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Keratoacanthoma Clinical Presentation

  • Author: Tsu-Yi Chuang, MD, MPH, FAAD; Chief Editor: William D James, MD  more...
 
Updated: Feb 29, 2016
 

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.

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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-keratoaca Keratoacanthoma (squamous cell carcinoma-keratoacanthoma or SCC-KA type) on inner canthus.
Keratoacanthoma of the left forehead. Keratoacanthoma of the left forehead.
Close-up view of the keratoacanthoma. Close-up view of the keratoacanthoma.
Keratoacanthoma lesion (squamous cell carcinoma-ke Keratoacanthoma lesion (squamous cell carcinoma-keratoacanthoma or SCC-KA type).
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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 ultraviolet light 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.[15] Additionally, a 2006 study suggested a strong association between cigarette smoking and the development of keratoacanthoma.[16]  

Trauma (iatrogenic or noniatrogenic), human papillomavirus (specifically types 9, 11, 13, 16, 18, 24, 25, 33, 37, and 57),[17, 18] genetic factors, and immunocompromised status also have been implicated as etiologic factors.

Merkel cell polyomavirus does not play a pathogenic role in keratoacanthoma.[19]

Twenty percent of patients who had metastatic melanoma and were treated with vemurafenib, a novel BRAF V600E inhibitor, may develop eruptive keratoacanthoma or squamous cell carcinoma.[20]

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.[21, 22, 23, 24]

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Contributor Information and Disclosures
Author

Tsu-Yi Chuang, MD, MPH, FAAD Clinical Professor, Department of Dermatology, Keck School of Medicine of the University of Southern California; Dermatologist, HealthCare Partners

Tsu-Yi Chuang, MD, MPH, FAAD is a member of the following medical societies: American Academy of Dermatology, American Society for Dermatologic Surgery, International Society of Dermatology

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Steven R Feldman, MD, PhD Professor, Departments of Dermatology, Pathology and Public Health Sciences, and Molecular Medicine and Translational Science, Wake Forest Baptist Health; Director, Center for Dermatology Research, Director of Industry Relations, Department of Dermatology, Wake Forest University School of Medicine

Steven R Feldman, MD, PhD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, North Carolina Medical Society, Society for Investigative Dermatology

Disclosure: Received honoraria from Amgen for consulting; Received honoraria from Abbvie for consulting; Received honoraria from Galderma for speaking and teaching; Received consulting fee from Lilly for consulting; Received ownership interest from www.DrScore.com for management position; Received ownership interest from Causa Reseasrch for management position; Received grant/research funds from Janssen for consulting; Received honoraria from Pfizer for speaking and teaching; Received consulting fee from No.

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Ryan Brashear, MD Staff Physician, Department of Dermatology, Indiana University School of Medicine

Ryan Brashear, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association

Disclosure: Nothing to disclose.

Arash Taheri, MD Research Fellow, Center for Dermatology Research, Department of Dermatology, Wake Forest University School of Medicine

Disclosure: Nothing to disclose.

References
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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).
 
 
 
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