Oral steroid improves bullous pemphigoid-like clinical manifestations in non-Herlitz junctional epidermolysis bullosa with COL17A1 mutation
- PMID: 17596158
- DOI: 10.1111/j.1365-2133.2007.08046.x
Oral steroid improves bullous pemphigoid-like clinical manifestations in non-Herlitz junctional epidermolysis bullosa with COL17A1 mutation
Abstract
Non-Herlitz junctional epidermolysis bullosa (JEB-nH), a nonlethal variant of junctional epidermolysis bullosa (JEB), is an autosomal recessive disorder characterized by separation of the dermal-epidermal junction. JEB-nH is caused by mutations in several genes and lack of the COL17A1 gene product may lead to skin fragility. A 41-year-old Japanese man with JEB-nH, featuring mutations in the gene encoding type XVII collagen, presented with great blisters over his entire body accompanied by severe itching and eosinophilia usually observed in bullous pemphigoid (BP). To our knowledge, our patient is the first with JEB-nH to be treated successfully with an oral steroid to control his skin affliction, symptoms and eosinophilia. This suggests that in the case of JEB-nH with eosinophilia caused by some secondary immune activation, oral steroids may constitute an alternate therapy to improve aggravated skin conditions and severe itching, both of which tend to show resistance to usual dermatological treatments.
Similar articles
-
Analysis of the COL17A1 in non-Herlitz junctional epidermolysis bullosa and amelogenesis imperfecta.Int J Mol Med. 2006 Aug;18(2):333-7. Int J Mol Med. 2006. PMID: 16820943
-
Autosomal dominant junctional epidermolysis bullosa.Br J Dermatol. 2009 May;160(5):1094-7. doi: 10.1111/j.1365-2133.2008.08977.x. Epub 2009 Dec 16. Br J Dermatol. 2009. PMID: 19120338
-
Localized and generalized forms of blistering in junctional epidermolysis bullosa due to COL17A1 mutations in the Netherlands.Br J Dermatol. 2007 May;156(5):861-70. doi: 10.1111/j.1365-2133.2006.07730.x. Epub 2007 Jan 30. Br J Dermatol. 2007. PMID: 17263807
-
Type XVII collagen gene mutations in junctional epidermolysis bullosa and prospects for gene therapy.Clin Exp Dermatol. 2003 Jan;28(1):53-60. doi: 10.1046/j.1365-2230.2003.01192.x. Clin Exp Dermatol. 2003. PMID: 12558632 Review.
-
Generalized atrophic benign epidermolysis bullosa.Adv Dermatol. 1997;13:87-119; discussion 120. Adv Dermatol. 1997. PMID: 9551142 Review.
Cited by
-
BP180 dysfunction triggers spontaneous skin inflammation in mice.Proc Natl Acad Sci U S A. 2018 Jun 19;115(25):6434-6439. doi: 10.1073/pnas.1721805115. Epub 2018 Jun 4. Proc Natl Acad Sci U S A. 2018. PMID: 29866844 Free PMC article.
-
The dysfunction of BP180/collagen XVII in keratinocytes promotes melanoma progression.Oncogene. 2019 Dec;38(50):7491-7503. doi: 10.1038/s41388-019-0961-9. Epub 2019 Aug 21. Oncogene. 2019. PMID: 31435021 Free PMC article.
-
A Case of Dystrophic Epidermolysis Bullosa Responding to Oral Corticosteroids.Indian J Dermatol. 2024 Mar-Apr;69(2):182-184. doi: 10.4103/ijd.ijd_702_23. Epub 2024 Apr 29. Indian J Dermatol. 2024. PMID: 38841237 Free PMC article. No abstract available.
-
Pathogenetic Therapy of Epidermolysis Bullosa: Current State and Prospects.Bull Exp Biol Med. 2021 May;171(1):109-121. doi: 10.1007/s10517-021-05182-8. Epub 2021 May 29. Bull Exp Biol Med. 2021. PMID: 34050833 Review.
-
Non-Cell-Autonomous Activity of the Hemidesmosomal Protein BP180/Collagen XVII in Granulopoiesis in Humanized NC16A Mice.J Immunol. 2020 Nov 15;205(10):2786-2794. doi: 10.4049/jimmunol.2000784. Epub 2020 Sep 30. J Immunol. 2020. PMID: 32998984 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical