Vancomycin-induced Linear IgA Bullous Dermatosis Research Articles

Vancomycin-induced linear IgA bullous dermatosis in a patient with cancer.

Vancomycin-induced linear IgA bullous dermatosis in a patient with cancer.

Vancomycin-induced linear IgA bullous dermatosis

Vancomycin-induced linear IgA bullous dermatosis

Severe Vancomycin-Induced Linear IgA Bullous Dermatosis Case Report

Linear IgA bullous dermatosis is a rare autoimmune blistering disease. Although multiple reports have documented drug exposure as a precipitating factor, formal studies validating the existence of drug-induced LABD are lacking. A 49-year-old man with history of intravenous drug use presented with left hip pain of 3 weeks duration after sustaining a fall. On presentation he was hemodynamically stable and physical examination was notable proximal left thigh tenderness with stiffness and limited range of movement. Laboratory diagnostics were remarkable for elevated inflammatory markers, with no evidence of leukocytosis. CT scan without contrast of the left lower extremity demonstrated severe left hip osteoarthritis without fracture or dislocation. The patient continued to experience severe pain, prompting incision and drainage of the left hip along with acetabuloplasty, removal of the femoral head, and stage I hip replacement with placement of prophylactic prosthetic cement spacer with vancomycin and tobramycin. Within 24 h of surgery, he developed multiple distinct maculopapular/bullous lesions of his torso and medial thigh that rapidly progressed. Punch biopsy was performed and due to involvement of ~ 20% body surface area, he was transferred to a tertiary center. H&E and immunostaining of the histological sample demonstrated linear IgA bullous disease mimicking Stevens-Johnson syndrome. The patient’s bullous lesions improved 2 weeks after discontinuation of vancomycin and initiation of therapy. This case demonstrates the importance of early recognition of the rare adverse effects of commonly used medications. Vancomycin is currently used more frequently given the recent rise in the prevalence of methicillin-resistant Staphylococcus aureus infection. Further studies are needed to understand the pathophysiology, genetic predisposition, and disease penetrance.

Transient and zosteriform vancomycin-induced linear IgA bullous dermatosis in a patient undergoing haemodialysis: drug-mediated IgA immunoreactivity against type VII collagen.

Transient and zosteriform vancomycin-induced linear IgA bullous dermatosis in a patient undergoing haemodialysis: drug-mediated IgA immunoreactivity against type VII collagen.

Unilateral vancomycin-induced linear IgA bullous dermatosis

Unilateral vancomycin-induced linear IgA bullous dermatosis

Linear IgA bullous dermatosis: A rare manifestation of vancomycin hypersensitivity

Vancomycin is one of the most widely used antibiotics and, because of its prevalent use, several common side effects have been well described, such as “red man” syndrome, agranulocytosis, and ototoxicity. In addition, it has been associated with hypersensitivity reactions including immunoglobulin E–mediated anaphylaxis, linear immunoglobulin A (IgA) bullous dermatosis (LABD), drug reaction with eosinophilia and systemic symptoms syndrome, acute interstitial nephritis, and Stevens-Johnson syndrome and toxic epidermal necrolysis. [1] Armstrong A.W. Fazeli A. Yeh S.W. et al. Vancomycin-induced linear IgA disease manifesting as bullous erythema multiforme. J Cutan Pathol. 2004; 31: 393-397 Crossref PubMed Scopus (39) Google Scholar Although a few case reports have documented vancomycin as the most frequent inciting factor for LABD, 1 Armstrong A.W. Fazeli A. Yeh S.W. et al. Vancomycin-induced linear IgA disease manifesting as bullous erythema multiforme. J Cutan Pathol. 2004; 31: 393-397 Crossref PubMed Scopus (39) Google Scholar , 2 Jones D.H. Todd M. Craig T.J. Early diagnosis is key in vancomycin-induced linear iga bullous dermatosis and Stevens-Johnson syndrome. J Am Osteopath Assoc. 2004; 104: 157-163 PubMed Google Scholar , 3 Minhas J.S. Wickner P.G. Long A.A. et al. Immune-mediated reactions to vancomycin: a systematic case review and analysis. Ann Allergy Asthma Immunol. 2016; 116: 544-553 Abstract Full Text Full Text PDF PubMed Scopus (55) Google Scholar , 4 Palmer R.A. Ogg G. Allen J. et al. Vancomycin-induced linear iga disease with autoantibodies to bp180 and lad285. Br J Dermatol. 2001; 145: 816-820 Crossref PubMed Scopus (64) Google Scholar formal studies validating the causal relation and eliminating reporting bias are lacking because it remains a relatively uncommon phenomenon.

053 Autoantibodies in vancomycin-induced linear IgA bullous dermatosis target type VII collagen in the presence of vancomycin

053 Autoantibodies in vancomycin-induced linear IgA bullous dermatosis target type VII collagen in the presence of vancomycin

A toxic epidermal necrolysis-like presentation of linear IgA bullous dermatosis treated with dapsone

Linear IgA bullous dermatosis is a rare autoimmune vesiculobullous disease characterized by linear deposition of IgA along the basement membrane zone. It is classically idiopathic, but may also arise secondary to drug exposure. A heterogeneous spectrum of clinical features has been described, including a rare, morbid variant mimicking toxic epidermal necrolysis. Herein, we present a case of vancomycin-induced linear IgA bullous dermatosis that manifested clinically as toxic epidermal necrolysis and resolved with dapsone therapy.

