Aetiology
Seborrhoeic keratoses have an ill-defined aetiology:
- genetic: there is a genetic predisposition with familial clustering; suggested autosomal dominant carriage (1)
- sun exposure: there is an association between extrinsic UV-induced skin aging and the development of seborrhoeic keratoses. Amyloid precursor protein (also a marker of cellular senescence) expression is higher in UV-exposed than in non-exposed skin and increases with age (2)
- viral: despite verrucous appearance in more advanced lesions, no evidence of papilloma virus involvement (3)
- visceral malignancy:
- possible association with the release of epidermal growth factors from internal malignancy
- evidence for this theory includes an association with acanthosis nigricans and the Leser-Trelat Sign (4)
- triggering agent may be transforming growth factor
- inflammatory dermatoses
References
- Hafner C, Hartmann A, van Oers JM, et al. FGFR3 mutations in seborrheic keratoses are already present in flat lesions and associated with age and localization. Mod Pathol. 2007;20:895-903.
- Li Y, Wang Y, Zhang W, et al. Overexpression of amyloid precursor protein promotes the onset of seborrhoeic keratosis and is related to skin ageing. Acta Derm Venereol. 2018 Jun 8;98(6):594-600.
- Lee ES, Whang MR, Kang WH. Absence of human papillomavirus DNA in nongenital seborrheic keratosis. J Korean Med Sci. 2001;16:619-622.
- Leser-Trélat syndrome in patients affected by six multiple metachronous primitive cancers. J Hematol Oncol. 2010; 3: 2.
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