Drug-induced Linear IgA Bullous Dermatosis Research Articles

Adult-onset linear IgA bullous dermatosis: a retrospective single-center cohort study of 81 patients and literature review.

Linear IgA bullous dermatosis (LABD) is a rare autoimmune blistering disorder that may be drug-induced or paraneoplastic. We aim to characterize features of LABD and determine differentiating factors among idiopathic, drug-induced, or malignancy-associated diseases. We conducted a single-center retrospective chart review of adult patients with linear IgA bullous dermatosis at a large tertiary referral center and a literature review of adult linear IgA bullous dermatosis. Eighty-one patients were included in the study. Ten patients (12.3%) had comorbid malignancy and nine (11.1%) had inflammatory bowel disease. Median disease duration was significantly shorter in both drug-induced (1.2 vs. 48.8 months; P < 0.001) and malignancy-associated (1.7 vs. 48.8 months; P < 0.001) LABD compared with idiopathic LABD. Recurrent episodes occurred significantly more often in idiopathic LABD compared to those with drug-induced (76.1 vs. 11.5%; P < 0.001) or malignancy-associated disease (76.1 vs. 33.3%; P = 0.019). Time to diagnosis was significantly shorter in the drug-induced (0.2 vs. 5.4 months; P < 0.001) and malignancy-associated groups (0.7 vs. 5.4 months; P = 0.049) compared with idiopathic; similarly, time to improvement was significantly shorter in both drug-induced (0.4 vs. 3.0 months; P < 0.001) and malignancy-associated disease (1.1 vs. 3.0 months; P = 0.016). Clinical morphology was indistinguishable between groups. Limitations included retrospective data collection, data from tertiary referral centers, and limited racial and ethnic diversity. Screening for underlying malignancy, as well as for a predisposing medication or possibly inflammatory bowel disease, may be advisable in patients with LABD, particularly when it is newly diagnosed.

Parasetamol ve Klorfeniramin Kombinasyonuna Bağlı Lineer Ig A Büllöz Dermatozu

Linear IgA bullous dermatosis (LABD) is an autoimmune, subepidermal vesiculobullous dermatosis. The etiology is unknown in most patients. Most recent case reports report drug-induced LABD cases. A 35 year-old male patient presented to our clinic with the complaint of tense bullous lesions located on trunk and extremities which started to occur after using a combinated drug including paracetamol and clorpheniramine. The lesions on the patient had responsed quickly to systemic and topical corticosteroid treatment, no new lesion had existed since fifth day of treatment and older lesions had begun to be epithelized. Clinical findings and histopathologic and direct immunoflourescent examination findings are important for differentiation between LABD and other bullous dermatoses. The clinical course is lighter than the idiopathic form in drug-induced LABD. Drug-induced LABD is rarely observed compared to idiopathic form. Many drugs can cause this condition. The reported drug lists and variety continue to increase. Dermatologists should be aware of the rare adverse effects that may occur as a result of drug use.

Treatment for syphilis unraveling gluten-sensitive linear IgA dermatosis

Linear IgA bullous dermatosis (LAD) is an acquired autoimmune blistering disorder which can develop following various drugs but not after banzathine penicillin injection. LAD has lower prevalence of associated gluten-sensitive enteropathy (GSE). We describe the case of a 20-year-old male with homosexual behavior who presented with multiple pruritic maculopapular lesions over the trunk, extremities, and palms for 2 months. Rapid plasma reagin (1:1280 titer) and treponema pallidum hemeagglutination tests were positive. A diagnosis of syphilis was made. The patient developed vesicular lesions following benzathine penicillin injection with histopathological and immunofluorescent features characteristic of LAD. Despite treatment, the patient continued developing new vesicles. Gluten-free diet (GFD) was advised, and the patient was further investigated for GSE. The patient responded well to GFD. We conclude that the prevalence of drug-induced LAD and associated GSE is quite low, but possibility exists. Hence, a diagnosis of GSE must be sought as patients might respond to GFD.

