A Morbilliform Variant of Vancomycin-Induced Linear IgA Bullous Dermatosis

Abstract

Background: Linear IgA bullous dermatosis is an autoimmune blistering disease characterized clinically by the presence of small tense blisters and immunologically by the presence of IgA at the dermal-epidermal junction. Idiopathic, systemic disease-related, and drugrelated versions of this disorder have been described, with the latter most commonly associated with vancomycin. Observations:We describe 2 patients with vancomycinassociated linear IgA bullous dermatosis who presented with a morbilliform eruption that lacked blistering. Lesional and perilesional tissue from each patient was examined by light microscopy and direct immunofluorescence. Histopathologic examination findings revealed vacuolar interface dermatitis with a mixed inflammatory infiltrate and occasional eosinophils, consistent with a drug eruption. Direct immunofluorescence revealed IgA deposited in a linear pattern at the dermoepidermal junction. In both patients, the results of indirect immunofluorescence using both IgG and IgA were negative.Conclusions: These cases highlight the existence of a new form of linear IgA bullous dermatosis presenting as a morbilliform drug eruption. Both patients were following extensive medication regimens, including use of multiple antibiotics. The diagnosis of linear IgA bullous dermatosis allowed us to target vancomycin as the likely allergen and begin treatment. In light of these findings, direct immunofluorescence may be a useful diagnostic adjunct in determining the cause of drug eruptions.

Vancomycin‐induced linear IgA bullous dermatosis presenting as generalized fixed drug eruption

“…For example, Armstrong et al described a case of vancomycin‐induced LABD manifesting as bullous erythema multiforme. Billet et al reported a morbilliform variant of vancomycin‐induced LABD, while Delbaldo et al characterized the utility of linear IgA deposits in drug‐induced epidermolysis bullosa aquisita . Similar to previous reports, our case lacked the prototypical vesicles and bullae in annular configurations and instead presented as dusky, violaceous patches, and plaques.…”

A case of vancomycin-associated linear IgA bullous dermatosis and IgA antibodies to the α3 subunit of laminin-332

“…A previous review of 47 VILABD cases revealed that the male‐to‐female ratio was 1·6 : 1 and the age of onset ranged from 32 to 92 years (mean 68 years). It was also reported that the skin lesions appeared 1 to 21 days (mean 9·8 days) after VCM administration, and that the symptoms were alleviated within 60 days (mean 20·5 days) after VCM discontinuation . In the present case, circulating IgA antilaminin‐332 antibodies were detected 2 days after VCM administration.…”

“…In most VILABD cases, the diagnoses of VILABD were confirmed by the rapid disappearance of the skin lesions after the discontinuation of VCM. In fact, IgA deposits seen by direct immunofluorescence were not detected when tested soon after the discontinuation of VCM or after the disappearance of skin lesions . In the present case, both the immunofluorescence titre and reactivity with the α3 subunit of laminin‐332 became negative after the skin lesion disappeared.…”

“…In fact, IgA deposits seen by direct immunofluorescence were not detected when tested soon after the discontinuation of VCM or after the disappearance of skin lesions. 1,33,40 In the present case, both the immunofluorescence titre and reactivity with the a3 subunit of laminin-332 became negative after the skin lesion disappeared. In addition, no recurrence was observed thereafter.…”

Vancomycin Hypersensitivity Reaction Presenting with Extensive Oral Ulcerations

“…Most importantly, though, our patient lacked a cutaneous rash. To our knowledge a case of vancomycin-induced LABD without a cutaneous rash has never been reported [7][8][9][10] and it is extremely rare for patients with vancomycin-induced LABD to lack visible cutaneous bullae in addition to other morphologic cutaneous abnormalities [10]. Our patient's clinical and serologic findings, along with a prompt response to methylprednisolone and discontinuation of vancomycin are most consistent with a diagnosis of vancomycin hypersensitivity reaction-associated diffuse oral ulcerations.…”