Optimizing the treatment for gastroesophageal reflux disease in young people: the role and place of rebamipide

Background. Gastroesophageal reflux disease (GERD) is a condition that results from the reflux of acidic stomach contents into the esophagus and causes heartburn or regurgitation. One of the key factors in the pathogenesis of this disease is the disruption of the protective function of the physiological antireflux barriers of the esophageal mucosa. Objective: to evaluate the effect of rebami­pide on the restoration of the esophageal protective barrier in the presence of erosive or non-erosive forms of gastroesophageal reflux disease in young patients. Materials and methods. Thirty young patients with GERD aged 18 to 45 years were examined. Accor­ding to the results of upper endoscopy, two groups were formed: group I — 15 individuals with erosive GERD and group II — 15 peop­le with non-erosive GERD, not associated with H.pylori. The control group consisted of 15 practically healthy individuals. Both groups of patients took proton pump inhibitors (PPIs) (pantoprazole) in standard doses and rebamipide for 30 days. The participants were examined for indicators of the NO system in the blood plasma before and after treatment: the general activity of total nitric oxide synthase (gNOS), inducible (iNOS), neuronal (nNOS) and endothelial (eNOS) forms of NOS; the functional activity of surface epithelial cells of the esophageal mucosa was assessed by the level of sialic acids and glycosaminoglycans. Results. Signs of endothelial dysfunction in GERD were manifested by a significant increase in the level of iNOS by 2.3 times in erosive GERD (p = 0.0048) and by 2.6 times in non-erosive GERD (p = 0.007) compared to the control group. eNOS activity was 1.2-fold lower than in the control group in both erosive (p = 0.0005) and non-erosive GERD (p = 0.0007). nNOS increased 1.6-fold (p = 0.04) in non-erosive GERD, but its level decreased significantly after treatment (p = 0.04). Nitrite (NO₂) levels were 2.6-fold higher in erosive GERD (p < 0.0001) and 1.8-fold higher in non-erosive GERD (p = 0.0022) compared to the control group. The normalization of sialic acid and glycosaminoglycan levels after treatment with the PPI + rebamipide complex (p < 0.0001 and p = 0.0001, respectively) is a confirmation of the restorative and protective functions of the esophageal mucosa in both erosive and non-erosive GERD in young patients. Conclusions. The addition of rebamipide to the PPI monotherapy had significant advantages in terms of correcting endothelial dysfunction indicators in patients with both erosive and non-erosive forms of GERD, contributing to the reduction of inflammatory infiltration of the epithelial layer and submucosal base of the esophageal mucosa, restoration of the epithelium, and healing of erosions, which has an important role in the protective and reparative processes of the esophageal mucosa. Although studies regarding the effect of rebamipide on the esophageal mucosal barrier are limited, the mechanisms of its action indicate a potential benefit. The data obtained may be guidelines for further clinical studies on the effectiveness of rebamipide in the treatment of gastroesophageal reflux disease.