Severe Drug-Induced Linear IgA Bullous Dermatosis: Not Everything is Steven Johnsons Syndrome

Severe Drug-Induced Linear IgA Bullous Dermatosis: Not Everything is Steven Johnsons Syndrome

Flame figures in linear IgA bullous dermatosis: a novel histopathologic finding

Linear IgA bullous dermatosis (LABD) is an autoimmune subepidermal blistering disease usually with a neutrophil rich inflammatory infiltrate, and characterized by linear IgA deposition at the basement membrane zone (BMZ), and neutrophil predominant dermal inflammation. We report a case of LABD with numerous eosinophils and flame figure formation, a unique histopathologic finding not previously reported. A 69-year-old woman presented with a rapidly progressive, intensely pruritic rash over forearms, breasts, axillae, hips, and thighs. Thelesions were comprised of annular vesicles and bullae with hemorrhagic crusts and erosions. The clinical differential diagnosis included bullous pemphigoid(BP), LABD, and epidermolysis bullosa aquisita (EBA). A biopsy from a bullous plaque on the wrist revealed a subepidermal blister with neutrophils and numerous eosinophils with flame figure formation.Direct immunofluorescent (DIF) microscopy revealed linear deposition of IgA at the BMZ. Although unusual, the combined findings supported a diagnosis of LABD. Increased eosinophils may be associated with drug-induced LABD and may explain the numerous eosinophils in our case. It is important to be aware of this finding as the pathology may easily be misdiagnosed as BP, or possibly bullousWells syndrome. This case emphasizes that combined clinical, pathologic, and DIF findings are essential in the diagnosis of bullous dermatoses.

Linear IgA bullous dermatosis: comparison between the drug-induced and spontaneous forms

Linear IgA bullous dermatosis (LABD) is a rare autoimmune blistering skin disorder characterized by linear deposits of IgA along the dermoepidermal junction, visualized by direct immunofluorescence (DIF). It is usually spontaneous and drug induced. To compare the clinical and histological forms of LABD. This retrospective single-centre cohort study concerned 28 patients diagnosed with LABD between 1 January 1995 and 31 December 2010. Imputability, determined according to the French imputability method (modified Bégaud score) and Naranjo score, enabled classification into drug-induced and spontaneous LABD groups. Clinical and histological features were compared by blinded analysis of images and histological patterns. Sixteen patients had spontaneous LABD and 12 had drug-induced LABD. Nikolsky sign and large erosions were significantly more frequent in drug-induced than spontaneous LABD (P = 0.003 and P = 0.03, respectively), with no between-group differences for erythematous plaques, target or target-like lesions, string of pearls, location, mucosal involvement or histological features. Drug-induced LABD was more severe than the spontaneous form, with lesions mimicking toxic epidermal necrolysis. Because LABD may be polymorphic and sometimes life threatening, DIF assay is recommended for all patients with Nikolsky sign and large erosions.

Is “Drug-Induced” Linear IgA Bullous Dermatosis a Separate Entity?

In the 1970s, linear IgA bullous dermatosis (LABD) was first described and differentiated from bullous pemphigoid and dermatitis herpetiformis, which have some overlapping features. In the 1980s, the drug vancomycin was pointed to as a causative agent. Most vancomycin recipients also take many other agents, which calls into question its role in LABD. Fortuna and colleagues reviewed the English-language literature on drug-induced LABD published …

Drug-induced linear IgA bullous dermatosis demonstrating the isomorphic phenomenon

Drug-induced linear IgA bullous dermatosis demonstrating the isomorphic phenomenon

The Role of the Isomorphic Phenomenon in Distinguishing Drug-Induced Linear IgA Bullous Dermatosis

The Role of the Isomorphic Phenomenon in Distinguishing Drug-Induced Linear IgA Bullous Dermatosis

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.

