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

1. 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.
2. 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.
3. Lee ES, Whang MR, Kang WH. Absence of human papillomavirus DNA in nongenital seborrheic keratosis. J Korean Med Sci. 2001;16:619-622.
4. Leser-Trélat syndrome in patients affected by six multiple metachronous primitive cancers. J Hematol Oncol. 2010; 3: 2.