Keratoacanthomas (KA) are rapidly growing papules that can enlarge from a 1 mm macule or papule to as large as 2.5 cm lesion in 3-8 weeks. Fully developed they are hemispheric, dome-shaped, skin colored nodules which often demonstrate a smooth crater filled with a central keratin plug. The smooth portion of the KA is often sharply demarcated and telangiectases may be found. There are four types of keratoacanthomas: Solitary, multiple, eruptive and keratoacanthoma centrifugum marginatum. KAs used to be considered a reactive condition or pseudomalignancy, but now most physicians consider KAs as low-grade squamous cell carcinomas (SCC). KAs may spontaneously regress and resolve without treatment and this is why in the past they were considered to be a “pseudomalignancy.” Any documented KA occurring in an immunocompromised patient should be managed as an SCC.
Solitary lesions most commonly occur on sun-exposed areas and by far and away are the most frequently observed type. Multiple Eruptive Keratoacanthomas (MEK) have been reported to occur in a single Scottish kindred and are referred to as the Ferguson Smith type. Generalized eruptive KAs are rarely observed, manifesting with between 40-60 lesions. The cause remains unknown, and is referred to as the Grzybowski type. The last form is Keratoacanthoma Centrifugum Marginatum (KCM), characterized by progressive peripheral expansion and central healing resulting in atrophy. Spontaneous involution may occur and the lesions may range from 5-30 cm in diameter.
HISTOLOGY: KAs demonstrate a central crater which is keratin-filled. At the base and sides of the crater the epithelium is acanthotic and composed of keratinocytes which are highly keratinized and have an eosinophilic, glassy cytoplasm. Surrounding the keratinocyte proliferation there is often a dense inflammatory infiltrate composed of neutrophilic microabscesses within the tumor with trapping of elastic fibers…these features are a clue to it being a KA versus a SCC.
ETIOLOGY: KAs arise from the infundibulum of the hair follicle. The pathogenitic mechanisms are unclear but may involve aberrant regulation of the WNT signal transduction pathways and mutations in the tumor suppression gene TP53. Risk factors include chronic UV light exposure, chemical carcinogens (cigarette smoking, industrial exposure), cutaneous trauma and human papillomavirus infections. In addition patients that are immunocompromised, have solid organ transplants, and a variety of genetic disorders (xeroderma pigmentosum, Muir-Tore syndrome, and incontinentia pigmenti) are predisposed to develop KAs. Additional associations have been reported with treatments such as psoralen-UVA phtochemotherapy, vemurafenib, dabrafenib and vismodegib.
TREATMENT: For the most part it is recommended to treat KAs just like SCCs which most often requires surgical excision with adequate margins. Nonsurgical therapy includes intralesional injections with 5-fluorouracil, bleomycin or methotrexate. For patients with GEK, the Grzybowski variant, treatment with oral retinoids, oral methotrexate and oral cyclophosphamide have been shown to be effective. For KCM variant recommended treatments include oral etretinate and oral methotrexate with prednisone are recommended. For solitary KAs I often perform a scoop shave removing the entire lesion if possible followed by aggressive fulguration of the base. If the deep margin continues to be involved I will often just watch for recurrence, due to the added treatment of fulguration, because if the lesion is going to recur it often does so within the next few weeks. If it does recur I surgically excise the remaining lesion. Otherwise, most of the time the lesions heal without recurrence. That’s been my experience… To read more click HERE, HERE and HERE.