Drug-induced linear IgA bullous dermatosis

A 73-year-old man was admitted to the University of California Davis Medical Center for treatment of a pleural effusion and congestive heart failure. His hospital course was complicated by asymptomatic sustained ventricular tachycardia requiring placement of an implantable cardiac defibrillator. The patient was treated with vancomycin and cefazolin during the procedure. After 3 days he developed tense vesicles over the dorsal aspect of the hands. Perilesional skin biopsy showed subepidermal cleavage with a neutrophilic infiltrate. Direct immunofluorescence revealed granular IgA and C3 deposition along the dermal epidermal junction. A diagnosis of drug-induced linear IgA bullous dermatosis secondary to vancomycin was established. Linear IgA bullous dermatosis is a rare autoimmune blistering disorder with clinical features that can overlap with bullous pemphigoid and dermatitis herpetiformis. Drug-induced linear IgA bullous dermatosis is a less common variant that is correspondingly less well characterized. Although a variety of medications have been implicated, vancomycin is the most common associated drug.

Drug-Induced Linear IgA Bullous Dermatosis

We report the case of a 69-year-old Japanese woman with multiple blistering lesions covering almost her whole body. Linear IgA and C3 depositions were seen at the basement membrane zone on direct immunofluorescence (IF). Linear IgA bullous dermatosis (LABD) is one of the autoimmune diseases resulting in subepidermal blisters. It is clinically similar to bullous pemphigoid and IF is required to distinguish the two diseases. In this case, the blistering lesions appeared after vancomycin treatment. This drug was strongly suspected as a cause of LABD in light of the clinical course of the patient even though a drug-lymphocyte stimulating test was negative. Among the various implicated causative drugs, vancomycin is the most commonly associated with LABD.

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

Linear IgA bullous dermatosis (LABD) is a rare autoimmune vesiculobullous disorder characterized by variable clinical presentations that may mimic bullous pemphigoid, dermatitis herpetiformis, cicatricial pemphigoid and erythema multiforme. A few cases of drug-induced LABD that clinically resembled toxic epidermal necrolysis (TEN) have been reported. A subset of patients with LABD have been found to be drug-induced; the most common drug being vancomycin. The diagnosis of LABD is confirmed by the presence of a linear band of IgA along the basement membrane zone on direct immunofluorescence microscopy. We report a case of a 77-year-old man who presented to us with vancomycin-induced LABD that presented clinically as TEN. He had a complete recovery over a 3-week period following discontinuation of the vancomycin and the addition of oral dapsone therapy. It is important to be aware that drug-induced LABD can mimic TEN.

A successful challenge in a patient with vancomycin-induced linear IgA dermatosis

Linear IgA bullous dermatosis (LABD), a subepidermal, blistering skin disease, is generally believed to be idiopathic. It has been reported in association with multiple medications, including vancomycin. In each case, complete clearance of the skin lesions occurred with discontinued use of the drug. A subsequent rechallenge reproduced the eruption within hours to days. To present a patient with vancomycin-associated LABD who underwent a successful challenge with the antibiotic 4 years after the initial reaction. The patient developed blistering lesions over her trunk and extremities 10 days after the initiation of vancomycin for sepsis. A biopsy specimen of a skin eruption was consistent with linear IgA dermatosis. Following discontinued use of the drug, her skin lesions resolved. Four years later, she required vancomycin for osteomyelitis. The patient underwent a vancomycin-graded challenge of 5 doses over 5 days. On day 1, she received 10 mg, and this was increased in a semilog fashion to 1,000 mg on day 5. She had no recurrence of her skin lesions. This is the first case, to our knowledge, to show a successful rechallenge in a patient with drug-associated LABD. Since the patient did not have a reaction to the challenge, it is possible that the IgA antibodies responsible for drug-induced LABD are only present transiently and diminish over time.

Vancomycin-associated linear IgA bullous dermatosis mimicking toxic epidermal necrolysis

Vancomycin is the most frequent trigger of drug-induced linear IgA bullous dermatosis. We describe a fulminant case of linear IgA bullous dermatosis in a 74-year-old man who experienced skin sloughing of 90% of his body surface after receiving vancomycin. (J Am Acad Dermatol 2003;48:S56-7.)

