Detection of circulating anti-skin antibodies by indirect immunofluorescence and by ELISA: a comparative systematic review and meta-analysis

BackgroundBoth enzyme-linked immunosorbent assays (ELISAs) and indirect immunofluorescence (IIF) are available for the diagnosis of autoimmune bullous diseases (AIBD). Many studies have reported on the performance of ELISAs and concluded that ELISAs could replace IIF. This study compares the diagnostic accuracy of ELISA and IIF for the detection of autoantibodies to desmoglein 1 (DSG1), desmoglein 3 (DSG3), bullous pemphigoid antigen 2 (BP180) and bullous pemphigoid antigen 1 (BP230) to support the diagnosis of pemphigus vulgaris (PV), pemphigus foliaceus (PF) and bullous pemphigoid (BP).MethodsA literature search was performed in the PubMed database. The meta-analysis was performed using summary values and a bivariate random effect model.ResultsThe five included studies on PV did not demonstrate significant differences between IIF and DSG3-ELISA (sensitivity 82.3% vs. 81.6%, p = 0.9284; specificity 95.6% vs. 93.9%, p = 0.5318; diagnostic odds ratio [DOR] 101.60 vs. 67.760, p = 0.6206). The three included studies on PF did not demonstrate significant differences between IIF and DSG1-ELISA (sensitivity 80.6% vs. 83.1%, p = 0.8501; specificity 97.5% vs. 93.9%, p = 0.3614; DOR 160.72 vs. 75.615, p = 0.5381). The eight included studies on BP showed that BP230-ELISA differed significantly from both IIF on monkey esophagus (MO) and BP180-ELISA with regard to DOR (11.384 vs. 68.349, p = 0.0008; 11.384 vs. 41.699, p = 0.0125, respectively)ConclusionsOur meta-analysis shows that ELISA performs as well as IIF for diagnosing PV, PF and BP.

Gambaran Dermal-Epidermal Junction Pada Bullous Pemphigoid Dan Epidermolysis Bullosa Acquisita

Epidermis and dermis of the skin attach each other because of the role of a structure which is called dermal-epidermal junction. The dermal-epidermal junction can be divided into three distinct zones named hemidesmosome-keratin intermediate filament complex, basement membrane, and anchoring fibril. Each part of the distinct zone has significant components for the integrity of the skin. Bullous pemphigoid is an autoimmune disorder caused by autoantibody against a 180-kDa molecule now called Bullous Pemphigoid Antigen 2 (BPAG2) or type XVII collagen within basement membrane. To date, the patophysiology and the components of dermal-epidermal junction that induce the blister formation remain unclear. Epidermolysis bullosa acquisita is an autoimmune disease with sub-epidermal blistering associated with autoimmunity to the collagen within anchoring fibrils. The pathophysiology and etiology—again—remain unknown.