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Porokeratosis (PK), first described in 1983, is a chronic parakeratotic skin disorder. Clinical types include porokeratosis of Mibelli (PM), disseminated superficial PK, disseminated superficial actinic porokeratosis (DSAP), facial PK, and ptychotropica porokeratosis (PP). Dermoscopic images of PK show an obvious annular margin with scales and an atrophied center.[1] Wood’s lamp pictures of PK present a diamond necklace‐like structure.[2] Gene mutations in mevalonate pathway enzymes, such as mevalonate kinase (MVK), phosphomevalonate kinase (PMVK), mevalonate decarboxylase (MVD), and farnesyl diphosphate synthase (FDPS), may be involved in the pathogenesis of PK.[3,4] In the present study, five sporadic patients with PK were recruited. Dermoscopic features were investigated, and genetic testing was conducted.

Dermoscopic Features and Gene Mutation in the Mevalonate Pathway of Five Sporadic Patients with Porokeratosis