Linear IgA bullous dermatosis in one of two piroxicam-induced eruptions: A distinct direct immunofluorescence trend revealed by the literature

Background: The report focuses first on two patients with piroxicam-induced bullous eruption, one whose disease was diagnosed as linear IgA bullous dermatosis (LABD) and the other with no disease-specific immunologic findings using immunofluorescence methods. A review of the literature points to a distinctive direct immunofluorescence feature of drug-induced LABD cases. Objective: Our purposes were to focus on divergent piroxicam reactions and to compare immunofluorescence findings in our and other reported drug-induced LABD cases to randomly occurring LABD cases. Methods: Direct and indirect immunofluorescence methods were used to study biopsy and serum samples from both cases and biopsy specimens of 40 other LABD cases. Results: Tense blisters developed in two patients medicated with piroxicam. Immunofluorescence studies demonstrated deposits of IgA at the basement membrane zone (BMZ) in case 1 and only non-disease-specific fibrin deposits at the BMZ in case 2. Within 1 month of discontinuation of piroxicam, all lesions were gone in both patients. Conclusion: In LABD cases proven by direct immunofluorescence, (1) the index of suspicion of drug induction should be higher in cases with only IgA and no IgG in the BMZ; (2) possibly up to two thirds of all LABD cases may be drug induced; and (3) the negative immunofluorescence findings in case 2 and other cases reported in the literature suggest that LABD is one of several host responses in drug-induced blistering diseases. (J Am Acad Dermatol 2001;45:691-6.)

Naproxen-Associated Linear IgA Bullous Dermatosis: Case Report and Review

Linear IgA bullous dermatosis (LABD) is an acquired autoimmune subepidermal blistering disorder in which linear deposits of IgA are found along the basement membrane. Idiopathic, systemic disorder-related, and drug-induced forms of LABD have been described. Drug-induced LABD occurs in association with drug administration and resolves when the offending agent is discontinued. Other forms of LABD assume a more chronic course. The nonsteroidal anti-inflammatory drugs piroxicam and diclofenac have been previously reported to induce LABD. To our knowledge, this article describes the first documented case of LABD associated with naproxen administration, which resolved after discontinuation of the drug.

Drug-induced linear IgA bullous dermatosis after vancomycin discontinuance in a patient with renal insufficiency

Linear IgA bullous dermatosis (LABD) is an autoimmune, subepidermal, vesiculobullous disease that has been commonly associated with the use of vancomycin hydrochloride. Lesions typically appear during vancomycin therapy, 24 hours to 15 days after the first dose. A 65-year-old white man with renal insufficiency developed pruritic, tense bullae on the right chest, right medial arm, right flank, abdomen, and right upper thigh 14 days after his last dose of vancomycin. Histopathologic examination and immunofluorescence studies were diagnostic of LABD. Vancomycin-related LABD may appear as long as 2 weeks after the drug is discontinued. (J Am Acad Dermatol 2000;42:316-23.)

Drug-induced linear IgA bullous dermatosis probably induced by furosemide

Linear IgA bullous dermatosis (LABD) is an autoimmune disease, characterized by linear deposition of IgA along the basement membrane zone. Drug-induced LABD is rare but increasing in frequency. A new case of drug-induced LABD associated with the administration of furosemide is described. (J Am Acad Dermatol 1999;41:103-5.)

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

Linear IgA bullous dermatosis (LABD) is an autoimmune subepidermal blistering disease that may be associated with drug exposure. Our purpose was to compare the clinical, pathologic, and immunofluorescence findings in drug-induced LABD with those in the idiopathic type. Six patients with an acute drug eruption were identified who had linear IgA deposition at the basement membrane zone (BMZ). Lesional tissue was examined by brightfield microscopy, and perilesional tissue was examined by direct immunofluorescence (DIF). The presence of circulating BMZ antibody was assayed by indirect immunofluorescence (IIF) on monkey esophagus (ME) and salt-split human skin (SS). Histopathologic examination showed subepidermal bullae with varying numbers of inflammatory cells. DIF showed linear IgA at the BMZ; three of the patients also had weak deposition of C3 at the BMZ. Serum from five patients was studied by IIF. One patient had circulating IgA BMZ antibodies in a titer of 1:80 on ME, localized to the dermal side on SS. All patients were free of lesions within 5 weeks after discontinuation of the drug. Drug-induced LABD is a self-limited eruption characterized by linear deposition of IgA without IgG at the BMZ. Most patients lack circulating antibodies. The distribution of lesions and the course of the disease differ from those of idiopathic LABD.