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Recent Advances in Dermatitis Herpetiformis
Kimiko Nakajima
Clinical and Developmental Immunology , 2012, DOI: 10.1155/2012/914162
Abstract: Dermatitis herpetiformis is an autoimmune bullous disease that is associated with gluten sensitivity which typically presents as celiac disease. As both conditions are multifactorial disorders, it is not clear how specific pathogenetic mechanisms may lead to the dysregulation of immune responses in the skin and small bowel, respectively. Recent studies have demonstrated that IgA and antibodies against epidermal transglutaminase 3 play an important role in the pathogenesis of dermatitis herpetiformis. Here, we review recent immunopathological progress in understanding the pathogenesis of dermatitis herpetiformis.
Dermatitis Herpetiformis: From the Genetics to the Development of Skin Lesions
Diletta Bonciani,Alice Verdelli,Veronica Bonciolini,Antonietta D'Errico,Emiliano Antiga,Paolo Fabbri,Marzia Caproni
Clinical and Developmental Immunology , 2012, DOI: 10.1155/2012/239691
Abstract: Dermatitis herpetiformis (DH) is a rare autoimmune disease linked to gluten sensitivity with a chronic-relapsing course. It is currently considered to be the specific cutaneous manifestation of celiac disease (CD). Both conditions are mediated by the IgA class of autoantibodies, and the diagnosis of DH is dependent on the detection of granular deposits of IgA in the skin. There is an underlying genetic predisposition to the development of DH, but environmental factors are also important. This paper describes these different factors and discusses the known mechanism that lead to the development of skin lesions.
Dermatitis herpetiformis bodies and autoantibodies to noncutaneous organs and mitochondria in dermatitis herpetiformis  [cached]
Ana Maria Abreu Velez,Hong Yi,Julia Griffin Girard,Zhe Jiao
Our Dermatology Online , 2012,
Abstract: Introduction: The precise nature of the previously described dermatitis herpetiformis bodies remains unknown.Aims: Our study was conducted to investigate the nature of dermatitis herpetiformis bodies in the skin in 7 cases of dermatitis herpetiformis, and to search for the presence of autoantibodies in other organsMethods: We utilized clinical, histopathologic, and immunologic methods to evaluate these patients.Results: Dermatitis herpetiformis bodies were found to be comprised of an amalgamation of immunoglobulins A and M, as well as molecules reactive with antibodies to armadillo repeat gene deleted in velo-cardio-facial syndrome, desmoplakins 1 and 2, and plakophilin 4. In addition, we found immunologic colocalization with selected autoantibodies associated with mitochondria in the skin, heart, kidney, and peripheral nerves. The dermatitis herpetiformis bodies did not demonstrate immunologic colocalization with tissue/epidermal transglutaminase.Conclusion: The complete biochemical nature of dermatitis herpetiformis bodies requires further characterization. Dermatitis herpetiformis bodies in these patients appear to be distinctly different than cytoid bodies. Further studies are required to determine if the antibodies to noncutaneous organs are pathogenic, and/or contribute to systemic morbility in dermatitis herpetiformis patients.
Dermatitis herpetiformis intolerant to dapsone in Aids  [cached]
Krishna K,Kavitha K
Indian Journal of Dermatology, Venereology and Leprology , 1999,
Abstract: A 35-year-old man with AIDS and pulmonary tuberculosis presented with lesions suggestive of dermatitis herpetiformis and intolerance to dapsone. He was managed successfully with a combination of nicotinamide 200 mg/day and indomethacin 75 mg/day, topical steroids and gluten free diet.
Dermatitis herpetiformis and rheumatoid arthritis
Singal Archana,Bhattacharya Sambit Nath,Baruah Manik Chandra
Indian Journal of Dermatology, Venereology and Leprology , 2002,
Abstract: A 35- year-old deaf and dumb woman with clinical and histopothological diagnosis of dermatitis herpetiforrnis (DH) is reported for its rare association with rheumatoid arthritis (PA).
