PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 14714018

[Dermatitis herpetiformis].

Petter Jensen Gjersvik·Jørgen R Rønnevig
View original source ↗Export metadata ↓

Abstract

Dermatitis herpetiformis is characterised by an intensely itchy, chronic, papulovesicular eruption, usually on elbows, knees and buttocks. The diagnosis is based on granular IgA deposits in the dermal papillae in a perilesional skin biopsy analysed by immunofluorescence microscopy. Most patients have subclinical celiac disease; a gluten-free diet is effective in most cases. IgA antibodies against tissue transglutaminase (TG2) may be involved in the pathogenesis of celiac disease with or without dermatitis herpetiformis, and an epidermal transglutaminase (TG3) may be the autoantigen in dermatitis herpetiformis. This article provides a short review intended for the general practitioner of the pathogenesis, diagnosis and treatment of dermatitis herpetiformis.

Explore related subjects

Celiac DiseaseDermatitis HerpetiformisGlutensHumansImmunoglobulin AEnglish AbstractJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Petter Jensen Gjersvik, Jørgen R Rønnevig. 2003-11-20. [Dermatitis herpetiformis].. https://pubmed.ncbi.nlm.nih.gov/14714018/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Involvement of macrophage migration inhibitory factor gene in celiac disease susceptibility.

The MIF gene has been associated with several diseases with inflammatory and autoimmune background, such as ulcerative colitis, rheumatoid arthritis and systemic lupus erythematosus. We aimed at testing the influence of two functional MIF promoter variants in celiac disease (CD) susceptibility. A (CAAT)(5-8) tetranucleotide repeat at position -794 and a single-nucleotide polymorphism at -173G/C were analyzed in the Spanish population (531 patients and 887 healthy controls). chi(2) statistics or Fisher exact test were used for comparisons. The -173C allele significantly increased risk ((CC+GC) vs GG: odds ratio (OR) (95% confidence interval (CI))=1.41 (1.10-1.81); P=0.005), as did carriage of the (CAAT)(7) allele (OR (95% CI)=1.36 (1.02-1.82); P=0.03) and of the haplotype (CAAT)(7)//-173C (OR (95% CI)=1.33 (1.00-1.76); P=0.04). Our data evidence for first time the role of the MIF gene increasing predisposition to CD. A common effect of MIF variants seems to underlie the etiology of these complex conditions.

Celiac Disease↗
PubMed2007

Association of KIR2DL5B gene with celiac disease supports the susceptibility locus on 19q13.4.

Genome-wide scans have detected linkage to celiac disease (CD) in several genomic locations, including 19q13.4. Killer immunoglobulin-like receptor (KIR) genes map to the region and encode receptors of natural killer (NK) cells and certain T cells that modulate cytolitic activity through interactions with HLA class I ligands, participating in the innate immune response. We performed KIR genotyping in a group of 70 CD patients of Basque origin and compared gene content, genotype and haplotype frequencies to ethnically matched blood-donors. The frequency of gene combination KIR2DL5B(+)/KIR2DL5A(-) was significantly higher in the disease group, and this result was confirmed in a second group of 343 CD patients and 160 controls of Spanish origin, suggesting an implication of this 'unexpressed' gene with increased susceptibility to CD (combined OR of 3.63 (95% CI: 1.76-7.51; P=0.0004)), possibly due to the lack of an efficient inhibitory signal. Our results support the role of the KIR gene cluster in celiac disease and replicate the CD-susceptibility locus at 19q13.4.

Celiac Disease↗