Necrolytic migratory erythema (NME) is a relatively rare inflammatory skin disease
characterized by repeated episodes of an irregular annular eruption in which a central
pustule develops, subsequently erodes, and then encrusts. Although NME is typically
associated with glucagonomas, recently, there have been a number of case reports in
patients with nutritional disorders such as malabsorption, short-bowel syndrome, and
inflammatory bowel disease [
[1]
]. Common features on blood chemistry are zinc deficiency, hypoaminoacidemia, and fatty
acid deficiency, which have been postulated as causative mechanisms for NME [
[1]
]. The exact etiology, however, still remains to be delineated. We here report two
NME cases, one associated with typical glucagonoma and the other with generalized
pustular psoriasis and malabsorption due to amyloidosis. Based on the previous report,
the number of epidermal Langerhans cells (LC), the cutaneous counterpart of dendritic
cells [
[2]
], was significantly reduced in the epidermis of the zinc deficiency rats [
[3]
]. We, therefore, conducted immunohistochemical analysis to evaluate the number of
LC in erythematous skin lesions of NME and revealed a remarkable decrease in the number
of CD1a-positive epidermal LC in two NME cases.Keywords
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References
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Article info
Publication history
Published online: July 12, 2010
Received:
August 21,
2007
Identification
Copyright
© 2007 Japanese Society for Investigative Dermatology. Published by Elsevier Inc. All rights reserved.
