scholarly journals A Case of Drug-Induced Bullous Pemphigoid With an Isomorphic Response and Updated Review of Koebnerization in Bullous Diseases

Cureus ◽  
2021 ◽  
Author(s):  
Austin B Ambur ◽  
Rajiv Nathoo ◽  
Sadia Saeed
Keyword(s):  
Bullous Pemphigoid ◽  
Drug Induced ◽  
Bullous Diseases

scholarly journals Hydrochlorothiazide vs Venlafaxine: Drug-induced Bullous Pemphigoid

Cureus ◽  
2019 ◽  
Author(s):  
Srikanth Naramala ◽  
Hussain Dalal ◽  
Sreedhar Adapa ◽  
Pallav Patel ◽  
Venu Madhav Konala
Keyword(s):  
Bullous Pemphigoid ◽  
Drug Induced

scholarly journals Drug-induced bullous pemphigoid – a case report with review

2018 ◽  
Vol 30 (4) ◽  
pp. 427 ◽  
Author(s):  
Kamala Rawson ◽  
Sankar Vinod ◽  
B Sreenivasan ◽  
Gigi Roy
Keyword(s):  
Case Report ◽  
Bullous Pemphigoid ◽  
Drug Induced

Mustard-gas skin lesion and bullous pemphigoid antigen

1994 ◽  
Vol 52 ◽  
pp. 254-255
Author(s):  
John P. Petrali ◽  
Susan B. Oglesby ◽  
Tracey A. Hamilton
Keyword(s):  
Bullous Pemphigoid ◽  
Sulfur Mustard ◽  
Repair Process ◽  
Chemical Warfare Agent ◽  
Mustard Gas ◽  
Basal Cells ◽  
Immunochemical Study ◽  
Bullous Pemphigoid Antigen ◽  
Type Iv ◽  
Bullous Diseases

Human dermal exposure to the chemical warfare agent, sulfur mustard gas (HD), results in the delayed formation of fluid filled bullae which are incapacitating, persistent and slow to heal. In animal investigations, the pathology is typically described as that occurring during a prevesication period and that of a vesication period. During the first 24 hours, the pathology involves the latent lethal targeting of epidermal basal cells, a disabling of hemidesmosomes (prevesication) and a progressive inflammatory edema of the lamina lucida all contributing to the formation of characteristic lucidolytic microvesicles persisting at the dermal epidermal junction (vesication). We are now investigating possible primary or secondary HD-induced effects on extracellular adherent structural proteins of the basement membrane microenvironment which may contribute to vesication or may influence the repair process. Proteins selected for immunochemical study were laminin, type IV collagen, bullous pemphigoid antigen (BPA), fibronectin and desmosomal protein.Effects on BPA were of special interest. Its epitopes, BPA1 and BPA2, have been anatomically localized to basal cell hemidesmosomes and lamina lucida, and its role as an autoimmune antigen in the etiology of clinical bullous diseases such as bullous pemphigoid is well documented.

scholarly journals Bullous pemphigoid in a 3-month-old infant: case report and literature review of this dermatosis in childhood

2013 ◽  
Vol 88 (6) ◽  
pp. 961-965 ◽  
Author(s):  
Eugenio Galdino de Mendonça Reis-Filho ◽  
Tainah de Almeida Silva ◽  
Luiza Helena de Lima Aguirre ◽  
Carmelia Matos Santiago Reis
Keyword(s):  
Case Report ◽  
Bullous Pemphigoid ◽  
Immunohistochemical Staining ◽  
Collagen Type ◽  
Laboratory Data ◽  
Collagen Type Iv ◽  
Prognostic Features ◽  
Type Iv ◽  
Bullous Diseases ◽  
Infant Case

Bullous pemphigoid is an autoimmune subepidermal blistering dermatosis that is uncommon in childhood. We report a case of a female infant, 3 months old, which presented clinical and laboratory data for the confirmatory diagnosis of bullous pemphigoid. The authors used immunohistochemical staining for collagen type IV that allowed the differentiation of bullous pemphigoid from other subepidermal bullous diseases. Opportunely we review the clinical, immunological, therapeutic and prognostic features of this pathology in children.

