Drug‐induced linear IgA disease with antibodies to collagen VII

Wakelin, S. H.; Allen, J.; Zhou, Shuang; Wojnarowska, Fenella

doi:10.1046/j.1365-2133.1998.02081.x

Cited by 62 publications

(47 citation statements)

References 35 publications

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“…In most of the cases reported previously, patients were also treated with multiple drugs at the time point when bullous lesions erupted. The identification of the causative drug was usually based just on temporal relationship and was only rarely confirmed by rechallenge [1, 2]. Our results indicate that both skin testing and LTT may be helpful in identifying the causative drugs, especially since rechallenge is not advisable due to the risk of eliciting a widespread exanthem in these patients.…”

Section: Discussionmentioning

confidence: 84%

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Drug-Induced Linear IgA Bullous Dermatosis Associated with Ceftriaxone- and Metronidazole-Specific T Cells

et al. 1999

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Background: Previous reports indicate that various drugs may induce linear IgA bullous dermatosis (LABD). The role of T cells and T-cell-derived cytokines in the pathomechanism of such skin lesions, however, has remained unclear. Objective: To describe a case of LABD induced by ceftriaxone and metronidazole in an 80-year-old female suffering from cholelithiasis with concomitant cholecystitis and provide evidence that drug-specific T cells and their cytokines may contribute to the development of LABD lesions. Methods: We performed flow cytometry analysis of peripheral blood T cells during LABD, epicutaneous testing (scratch-patch) and lymphocyte proliferation analysis (LTT) with the suspected drugs, routine histological and immunohistochemical examination of the acute skin lesions during LABD as well as of the positive epicutaneous test reactions and measurement of cytokines (IL-4, IL-5, IL-10, TNF-á, IFN-ã) in the supernatant of the LTT cultures. Results: An increased number mainly of activated CD8+ cells was detected in the peripheral blood during LABD. T cell sensitization to ceftriaxone and metronidazole was confirmed by epicutaneous testing and LTT, indicating that these methods may be useful in identifying the causative drugs. Enhanced cytokine levels, particularly of IL-5, were found in the supernatant of the LTT stimulated with ceftriaxone and metronidazole. Furthermore, in situ expression of IL-5 was confirmed in the patient’s skin lesions by immunohistochemistry. Conclusion: Our findings suggest that in addition to IgA antibodies drug-specific T cells and their subsequent release of cytokines may play an important role in the pathogenesis of drug-induced LABD.

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Section: Discussionmentioning

confidence: 84%

“…Although usually idiopathic, previous reports have suggested a rare association with the administration of various drugs [1, 2]. However, the pathogenesis of drug-induced LABD has remained unclear and, in particular, no data on involvement of drug-specific T cells are available so far.…”

Section: Introductionmentioning

confidence: 95%

Drug-Induced Linear IgA Bullous Dermatosis Associated with Ceftriaxone- and Metronidazole-Specific T Cells

et al. 1999

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“…In the case of druginduced LABD, there are far fewer cases that have been reported, and thus it has been harder to characterize the target antigen involved. Two studies have found antibodies to the 230kD antigen, the 97kD antigen, and type-VII collagen in nonvancomycin drug-induced LABD 14,15 , and one study reported two patients with vancomycin-induced LABD with autoantibodies against BP180 and LAD 285 10 . The severity of the reaction does not appear to correlate with serum vancomycin levels.…”

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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“…Vancomycin is the most common drug responsible for linear IgA-bullous disease [9]. Other, more severe, drug allergic reactions to vancomycin include Stevens-Johnson syndrome and toxic epidermal necrolysis [10].…”

Section: Vancomycinmentioning

confidence: 99%

Evaluation and management of pediatric drug allergic reactions

Buchmiller¹,

Khan

2007

Curr Allergy Asthma Rep

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Drug allergy is a common reason for consulting an allergist. Determining whether a particular drug is involved can be accomplished with a careful history and physical examination, knowledge of the common and idiosyncratic reactions of the drugs in question, and selective skin testing. If a drug reaction is suspected, alternatives exist to allow continued appropriate treatment. A practical approach to the pediatric patient is outlined along with a general discussion of common drug allergic reactions encountered in clinical practice.

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Drug‐induced linear IgA disease with antibodies to collagen VII

Cited by 62 publications

References 35 publications

Drug-Induced Linear IgA Bullous Dermatosis Associated with Ceftriaxone- and Metronidazole-Specific T Cells

Drug-Induced Linear IgA Bullous Dermatosis Associated with Ceftriaxone- and Metronidazole-Specific T Cells

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

Evaluation and management of pediatric drug allergic reactions

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