Keratoacanthoma Clinical Presentation
- Author: Tsu-Yi Chuang, MD, MPH; Chief Editor: Dirk M Elston, MD more...
History
Keratoacanthoma (KA) typically grows rapidly, attaining 1-2 cm within weeks, followed by a slow involution period lasting up to 1 year and leaving a residual scar if not excised preemptively. Since expedient therapy almost always is instituted, the true natural course of the tumor cannot be confirmed with certainty.
Physical
Pertinent physical findings in keratoacanthoma (KA) are limited to the skin. Lesions typically are solitary and begin as firm, roundish, skin-colored or reddish papules that rapidly progress to dome-shaped nodules with a smooth shiny surface and a central crateriform ulceration or keratin plug that may project like a horn. Most keratoacanthomas occur on sun-exposed areas. The face, neck, and dorsum of the upper extremities are common sites. Truncal lesions are rare. Lesions usually are skin-colored to pinkish-red. Unaffected skin retains its normal appearance. Note the images below.
Keratoacanthoma (squamous cell carcinoma-keratoacanthoma or SCC-KA type) on inner canthus.
Keratoacanthoma of the left forehead.
Close-up view of the keratoacanthoma.
Keratoacanthoma lesion (squamous cell carcinoma-keratoacanthoma or SCC-KA type). Causes
The definitive cause of keratoacanthoma (KA) remains unclear; however, several potentiating factors should be considered. Epidemiologic data of keratoacanthoma is notably similar to SCC and Bowen disease (SCC in situ) concerning age, sex, and the anatomic site of lesions. These data strongly support a common etiology among keratoacanthoma, SCC, and Bowen disease. Epidemiologic data support sunlight as an important etiologic factor.
Industrial workers exposed to pitch and tar have been well established as having a higher incidence of keratoacanthoma, as well as SCC.[13] Additionally, a 2006 study suggested a strong association between cigarette smoking and the development of keratoacanthoma.[14]
Trauma, human papillomavirus (specifically types 9, 11, 13, 16, 18, 24, 25, 33, 37, and 57),[15, 16] genetic factors, and immunocompromised status also have been implicated as etiologic factors.
Finally, research has identified that up to one third of keratoacanthomas harbor chromosomal aberrations. Recurrent aberrations include gains on 8q, 1p, and 9q with deletions on 3p, 9p, 19p, and 19q. One other report identified a 46,XY,t(2;8)(p13;p23) chromosomal aberration.[17, 18]
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