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Improvement of hereditary palmoplantar keratoderma with oral trametinib
Author(s) -
Song Hannah,
Dzuali Fiatsogbe,
Chi Susan N.,
Treat James R.,
Huang Jennifer T.
Publication year - 2018
Publication title -
pediatric dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.542
H-Index - 73
eISSN - 1525-1470
pISSN - 0736-8046
DOI - 10.1111/pde.13731
Subject(s) - medicine , palmoplantar keratoderma , trametinib , dermatology , keratoderma , hyperkeratosis , genetics , mapk/erk pathway , biology , kinase
Abstract We report a child with a past medical history notable for congenital deafness, palmoplantar keratoderma ( PPK ), and hypothalamic glioma who initiated a MEK inhibitor trametinib for cancer‐directed therapy at 11 years of age and was incidentally noted to have marked improvement in his PPK . Trametinib withdrawal led to worsening in the patient's PPK . We speculate that the patient's PPK improved because of trametinib, given the temporal relationship between trametinib therapy and PPK severity, observed both after introduction and withdrawal of trametinib therapy. The upregulation of MAPK signaling may be involved in the pathogenesis of keratinocyte proliferation in at least some forms of PPK , given that downstream inhibition of MAPK signaling led to an improvement in the patient's PPK .