Assessment of the role of EGF +61A/G and EGFR R497K polymorphism in patients with inflammatory bowel disease: A case-control study

Abstract

Aim: Epidermal growth factor (EGF) and epidermal growth factor receptor (EGFR) play an important role in the regulation of cell growth, survival, migration, apoptosis, proliferation, and differentiation. We aimed to investigate the presence of EGF (+61A/G) and EGFR R497Kpolymorphisms in patients with inflammatory bowel disease (IBD) and their associations with clinical features of the patients.Methods: This case-control study included 91 IBD patients (45 Crohn’s disease (CD) patients and 46 ulcerative colitis (UC) patients) and 129 healthy controls (HC).  EGF and EGFR were genotyped by polymerase chain reaction and restriction fragment length polymorphism techniques to elucidate their association with clinical outcomes. The disease activity for UC and CD were assessed by Truelove-Witts index (TW) and Crohn's disease activity index (CDAI), respectively. The Montreal classification was used for disease involvement and behavior.Results: EGFR497 AA genotype was significantly decreased in patients with UC compared with CD and HC. In addition, the patients with UC who had EGF +61 A allele had increased risk of moderate and severe disease (p=0.28; OR= 3.13; 95% CI=0.34-28.73). The patients with CD who had the EGF61 AG genotype were found to increased risk for the presence of penetrating disease (p=0.14; χ2=5.59; OR=5.00; 95% CI=1.26-19.83). EGF +61 A genotype carriers also had higher CDAI scores (p=0.19; OR=4.00; 95% CI=0.44-36.14). In addition, A+ carriers were also found to have higher requirement for anti-TNF treatment (p=0.11; OR=5.0; 95% CI=0.56-44.4). Conclusion: In this study, EGFR 497 AA genotype was found to decrease significantly in patients with UC compared to HC and CD patients. To enlighten the mechanism, further studies with larger sample groups are needed to clarify the role of the EGF (+61A/G) and EGFR R497K genes polymorphism, and development of the etiology and pathogenesis of IBD