The isomorphic response in vancomycin-induced linear IgA bullous dermatosis

The isomorphic response in vancomycin-induced linear IgA bullous dermatosis

Vancomycin-induced linear IgA bullous dermatosis

Vancomycin-induced linear IgA bullous dermatosis

Vancomycin-induced linear IgA bullous dermatosis: associations

Linear IgA bullous dermatosis (LABD) is a rare autoimmune blistering disease. LABD is consideredmostly idiopathic, butsome cases have been reported to be drug-induced, mainly associated with vancomycin (VCM).We present two cases of LABD possibly associated with VCM used for cardiac surgery prophylaxis; inthe presented cases, the eruptions occurred only after VCM withdrawal, therefore leaving a questionabout the relationship between VCM and LABD in these cases.We reviewed previous reports of VCM-induced LABD and analyzed the following parameters: gender,age, recent medical history, concurrent medication, latency period, progression after withdrawal,time to resolution, treatment, and rechallenge. The causal relationship between VCM and LABD was often unclear; patients frequently hadconcurrent medication and symptoms frequently began and/or progressed after VCM withdrawal. Amongthe 46 reviewed patients in addition to our two cases (n=48), 20 (42%) had recent history ofcardiac procedure, cardiac infection, congestive heart failure, or aortic aneurism. Further investigation is needed to ascertain the association between LABD, VCM, andheart disease.

Vancomycin-induced linear IgA bullous dermatosis with isomorphic phenomenon

Vancomycin-induced linear IgA bullous dermatosis with isomorphic phenomenon

Vancomycin-induced linear IgA bullous dermatosis with isomorphic response

Linear IgA bullous dermatosis (LABD) is occasionally induced by certain drugs, of which vancomycin is the most common. We herein describe a case of vancomycin-induced LABD on the trunk and extremities. Our case was unique in which tense bulla was induced on the old operation scars. A 92-year-old man developed diffuse erythema and bullas on his trunk and extremities. Also, blister formation was observed on the operation scar on the abdomen. A biopsy specimen showed subepidermal split with neutrophilic and lymphocytic infiltration in the upper dermis. Direct immunofluorescence showed a linear IgA deposition at the basement membrane zone. His skin conditions were improved by stoppage of vancomycin and topical corticosteroids. We should know about the occurrence of LABD in patients under vancomycin treatment.

Linear IgA bullous dermatosis herpeticum: Disseminated herpes simplex virus infection within the lesions of vancomycin-induced linear IgA bullous dermatosis

Linear IgA bullous dermatosis herpeticum: Disseminated herpes simplex virus infection within the lesions of vancomycin-induced linear IgA bullous dermatosis

Possible Dual Immunoreactivity for Laminin-332 and Type VII Collagen in a Case with Vancomycin-Induced Linear Iga Bullous Dermatosis Manifesting as Erythroderma

We report a unique case of vancomycin-induced linear IgA bullous dermatosis (LABD) presenting as erythroderma. Direct immunofluorescence showed a linear IgA deposition at the dermal side of the basement membrane zone (BMZ), and double immunostaining using patients’ skin as a substrate revealed that the in vivo IgA signal co-localized with laminin-332 and type VII collagen. Our case is the first documentation of vancomycin-induced LABD, in which the pathogenic IgA deposit would concomitantly recognize the two distinct antigens at the dermal BMZ.

Mechanical forces exacerbate vancomycin-induced linear IgA bullous dermatosis

Mechanical forces exacerbate vancomycin-induced linear IgA bullous dermatosis

Vancomycin-induced linear IgA bullous dermatosis mimicking toxic epidermal necrolysis

Vancomycin-induced linear IgA bullous dermatosis mimicking toxic epidermal necrolysis

Localized Palmar Vancomycin-Induced Linear IgA Bullous Dermatosis Occurring at Supratherapeutic Levels

Localized Palmar Vancomycin-Induced Linear IgA Bullous Dermatosis Occurring at Supratherapeutic Levels

A Morbilliform Variant of Vancomycin-Induced Linear IgA Bullous Dermatosis

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 drug-related versions of this disorder have been described, with the latter most commonly associated with vancomycin. We describe 2 patients with vancomycin-associated 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. 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.

A Young Man with Pyomyositis and Bullous Disease

Diagnosis: linear IgA bullous dermatosis (LABD). Direct immunofluorescence staining of the skin biopsy specimen obtained from the left thigh, the predominant site of the outbreak of multiple small bullae (figures 1 and 2), revealed the presence of linear IgA deposits along the basement membrane (figure 3) consistent with the diagnosis of LABD related to vancomycin therapy. LABD is an autoimmune subepidermal vesiculobullous disease characterized by IgA deposition in a linear pattern along the basement membrane zone [1]. The disease is mediated by autoantibodies directed against several components of the basement membrane zone [2, 3]. Among antimicrobial drugs, vancomycin is the agent that is most frequently involved in cases of drug-induced LABD. Vancomycin-induced LABD is not dose dependent and has heterogenous presentation, ranging from benign erythema multiforme to toxic epidermal necrolysis [4–6]. The lesions appear 1–15 days after initiation of vancomycin therapy. Spontaneous and complete healing occurs after withdrawal of vancomycin therapy. However, new lesions could still appear up to 2 days after withdrawal of treatment with the drug. The use of steroids and dapsone do not seem to improve the outcome [4]. Rechallenge reproduces the disease with more-rapid and moresevere onset; however, successful rechallenge has been reported [7]. In our patient, vancomycin therapy was switched to daptomycin therapy, and the patient’s bullous rash resolved several days later.