The Role of E-Cadherin in the Assessment of Esophageal Mucosal Damage in Patients with Gastroesophageal Reflux Disease Associated with Obstructive Sleep Apnea/Hypopnea Syndrome

Aim. To evaluate the E-cadherin content in the blood plasma of individuals with suffering from both gastroesophageal reflux disease (GERD) and GERD combined with obstructive sleep apnea/hypopnea syndrome (OSAHS).

Materials and methods. 120 patients with GERD and/or OSAHS were examined. All the patients underwent esophagogastroduodenoscopy with the biopsy of the lower third of the esophagus in order to perform GERD morphological verification. The diagnostics of respiratory disorders during sleeping was performed using computer pulse oximetry. Group 1 (n = 29) consisted of GERD patients, group 2 (n = 35) of patients with GERD in combination with OSAHS, group 3 (n = 30) of patients with OSAHS, group 4 (n = 26) was the comparison group. The concentration of E-cadherin in the blood plasma was determined using enzyme immunoassay.

Results. There were no statistically significant differences in the plasma level of the N-terminal E-cadherin fragment between GERD patients and the comparison group (0.207 (0.128; 0.295) and 0.128 (0.067; 0.281) ng/ml, respectively, p = 0.082). However, the patients with erosive esophagitis were characterized by a higher content of E-cadherin in the blood plasma than those of the comparison group (0.284 (0.176; 0.858) and 0.128 (0.067; 0.281) ng/ml,  respectively, p = 0.03). In patients with GERD and OSAHS, statistically significantly higher plasma concentrations of E-cadherin were observed as compared to GERD patients (0.379 (0.277; 0.538) and 0.2007 (0.128; 0.295) ng/ml,  respectively, p = 0.017). A positive dependence of E-cadherin concentration in the blood plasma on the apnea/hypopnea index was found (r = 0.43, p <0.05).

Conclusions. OSAHS negatively affects the state of histoarchitecture of the esophageal mucosa of GERD patients, as evidenced by an increase in N-terminal E-cadherin in the blood plasma and may indicate a loss of E-cadherin in the esophageal mucosa with the development of an impaired function of tight junctions. 

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