physical examination reveals a 2.0-cm firm nodule with a crusted center.
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Keratoacanthoma (KA) is a commonly encountered tumor that originates from the pilosebaceous unit (hair follicle, hair shaft, and sebaceous gland). The lesion is usually dome-shaped, rapidly growing, and contains a central debris-laden core.1
The etiology of KA has been linked to ultraviolet light exposure and lesions have a predilection for sun-exposed areas such as the face and forearms.1 Keratoacanthomas have also been linked to trauma and several subtypes of the human papillomavirus (HPV) infections, although a study by Lu et al could not find any role of HPV types in the etiology of KAs.2 These tumors have been induced by treatment with the BRAF V600E inhibitor vemurafenib in patients with metastatic melanoma.3 Keratoacanthomas have also been associated with prolonged exposure to coal tar and cigarette smoke.4,5
Diagnosis of KA is confirmed by biopsy, which reveals well-differentiated squamous epithelium exhibiting a mild degree of pleomorphism and evidence of the keratin plug. Differentiating KA from squamous cell carcinoma (SCC) may be challenging;many clinicians consider the neoplasm to be a low-grade SCC. 6,7 Although KA tumors may spontaneously regress, metastatic spread has been reported8 and full excision, when anatomically feasible, is the treatment of choice.1
Zachary Sabaday, PA-C, is a physician assistant at the DermDox Dermatology Centers, PC, in Sugarloaf, Pennsylvania. Stephen Schleicher, MD, is director of the DermDox Center for Dermatology in Pennsylvania, associate professor of medicine at Commonwealth Medical College, and clinical instructor of dermatology at Arcadia University and Kings College.
1. Kwiek B, Schwartz RA. Keratoacanthoma (KA): an update and review. J Am Acad Dermatol. 2016;74(6):1220-1233. doi:10.1016/j.jaad.2015.11.033
2. Lu S, Syrjänen SL, Havu VK, Syrjänen S. Known HPV types have no association with keratoacanthomas. Arch Dermatol Res. 1996;288(3):129-132. doi:10.1007/BF02505821
3. Chapman PB, Hauschild A, Robert C, et al; BRIM-3 Study Group. Improved survival with vemurafenib in melanoma with BRAF V600E mutation. N Engl J Med. 2011;364(26):2507-2516. doi:10.1056/NEJMoa1103782.
4. Letzel S, Drexler H. Occupationally related tumors in tar refinery workers. J Am Acad Dermatol. 1998;39(5 Pt 1):712-720. doi:10.1016/s0190-9622(98)70043-x
5. Miot HA, Miot LD, da Costa AL, Matsuo CY, Stolf HO, Marques ME. Association between solitary keratoacanthoma and cigarette smoking: a case-control study. Dermatol Online J. 2006;12(2):2.
6. Kern WH, McCray MK. The histopathologic differentiation of keratoacanthoma and squamous cell carcinoma of the skin. J Cutan Pathol. 1980;7:318-325. doi:10.1111/j.1600-0560.1980.tb01202.x
7. Cribier B, Asch P, Grosshans E. Differentiating squamous cell carcinoma from keratoacanthoma using histopathological criteria. Is it possible? A study of 296 cases. Dermatology. 1999;199(3):208-212. doi:10.1159/000018276
8. Piscioli F, Boi S, Zumiani G, Cristofolini M. A gigantic, metastasizing keratoacanthoma. Report of a case and discussion on classification. Am J Dermatopathol. 1984;6:123-129.