Gene Expression Profiling in Dermatitis Herpetiformis Skin Lesions  [PDF]
M. Dolcino,E. Cozzani,S. Riva,A. Parodi,E. Tinazzi,C. Lunardi,A. Puccetti
Journal of Immunology Research , 2012, DOI: 10.1155/2012/198956
Abstract: Dermatitis herpetiformis (DH) is an autoimmune blistering skin disease associated with gluten-sensitive enteropathy (CD). In order to investigate the pathogenesis of skin lesions at molecular level, we analysed the gene expression profiles in skin biopsies from 6 CD patients with DH and 6 healthy controls using Affymetrix HG-U133A 2.0 arrays. 486 genes were differentially expressed in DH skin compared to normal skin: 225 were upregulated and 261 were downregulated. Consistently with the autoimmune origin of DH, functional classification of the differentially expressed genes (DEGs) indicates a B- and T-cell immune response (LAG3, TRAF5, DPP4, and NT5E). In addition, gene modulation provides evidence for a local inflammatory response (IL8, PTGFR, FSTL1, IFI16, BDKRD2, and NAMPT) with concomitant leukocyte recruitment (CCL5, ENPP2), endothelial cell activation, and neutrophil extravasation (SELL, SELE). DEGs also indicate overproduction of matrix proteases (MMP9, ADAM9, and ADAM19) and proteolytic enzymes (CTSG, ELA2, CPA3, TPSB2, and CMA1) that may contribute to epidermal splitting and blister formation. Finally, we observed modulation of genes involved in cell growth inhibition (CGREF1, PA2G4, and PPP2R1B), increased apoptosis (FAS, TNFSF10, and BASP1), and reduced adhesion at the dermal epidermal junction (PLEC1, ITGB4, and LAMA5). In conclusion, our results identify genes that are involved in the pathogenesis of DH skin lesions. 1. Introduction Dermatitis herpetiformis (DH) is an autoimmune subepidermal blistering skin disease characterized by intense pruritic papulovesicular eruptions mainly localized on extensor surfaces [1]. DH typically develops in patients with celiac disease (CD). The two conditions share the same genetic background (HLA genes DQ2–DQ8), improve following a gluten-free diet (GFD), and are mediated by IgA autoantibodies [2]. IgA antibodies against tissue transglutaminase (tTG) are detectable both in CD and DH, while autoantibodies directed against epidermal transglutaminase (eTG) are a typical serological marker of patients with DH [3]. The key feature of DH is a granular deposition of IgA within the tips of dermal papillae and along the basement membrane of perilesional skin. eTG has been shown to colocalize with such IgA deposits [4]. Typical histopathologic features of DH consist of accumulation of neutrophils and a few eosinophils with formation of papillary microabscesses which then coalescence to form a subepidermal bulla. Moreover, a perivascular cellular infiltrate composed mainly by CD4+ lymphocytes is also present [5]. In
The Expression of Selected Proapoptotic Molecules in Dermatitis Herpetiformis
Zebrowska Agnieszka,Erkiert-Polguj Anna,Wagrowska-Danilewicz Malgorzata,Danilewicz Marian,Sysa-Jedrzejowska Anna,Anna Cynkier,Waszczykowska Elzbieta
Clinical and Developmental Immunology , 2012, DOI: 10.1155/2012/178340
Abstract: The role of the process of apoptosis is investigated in the pathogenesis of many autoimmune diseases; however at present, there is not much information about its role in dermatitis herpetiformis. Skin biopsies were taken from 18 DH patients and from 10 healthy subjects. The localization and expression of Bax, Fas, FasL, TRAIL, TRAIL-R in skin lesions, and perilesional skin were studied by immunohistochemistry. Expression of Bax, Fas, and Fas ligand was detected in the keratinocytes in skin biopsies from DH patients. Expression of TRAIL and TRAIL receptor was confirmed in epidermis, infiltration cells, and some fibroblasts. The expression of examined molecules in biopsies from healthy people was observed only in single cells. There were statistically significant differences between lesional, perilesional, and healthy skin of control group in Bax expression analysis and between lesional skin and control group in Fas, FasL, and TRAIL expression. There were statistically significant differences between control group and perilesional skin in Bax and FasL expression. Our results show that selected proapoptotic molecules may take part in pathogenesis of dermatitis herpetiformis, but the role of apoptosis in this process is not clear.
Newly Described Clinical and Immunopathological Feature of Dermatitis Herpetiformis
Veronica Bonciolini,Diletta Bonciani,Alice Verdelli,Antonietta D'Errico,Emiliano Antiga,Paolo Fabbri,Marzia Caproni
Clinical and Developmental Immunology , 2012, DOI: 10.1155/2012/967974
Abstract: Dermatitis herpetiformis (DH) is an inflammatory cutaneous disease with typical histopathological and immunopathological findings clinically characterized by intensely pruritic polymorphic lesions with a chronic-relapsing course. In addition to classic clinical manifestations of DH, atypical variants are more and more frequently reported and histological and immunological are added to them, whereas the impact on quality of life of patients with DH is increasingly important to a certain diagnosis. The aim of this paper is to describe all the possible clinical, histological, and immunological variants of DH in order to facilitate the diagnosis of a rare disease and, therefore, little known.
Dermatitis herpetiformis – analiza kliniczna 63 chorych
Jolanta Rujner,Aleksandra Bielejec
Polish Gastroenterology , 1998,
Abstract: U 63 chorych na dermatitis herpetiformis (dh), w tym 25 p ci eńskiej w wieku 5,49-18 lat (–x=14,18 roku) i 38 p ci m skiej w wieku 4,25-36,09 roku (–x=15,09 roku), oceniono wiek wyst pienia zmian skórnych, morfologi bioptatu jelita cienkiego, obecno IgAEmA oraz wspó wyst powanie innych chorób w porównaniu z ich cz sto ci u 500 chorych na celiaki bez skórnej manifestacji.
Celiakia latentna u 18-letniej dziewczyny z dermatitis herpetiformis
Jolanta Rujner,Hanna Gregorek,Maria Zegad?o-Mylik,Bogdan Wo?niewicz
Polish Gastroenterology , 1998,
Abstract: Przedstawiamy 18-letni chor na dermatitis herpetiformis, u której do ponownego zaniku kosmków jelita cienkiego dosz o dopiero po 4,5-letniej prowokacji glutenem.
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