Vancomycin-induced linear IgA bullous disease presenting as toxic epidermal necrolysis

Waldman, Mark A.; Black, Douglas; Callen, Jeffrey P.

doi:10.1111/j.1365-2230.2004.01649.x

Cited by 81 publications

(60 citation statements)

References 11 publications

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“…Including our case, 7 cases have been reported in the USA, 3 in France, 1 in the Slovak Republic, 1 in Germany, 1 in Ireland, 1 in Australia, 1 in Portugal, and 1 in Taiwan [2,11,12,13,14,15,16,17,18,19,20,21,22,23,24]. Patients in these reports ranged in age from 41 to 91 years, with an average age of 69.…”

Section: Discussionmentioning

confidence: 99%

Linear IgA Bullous Disease Presenting as Toxic Epidermal Necrolysis: A Case Report and Review of the Literature

Kakar

Paugh

Jaworsky³

2013

Dermatology

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A 91-year-old female presented with widespread skin sloughing and bullae clinically mimicking toxic epidermal necrolysis (TEN). The patient was on multiple antibiotics, including vancomycin and piperacillin/tazobactam. Histopathology and direct immunofluorescence were consistent with a diagnosis of linear IgA bullous disease (LABD). In a PubMed review of the literature from 1975 to the present, there have been 15 cases of LABD presenting as TEN clinically and with characteristic linear IgA deposits on direct immunofluorescence studies. Vancomycin and phenytoin were the most commonly implicated medications. Twelve patients saw a resolution or healing of skin lesions after discontinuation of the implicated medication. There were, however, 5 patients who died of complications related to their comorbidities. It is important to include LABD in the differential diagnosis when evaluating patients who clinically present with TEN.

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Section: Discussionmentioning

confidence: 99%

Linear IgA Bullous Disease Presenting as Toxic Epidermal Necrolysis: A Case Report and Review of the Literature

Kakar

Paugh

Jaworsky³

2013

Dermatology

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“…The histological features may be similar to other vesiculobullous diseases, but direct immunofluorescence microscopy commonly demonstrates a characteristic linear band of IgA along the basement membrane zone. Due to the heterogeneous clinical features, LABD must be differentiated from a number of diseases including pemphigus vulgaris, bullous pemphigoid, dermatitis herpetiformis, and erythema multiforme 7,9 . The etiology of LABD is yet to be fully elucidated, but some have reported the presence of a group of autoantigens that have been found to be targets in the idiopathic form of LABD.…”

Section: Discussionmentioning

confidence: 99%

“…Several drugs have been implicated as the cause of LABD, vancomycin being the most frequent [6][7][8][9][10][11][12] . LABD can occur anytime from 1 day to 1 month following the initial administration of vancomycin 10 .…”

Section: Discussionmentioning

confidence: 99%

Vancomycin-induced Linear IgA Bullous Dermatosis: A Case Report and Review of the Literature

2008

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Linear IgA bullous dermatosis (LABD) is a rare autoimmune bullous disease that can either occur without any apparent cause or be induced by the administration of certain drugs, the most common of which is vancomycin. We present a case of a 45-year-old woman who was diagnosed with vancomycin-induced LABD by the presence of a characteristic linear band of IgA along the basement membrane zone on direct immunofluorescence microscopy. Our patient showed complete recovery after a 2-week period during which vancomycin administration was discontinued. (Ann Dermatol (Seoul) 20(2) 102∼106, 2008)

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“…2A, eosinophils; arrowheads), as earlier described (26,27). When collagen gels containing IgA-coated beads or BSA-coated beads as control were incubated with granulocytes and stained with H&E to distinguish neutrophils from eosinophils, neither neutrophils nor eosinophils migrated toward BSA-coated beads.…”

Section: Iga Induces Both Neutrophil and Eosinophil Migrationmentioning

confidence: 99%

Blocking Fcα Receptor I on Granulocytes Prevents Tissue Damage Induced by IgA Autoantibodies

Steen

Bakema

Sesărman

et al. 2012

The Journal of Immunology

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IgA represents the most prominent Ab class at mucosal surfaces and the second most prevalent Ab in human blood after IgG. We recently demonstrated that cross-linking of the granulocyte IgA FcR (FcαRI) by IgA induces a chemotactic-driven positive-feedback migration loop, hereby amplifying recruitment of granulocytes to IgA deposits. Therefore, we postulated that aberrant IgA–Ag complexes, which can be found in tissues in IgA-mediated diseases, are responsible for tissue damage by inducing continuous granulocyte migration and activation. Using an IgA-dependent skin-blistering disease as a model system, we demonstrated colocalization of FcαRI-positive granulocyte infiltrates with IgA in cryosections of lesional skin of patients suffering from this disease. Furthermore, we showed granulocyte migration to IgA deposits injected in human skin explants and in murine skin of FcαRI transgenic mice in vivo. Importantly, ex vivo migration and tissue damage were inhibited by blocking FcαRI, indicating that these events are dependent on the interaction of IgA autoantibodies with FcαRI. Thus, interrupting the granulocyte migration loop by blocking FcαRI reduces tissue damage in diseases with aberrant IgA–immune complexes. As such, our results may lead to development of new therapies for IgA-mediated chronic inflammatory diseases, hereby decreasing severe morbidity and improving quality of life for these patients.

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Vancomycin-induced linear IgA bullous disease presenting as toxic epidermal necrolysis

Cited by 81 publications

References 11 publications

Linear IgA Bullous Disease Presenting as Toxic Epidermal Necrolysis: A Case Report and Review of the Literature

Linear IgA Bullous Disease Presenting as Toxic Epidermal Necrolysis: A Case Report and Review of the Literature

Vancomycin-induced Linear IgA Bullous Dermatosis: A Case Report and Review of the Literature

Blocking Fcα Receptor I on Granulocytes Prevents Tissue Damage Induced by IgA Autoantibodies

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