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Lichen sclerosus et atrophicus‐like lesions in mycosis fungoides

gene mutations have been reported in similar conditions we investigated our patient’s loricrin gene, but detected no mutation. In Table 1, we summarize the data of four Japanese patients with EKV who were investigated genetically. These suggest several specific features for Japanese patients with EKV: (i) all four patients were female; (ii) no patient had a positive family history; and (iii) no patient had mutations in GJB3 or GJB4. It is possible that there are some ethnic differences in pathogenesis of EKV. In Japanese patients, EKV is assumed to be inherited in a recessive manner. Ultrastructural study of patient 3 disclosed an increased amount of gap junctions in the epidermis. Therefore, another connexin gene or another gene that is essential for the formation of gap junctions might be responsible for EKV in Japanese patients. Also in a Dutch family, van Steensel et al. 11 have recently reported a new type of erythrokeratoderma in which no connexin or loricrin mutations were identified. In summary, our patient had no mutation in GJB3 or GJB4 or the loricrin gene and may be classified as having another type of EKV caused by an unidentified gene.