- Most common is a solitary, rapidly proliferating, dome-shaped, erythematous or flesh-colored papule or nodule with a central keratinous plug, typically reaching 1 to 2 cm in diameter.
- Clinically and microscopically resemble squamous cell carcinoma (SCC)
- Other presentations include grouped, multiple, keratoacanthoma (KA) centrifugum marginatum, intraoral, subungual, regressing, nonregressing, generally eruptive (1).
- Majority are benign and resolve spontaneously, but lesions do have the potential for invasion and metastasis, therefore require treatment.
- Three clinical stages of KAs (1):
- Proliferative: rapid growth of the lesion over weeks to several months
- Maturation/stabilization: Lesion stabilizes and growth subsides.
- Involution: spontaneous resolution of the lesion, leaving a hypopigmented, depressed scar; most but not all lesions will enter this stage.
- System(s) affected: integumentary
- Greatest incidence age >50 years but may occur at any age
- Presentation increased during summer and early fall seasons
- Most frequently on sun-exposed, hair-bearing skin but may occur anywhere
- Predominant sex: male > female (2:1)
- Most commonly in fair-skinned individuals; highest rates in Fitzpatrick I to III
- 104 cases per 100,000 individuals
Etiology and Pathophysiology
- Derived from an abnormality causing hyperkeratosis within the follicular infundibulum
- Squamous epithelial cells proliferate to extend upward around the keratin plug and proceed downward into the dermis; followed by invasion of elastic and collagen fibers
- Cellular mechanism responsible for the hyperkeratosis is currently unknown; role of human papillomavirus (HPV) has been discussed but has no established causality (2).
- Regression may be due to immune cytotoxicity or terminal differentiation of keratinocytes.
- Multiple etiologies have been suggested:
- UV radiation
- May be provoked by surgery, cryotherapy, chemical peels, or laser therapy
- Viral infections: HPV or Merkel cell polyomavirus
- Genetic predisposition: Muir-Torre syndrome, xeroderma pigmentosum, Ferguson-Smith syndrome
- BRAF inhibitors (1)
- Chemical carcinogen exposure
- Mutation of p53 or H-ras
- Ferguson-Smith (AD)
- Witten-Zak (AD)
- Muir-Torre (AD)
- Xeroderma pigmentosum (AR)
- Grzybowski (sporadic)
- Incontinentia pigmenti (XLD)
- UV exposure/damage: outdoor and/or indoor tanning
- Fitzpatrick skin type I to III
- Trauma (typically appears within 1 month of injury): laser resurfacing, surgery, cryotherapy, tattoos
- Chemical carcinogens: tar, pitch, and smoking
- Immunocompromised state
- Discoid lupus erythematosus
- HPV infection
Commonly Associated Conditions
- Frequently, the patient has concurrent sun-damaged skin: solar elastosis, solar lentigines, actinic keratosis, nonmelanoma skin cancers (basal cell carcinoma, SCC).
- In Muir-Torre syndrome, KAs are found with coexisting sebaceous neoplasms and malignancy of the GI and GU tracts; may have sebaceous differentiation known as a seboacanthoma
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