Keratoacanthomas Arising in Hypertrophic Lichen Planus

Allen, J. V.

doi:10.1001/archderm.1981.01650080073035

Cited by 27 publications

(13 citation statements)

References 8 publications

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“…We have only been able to find one previous report describing a woman who developed three KAs in HLP of 1 year’s duration. 3 In contrast, our patient was a man who developed only one KA in HLP of more than 20 years’ duration. In both cases, pathogenetic mechanisms such as chronic inflammation, chronic corticosteroid therapy and chronic mechanical trauma should be considered.…”

Section: Dermatoses That May Precede Reactive Keratoacanthomasmentioning

confidence: 75%

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Keratoacanthoma arising in hypertrophic lichen planus

Badell

Marcoval

Gallego

et al. 2000

British Journal of Dermatology

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Section: Dermatoses That May Precede Reactive Keratoacanthomasmentioning

confidence: 75%

“… 2 We describe a patient who developed a KA within HLP; to our knowledge, only one case has previously been reported. 3 …”

Section: Dermatoses That May Precede Reactive Keratoacanthomasmentioning

confidence: 99%

Keratoacanthoma arising in hypertrophic lichen planus

Badell

Marcoval

Gallego

et al. 2000

British Journal of Dermatology

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“…Reactive KAs are also seen in a host of diseases such as psoriasis, lichen planus, prurigo nodularis, gravitational dermatitis and skin grafts (L.S., personal communication) and other skin diseases. Treatment with topical agents or use of procedures for treatment of skin diseases may also induce KA formation.…”

Section: Reactive Kasmentioning

confidence: 99%

Squamous cell carcinoma and keratoacanthomas are biologically distinct and can be diagnosed by light microscopy: a review

et al. 2016

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Keratoacanthomas (KAs) are self-limiting squamoproliferative lesions usually seen on sun damaged skin. These tumours are in many ways enigmatic, and the relation between KAs and squamous cell carcinoma is still a contested topic. In this review the biology and histology of KAs will be discussed, and based on morphology, clinical outcome and recent genetic analysis of the tumour types, we conclude that KAs and SCCs are two distinct biological entities which can usually be distinguished by conventional microscopy. The sentinel observation of rapid and frequent appearance of KAs after BRAF treatment of malignant melanoma patients has paved the way for a more general understanding of the pathogenesis leading to the appearance of KAs in patients with inflammation in the skin. In BRAF treated patients, the KAs are a consequence of paradoxical activation of the MAP kinase pathway. Similarly, any external trauma or pharmaceutical interventions resulting in inflammation in the skin will activate the MAP kinase pathway. Such inflammation-mediated MAP kinase activation in the skin will result in the development of KAs through the same pathway as demonstrated for BRAF treated patients. It is characteristic that skin tumours following short acting inflammatory stimulation of severely sun damaged skin develop almost exclusively into KAs, whereas it is exceedingly rare that such inflammatory conditions lead to formation of SCCs. The understanding that inflammatory reactions in sun-damaged skin may activate pathways specifically leading to the formation of KAs may spare the patient the discomfort and disfigurement of needless overtreatment.

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“…In its most severe forms, hypertrophic LP mimics well‐differentiated squamous cell carcinoma (SCC). This is further complicated by reports of SCC and keratoacanthoma arising in hypertrophic LP …”

mentioning

confidence: 99%