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Multiple cutaneous myxoid cysts with transepidermal elimination

eruptions without acantholysis reflect that our case was predominantly mediated by cellular autoimmunity rather than humoral immunity. The most striking and unusual clinical feature of our case was that there was no mucosal involvement. The underlying cause of the absence of mucosal involvement in our patient remains unknown. Amagai et al. reported that almost all patients with PNP have circulating anti-Dsg3 autoantibodies and demonstrated that anti-Dsg autoantibodies were involved in the pathogenesis of blister formation. If this postulation is correct, we can suspect that the absence of detectable antiDsg3 autoantibodies in our patient may be responsible for the absence of both mucosal and cutaneous acantholytic lesions. However, the pathomechanism of oral lesions in PNP is still unclear and may be more complex than in classic pemphigus vulgaris, because PNP produces autoantibodies against multiple antigens, including plakin family proteins as well as Dsgs. Several cases of PNP without anti-Dsg autoantibodies have been reported; however, the patients still had oral and cutaneous acantholytic lesions. Thus, the absence of anti-Dsg3 autoantibodies in itself is insufficient to explain the absence of mucosal involvement in our patient. Moreover, cell-mediated immune responses like lichen planus and EM also cause cytotoxicity to mucosal epithelia. This case is a further example showing diversity of clinical manifestations of PNP. Further studies are necessary to elucidate the underlying pathomechanism causing clinical diversity of PNP.