Expression of epidermal growth factor receptor (EGFR) in systemic sclerosis patients (SSc) and gastro-oesophageal reflux disease (GORD)

• Published in: Immunology letters Vol. 265; pp. 31 - 36
• Main Authors: Pasta, Andrea, Calabrese, Francesco, Djahandideh Sheijani, Shirin, Furnari, Manuele, Giannini, Edoardo G., Grillo, Federica, Marabotto, Elisa, Mastracci, Luca, Murdaca, Giuseppe, Negrini, Simone, Savarino, Edoardo Vincenzo, Savarino, Vincenzo, Zentilin, Patrizia
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.02.2024
• Subjects: Epidermal growth factor receptor; ErbB Receptors; Esophagitis; Gastroesophageal Reflux - diagnosis; Gastroesophageal Reflux - pathology; Gastroesophageal reflux disease; Humans; Microscopic esophagitis; Retrospective Studies; Scleroderma, Systemic; Systemic sclerosis; Microscopic esophagitis; Systemic sclerosis; Gastroesophageal reflux disease; Epidermal growth factor receptor
• ISSN: 0165-2478; 1879-0542; 1879-0542
• DOI: 10.1016/j.imlet.2023.106834

•SSc leads to a fibrotic process and EGFR expression is increased in damaged tissues.•EGFR is overexpressed in the esophagus of SSc patients without microscopic esophagitis.•Microscopic esophagitis is associated with increased EGFR expression in all subjects. Systemic sclerosis (SSc) affects the connective tissue and leads to an abnormal fibrotic process in the skin and internal organs. Epidermal Growth Factor Receptor (EGFR) is able to induce cell proliferation and differentiation, and its expression is increased in SSc patients with pulmonary artery hypertension and in skin biopsies in patients with scleroderma. To date, no data on esophageal expression of EGFR are available in SSc patients. We aimed to evaluate whether the pro-fibrogenic pathways of SSc may affect EGFR expression in the esophagus. A retrospective analysis included patients with SSc and control subjects suffering from gastroesophageal reflux symptoms. Endoscopic assessment and histopathologic analyses were performed in all subjects and the presence of microscopic esophagitis was used to distinguish patients with normal esophageal mucosa and subjects with non-erosive reflux disease. EGFR expression was measured in all subjects. A total of 35 patients with SSc were included, while the control group included 67 non-SSc patients. EGFR expression at the Z-line was higher in SSc patients than non-SSc patients in absence of microscopic esophagitis (median 65 %, IQR 56–71 % vs 42 %, IQR 37–54 %, p < 0.001). Microscopic esophagitis was found in 60 % of patients with SSc and 62.7 % of control patients, and EGFR expression was significantly higher in patients presenting microscopic esophagitis both in SSc and non-SSc patients. The EGFR hyperexpression may be due to SSc and/or reflux-related damage in patients with microscopic esophagitis. Further studies are warranted to answer open questions and provide a possible role of EGFR in terms of diagnosis, prognosis, and therapy.