Advances in medical sciences · 2014
A distinct salivary secretory response mediated by the esophago-salivary reflex in patients with Barrett's esophagus: its potential pathogenetic implications.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Yandrapu Harathi, Marcinkiewicz Marek, Poplawski Cezary, Namiot Zbigniew, Zbroch Tomasz, Sarosiek Jerzy
Аннотация
PURPOSE: A significantly compromised epidermal growth factor (EGF) secretion by basal parotid saliva may contribute to the development of Barrett's esophagus (BE). The rate of secretion of EGF as well as a wide spectrum of protective factors in total basal and stimulated saliva in BE patients remains to be explored. We therefore studied the rate of secretion of salivary buffers, glycoconjugate, protein, EGF, transforming growth factor α (TGFα) and prostaglandin E₂ (PGE₂), evoked by esophago-salivary reflex, in patients with BE and controls (CTRL).
MATERIAL/METHODS: Salivary secretion was collected during basal condition, mastication, and intraesophageal mechanical and chemical stimulations respectively, mimicking the natural gastroesophageal reflux scenario.
RESULTS: Salivary pH in BE was significantly lower than in controls during mechanical (p<0.001) and chemical stimulations (p<0.001). Bicarbonate and protein outputs in BE were significantly lower during mechanical (p<0.05) and chemical stimulations (p<0.01). The non-bicarbonate and glycoconjugate outputs in BE were lower during chemical stimulation (p<0.05) and during mechanical (p<0.05) and chemical stimulations (p<0.05) respectively. The rate of salivary EGF output in BE was significantly lower during mechanical stimulation (p<0.05). We observed a higher TGFα output during mastication (p<0.05) and PGE2 secretion during basal and masticatory condition (p<0.05) in BE.
CONCLUSIONS: Patients with BE demonstrated significantly compromised salivary pH and rate of secretion of bicarbonate, non-bicarbonate, glycoconjugate, protein and EGF. This impairment could potentially predispose to the development of accelerated esophageal mucosal injury. Potential restoration of this impairment by masticatory stimulation of salivary secretion using sugarless chewing gum justifies further clinical exploration.
MATERIAL/METHODS: Salivary secretion was collected during basal condition, mastication, and intraesophageal mechanical and chemical stimulations respectively, mimicking the natural gastroesophageal reflux scenario.
RESULTS: Salivary pH in BE was significantly lower than in controls during mechanical (p<0.001) and chemical stimulations (p<0.001). Bicarbonate and protein outputs in BE were significantly lower during mechanical (p<0.05) and chemical stimulations (p<0.01). The non-bicarbonate and glycoconjugate outputs in BE were lower during chemical stimulation (p<0.05) and during mechanical (p<0.05) and chemical stimulations (p<0.05) respectively. The rate of salivary EGF output in BE was significantly lower during mechanical stimulation (p<0.05). We observed a higher TGFα output during mastication (p<0.05) and PGE2 secretion during basal and masticatory condition (p<0.05) in BE.
CONCLUSIONS: Patients with BE demonstrated significantly compromised salivary pH and rate of secretion of bicarbonate, non-bicarbonate, glycoconjugate, protein and EGF. This impairment could potentially predispose to the development of accelerated esophageal mucosal injury. Potential restoration of this impairment by masticatory stimulation of salivary secretion using sugarless chewing gum justifies further clinical exploration.