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Updated: Aug 14, 2026

Recognition of Epidermal Transglutaminase by IgA and Tissue Transglutaminase 2 Antibodies in a Rare Case of Rhesus Dermatitis
Published on: December 15, 2011
[Vancomycin-induced linear IgA dermatosis]
Thomas Brinkmeier1, Bernd Angelkort, Peter J Frosch
1Hautklinik, Klinikum Dortmund gGmbH und Universität Witten/Herdecke. t.brinkmeier@derma.de
Abstract:
Linear IgA disease is a rare autoimmune bullous skin disorder that may be idiopathic or drug-induced. The mechanisms of loss of self-tolerance to target antigens of the dermo-epidermal junction are unclear and may be variable. Regardless of the etiology, the clinical presentation is quite heterogeneous. Frozen sections of a blister roof are helpful in early diagnosis to rule out full-thickness epidermal necrosis or subcorneal separation as seen in toxic epidermal necrosis or staphylococcal scaled skin syndrome, respectively. Drug-induced cases of linear IgA disease typically resolve quickly once the causative agent is withdrawn. Vancomycin is the best-documented insiting drug in the literature. The significance of further associations such as malignancy or different autoimmune diseases is uncertain. Review of medication exposures after diagnosis is crucial in identifying possible offending agents. We present a patient with vancomycin-induced linear IgA disease in whom the drug was immediately discontinued because of the characteristic clinical presentation and rapid histopathological examination. The development of new blisters stopped within 24 hours and the skin healed within 2 weeks.
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