Antigen identification in drug-induced bullous pemphigoid

1993 ◽  
Vol 29 (5) ◽  
pp. 879-882 ◽  
Author(s):  
Eileen Pazderka Smith ◽  
Ted B. Taylor ◽  
Laurence J. Meyer ◽  
John J. Zone
Keyword(s):  
Bullous Pemphigoid ◽  
Drug Induced

Gliptin-Induced Bullous Pemphigoid: Canadian Case Series of 10 Patients

2020 ◽  
pp. 120347542097234
Author(s):  
Miriam Armanious ◽  
Mohn’d AbuHilal
Keyword(s):  
Bullous Pemphigoid ◽  
Case Series ◽  
Rapid Improvement ◽  
Drug Induced ◽  
Dipeptidyl Peptidase 4 ◽  
Early Withdrawal ◽  
Immune Mediated ◽  
Dipeptidyl Peptidase 4 Inhibitors ◽  
Causative Agents

Background Bullous pemphigoid (BP) is a chronic immune-mediated vesiculobullous disorder. Recently, several reports have described dipeptidyl peptidase-4 inhibitors, also known as gliptins, as causative agents for drug-induced BP. Objective To report and describe clinical and histologic characteristics of 10 cases of gliptin-induced BP. Results We identified 10 patients with gliptin-induced BP. Nine were secondary to linagliptin, and 1 case was attributed to sitagliptin. All patients showed significant improvement after withdrawal of gliptin medications and proper medical treatment. There has been no evidence of relapse after 4 months of follow-up. Conclusion This report supports the proposed association between gliptins and BP. Physicians should be aware of this potential adverse effect, as gliptin-induced BP can be reversible once identified and the responsible medication is stopped. Early withdrawal of the offending drug and proper treatment can lead to rapid improvement and reduced morbidity.

Drug-Induced Bullous Pemphigoid Caused by a Generic Canadian Medication Obtained Over the Internet

2005 ◽  
Vol 141 (11) ◽  
Author(s):  
Laura K. Ferris ◽  
Drazen Jukic ◽  
Joseph C. English ◽  
Matthew J. Zirwas
Keyword(s):  
Bullous Pemphigoid ◽  
The Internet ◽  
Drug Induced

IgE-mediated mechanisms in bullous pemphigoid and other autoimmune bullous diseases

2015 ◽  
Vol 12 (3) ◽  
pp. 267-277 ◽  
Author(s):  
Nina van Beek ◽  
Franziska S. Schulze ◽  
Detlef Zillikens ◽  
Enno Schmidt
Keyword(s):  
Bullous Pemphigoid ◽  
Autoimmune Bullous Diseases ◽  
Bullous Diseases ◽  
Ige Mediated

scholarly journals Bullous pemphigoid in diabetic patients treated by gliptins: the other side of the coin

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Karim Chouchane ◽  
Giovanni Di Zenzo ◽  
Dario Pitocco ◽  
Laura Calabrese ◽  
Clara De Simone
Keyword(s):  
Bullous Pemphigoid ◽  
Complement C3 ◽  
Direct Immunofluorescence ◽  
Diabetic Patients ◽  
Type 2 Diabetic Patients ◽  
Drug Induced ◽  
Inflammatory Phenotype ◽  
Linear Band ◽  
Circulating Autoantibodies

AbstractBullous pemphigoid (BP) is the most common autoimmune bullous skin disease that affects primarily patients older than 60 years. The majority of BP cases are spontaneous, but BP can also be triggered by certain drugs’ exposures. Since 2011, a growing number of observations has been reporting cases of BP in Type 2 diabetic patients. These forms have been linked to the use of a new category of anti-diabetic drugs called dipeptidyl peptidase inhibitors (DPP-4i) or gliptins, but to date, the exact pathophysiological mechanisms underlying this association are not completely elucidated. Although conventional and gliptin-associated BP are thought to share similar clinical and histopathological features, our thorough review of the most recent literature, shows that these 2 forms are quite distinct: DPP-4-i-associated BP seems to appear at an earlier age than spontaneous BP, it may manifest either as a noninflammatory or inflammatory phenotype, while the conventional form presents with a typical inflammatory phenotype. Additionally, an important distinctive histological feature was recently shown in Gliptin-associated BP: these forms may present a less significant eosinophils infiltrate in the upper dermis of peri-blister lesions compared to the skin of patients with spontaneous BP, and this seems a specific feature of the clinically non-inflammatory forms. In accordance with previous literature, we found that the direct immunofluorescence (DIF) gives identical findings in both DPP-4i-associated and conventional forms of BP which is an IgG and complement C3 deposition as a linear band at the dermal–epidermal junction in perilesional skin. Indirect immunofluorescence shows the presence of IgG circulating autoantibodies in the patient's serum which titer does not differ between spontaneous and DPP-4i-associated BP, while the specificity of these autoantibodies, may be different in spontaneous, induced non-inflammatory and induced inflammatory forms, epitope spreading phenomenon seems to play a role in determining these specificities. Further research, based on integrated epidemiological, clinical, histo-immunological and pharmacogenomic approaches, may give more insight into these forms of BP. This combined approach will allow to better define BP endotypes and to unveil the mechanism of spontaneous or drug-induced breakage of the immunotolerance to skin self-antigens.

Sign in / Sign up

Export Citation Format

Share Document