Pemphigus & Pemphigoid
- Bullous pemphigoid (BP) is an autoantibody-mediated blistering disease that is often associated with neurologic disease. BP antibodies target two epidermal adhesion molecules, known as BP180 and BP230. Homologues to these proteins are found in the brain, and it is hypothesized that neurologic disease leads to the production of autoantibodies that can cross-react with their cutaneous forms. To better understand the link between BP and neurologic disease, we evaluated primary demographic features (age, sex, race, ethnicity, and elapsed time between onset of skin symptoms and BP diagnosis), severity of BP, and IgG and IgE autoantibody levels in BP control individuals and patients with BP with preceding Parkinson disease, dementia, and stroke.
- Dipeptidyl peptidase-4 inhibitor (DPP-4i) has been widely used to treat type 2 diabetes. DPP-4 inactivates incretins by catalyzing the cleavage of those proteins to inactive forms (Drucker, 2007). DPP-4i works by inhibiting the action of this enzyme and improves glycemic control (Aschner and Kipnes, 2006). DPP-4i has been known as a safe drug; however, an increased risk of bullous pemphigoid (BP) during DPP-4i exposure has been reported in diabetic patients administered DPP-4i (Béné et al., 2016).
- Bullous pemphigoid (BP) is a major autoimmune blistering skin disorder, in which a majority of the autoantibodies (autoAbs) target the juxtamembranous extracellular noncollagenous 16A domain (NC16A) domain of hemidesmosomal collagen XVII. BP-autoAbs may target regions of collagen XVII other than the NC16A domain; however, correlations between epitopes of BP-autoAbs and clinical features have not been fully elucidated. To address correlations between the clinical features and specific epitopes of BP-autoAbs, we evaluated the epitope profiles of BP-autoAbs in 121 patients.