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Trappin-2/Elafin and Clusterin serum levels in Pemphigus Vulgaris and correlation with the severity score: a case–control study in Assiut University

Research Authors
Badran Y. Aya1, Shehata Refaat Rofaida1, Abd-Elkader S. Alaa2, Kamel A. Amira3, Abd-Elsamea S. Fatma4, Gomaa S. Ahmed 1 1Department of Dermatology, Venereology and Andrology, Faculty of Medicine, Assiut University, Assiut, Egypt 2Department of Clinical P
Research Date
Research Department
Research Journal
Egyptian Journal of Dermatology and Venereology
Research Member
Research Vol
2021, 42:53–59
Research Year
2021
Research Abstract

Background: Trappin-2/Elafin, a 9.9 kDa molecule derived from Preproelafin, is primarily found in immune cells, skin, lungs, and other organs. Clusterin, a heterodimeric glycoprotein, is involved in processes like lipid interaction, apoptosis regulation, complement system modulation, and response to stress and autoimmune damage. Both proteins have been studied in various diseases with immune involvement, but their role in pemphigus vulgaris (PV) remains unclear.

Methods: This study aimed to investigate the serum levels of Trappin-2/Elafin and Clusterin in PV patients and their potential correlation with disease severity using the pemphigus disease area index. Serum levels were quantified using enzyme-linked immunosorbent assay (ELISA) in 50 PV patients and 40 healthy controls.

Results: showed significantly higher serum levels of Trappin-2/Elafin and Clusterin in PV patients compared to controls (P<0.001). However, no correlation was found between these levels and disease severity. The elevated Trappin-2/Elafin levels suggest chronic inflammation, autoimmunity, and tissue damage, while increased Clusterin levels indicate autoimmune damage, stress, or transforming growth factor stimulation.

Conclusion: While Trappin-2/Elafin and Clusterin are elevated in PV patients, their increase is not disease-specific, nor are they reliable markers of disease severity. These findings highlight their roles in broader inflammatory and autoimmune processes rather than PV-specific pathogenesis.