Drug-induced linear IgA bullous dermatosis: Report of six cases and review of the literature

Kuechle, Melanie K.; Stegemeir, Eva; Maynard, Bruno; Gibson, Lawrence E.; Leiferman, Kristin M.; Peters, Margot S.

doi:10.1016/s0190-9622(94)70015-x

Cited by 178 publications

(119 citation statements)

References 22 publications

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“…4,7,8 However, the lesions may continue evolving for several weeks due to persistent autoimmunity that might take months to subside. 1,10 Our patient healed progressively within 2 weeks after stopping TMP-SMX.…”

Section: Figurementioning

confidence: 77%

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Childhood linear IgA bullous disease induced by trimethoprim-sulfamethoxazole

Nantel-Battista¹,

Dhaybi²,

Hatami³

et al. 2010

J Dermatol Case Rep

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Background: Linear IgA bullous disease (LABD) is a rare mucocutaneous autoimmune subepidermal blistering disease that can affect children mostly of pre-school age. As many as two-thirds of LABD are related to drug ingestion, particularly certain antibiotics, non-steroidal anti-inflammatory drugs and diuretics.Main observation: We describe a 3-year-old boy who presented a CMV infection followed by LABD induced by trimtheporim-sulfametoxazole. To our knowledge, this is the first reported case of trimethoprim-sulfamethoxazole that was confirmed by a rechallenge.Conclusions: Most cases of drug-induced LABD are patients being treated with multiple systemic drugs that could induce the LABD. In the lack of suitable alternative treatment, the identification of the causative drug can be achieved by a rechallenge under close medical surveillance.

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Section: Figurementioning

confidence: 77%

“…medical literature. 3,10,11 The only pediatric possible TMP-SMX-induced LABD was a 5-year-old child presenting acute lymphoblastic leukemia (ALL) in remission who received prophylactic treatment with TMP-SMX. 3 Our patient is the first case of LABD induced by TMP-SMX that was confirmed by a rechallenge.…”

Section: Figurementioning

confidence: 99%

Childhood linear IgA bullous disease induced by trimethoprim-sulfamethoxazole

Nantel-Battista¹,

Dhaybi²,

Hatami³

et al. 2010

J Dermatol Case Rep

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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: 78%

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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“…Examples of granular linear deposition at the BMZ have also been identified. [Kuechle, et al, 1994] In addition, C3 deposition at the BMZ is also found on occasion. [Kuechle, et al, 1994] …”

Section: Histologymentioning

confidence: 96%