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How should we manage multiple skin ulcers associated with calciphylaxis?

ceous cyst. In our case, the lesion was initially diagnosed as pilomatrixoma but the diagnosis was revised after histological examination. The histopathological appearance of SCN consists of a homogeneous, basophilic mass with granules of various sizes in the upper dermis. Evans et al. reported that six of 21 cases showed ulceration and transepidermal elimination of calcium. In our case, we think that the megascopic pit of the nodule corresponds to microscopic transepidermal elimination of calcium. Several theories regarding the pathogenesis of SCN have been proposed, including sweat gland duct hamartoma, calcium deposition in pre-existing lesions such as a hamartoma or nevus, mast cell degranulation with secondary calcification, traumatic calcification secondary to repetitive irritation, and dystrophic calcification due to dermal injury. Recently, Kim et al. proposed that mutation of GNAS1, a gene involved in the regulation of osteogenesis and endocrine homeostasis, may play a role of pathogenesis of SCN. Further studies are required to improve our understanding of the cause and histogenesis of SCN. The management of SCN is surgical removal followed by histopathological evaluation. To avoid misdiagnosis, SCN should be considered in the differential diagnosis of a solitary hard nodule in children.