Identification of a de novo keratin 1 mutation in epidermolytic hyperkeratosis with palmoplantar involvement

Eur J Dermatol. 2006 Sep-Oct;16(5):507-10.

Abstract

Epidermolytic hyperkeratosis (EHK) (OMIM 113800) is a generalized skin disease with mostly autosomal dominant inheritance, caused by mutations in keratin 1 or keratin 10. These genes are expressed in suprabasal epidermal layers, resulting in abnormal keratin-intermediate filament cytoskeleton. We present a male patient with generalized hyperkeratosis involving palms and soles. In lesional skin massive hyperkeratosis and cytolysis in the suprabasal layers of the epidermis were observed. Immunohistochemistry staining for keratin 1 (and keratin 10) showed abnormal clumping in suprabasal keratinocytes. By electron microscopy perinuclear intermediate filament clumps were detected in the keratinocytes. A heterozygous missense mutation, designated L187F, was identified in exon 1 of the keratin 1 gene by direct sequencing. This mutation was not detected in his unaffected parents, indicative of a de novo mutational event. The homologous mutation (L187F, also designated L7F) in basal keratin genes keratin 5 or -14 causes epidermolysis bullosa simplex. The amount of keratin 1-mRNA in the patient's skin was not altered compared to controls. We propose that the severe EHK phenotype observed in our patient results from a dominant negative effect of the L187F mutant Keratin 1 allele exerted on keratin 10, the associated partner-keratin. These findings should be helpful for genetic counseling, prenatal diagnosis and studying molecular structure-function relationship in EHK.

Publication types

  • Case Reports

MeSH terms

  • Adult
  • Humans
  • Hyperkeratosis, Epidermolytic / genetics*
  • Hyperkeratosis, Epidermolytic / pathology
  • Keratin-1 / genetics*
  • Keratoderma, Palmoplantar / genetics*
  • Keratoderma, Palmoplantar / pathology
  • Male
  • Mutation, Missense
  • RNA, Messenger / analysis

Substances

  • Keratin-1
  • RNA, Messenger

Associated data

  • OMIM/113800