Canan Caymaz-Bor

Gastroesophageal Reflux Disease in a Low-Income Region in Turkey

OBJECTIVES:Detailed population-based data regarding the prevalence and symptom profile of gastroesophageal reflux disease (GERD) in underdeveloped and developing Caucasian countries are lacking. The aim of this study was to determine the prevalence and clinical spectrum of GERD in a low-income region in Turkey.METHODS:We used a previously validated reflux questionnaire, which was translated into Turkish and culturally adapted. The questionnaire was applied to 630 randomly selected participants greater than 20 yr old living in a population of 8,857 adults, with a low mean income of

Effect of heat stress on rabbit esophageal epithelium

75/person/month. The reliability and reproducibility of the questionnaire were calculated using the kappa statistic (test-retest). Endoscopy and/or 24-h intraesophageal pH monitoring were used to ascertain its validity in identifying patients with reflux.RESULTS:The prevalence of GERD symptoms was 10% for heartburn, 15.6% for regurgitation, and 20% for either symptom experienced at least weekly (95% CI). Heartburn and regurgitation were associated with noncardiac chest pain (37.3%), dysphagia (35.7%), dyspepsia (42.1%), odynophagia (35.7%), globus, hoarseness, cough, hiccup, nausea, vomiting, belching, and NSAID use, but not with body mass index in both frequent and occasional symptom groups. The prevalence of heartburn symptoms, but not regurgitation, increased significantly with age.CONCLUSIONS:The prevalence of GERD in a low-income population in Turkey was similar to that of developed countries, although with a different symptom profile, namely, a lower incidence of heartburn and a higher incidence of regurgitation and dyspepsia. These findings support the contention that there are a large number of patients worldwide in underdeveloped nations with poorly recognized and largely undertreated GERD.

Effect of ethanol on the structure and function of rabbit esophageal epithelium

Hot beverages expose the esophageal epithelium to temperatures as high as 58 degrees C. To study the impact of such temperatures, rabbit esophageal epithelium was exposed to luminal heat or both luminal and serosal heat while mounted in Ussing chambers. Luminal heat, mimicking exposure to hot beverages, reduced potential difference (PD) and resistance (R) when applied at >/=49 degrees C and reduced short-circuit current (Isc) at >/=60 degrees C. At >/=60 degrees C, subepithelial blisters developed. Higher temperatures reduced R only moderately and reversibly. In contrast, the Isc declined sharply and irreversibly once threshold was reached. Luminal and serosal heat also reduced PD, Isc, and R, although the threshold for reduction in Isc was now similar to that for R. Additionally, luminal and serosal heat reduced Isc more than R for any given temperature and resulted in blisters at lower temperatures (50 degrees C) than luminal heat alone. The heat-induced decline in Isc was attributed in part to inactivation of Na-K-ATPase activity, although other transport systems could have been equally affected, and the decline in R to an increase in paracellular permeability. The latter effect on R also contributed to an increase in tissue sensitivity to luminal acid damage. Consumption of hot beverages exposes the esophagus to temperatures that can negatively impact epithelial structure and function. Impaired barrier function by heat increases the risk of esophageal damage by subsequent contact with (refluxed) gastric acid. These findings help explain in part the association between esophageal disease and consumption of hot beverages.Hot beverages expose the esophageal epithelium to temperatures as high as 58°C. To study the impact of such temperatures, rabbit esophageal epithelium was exposed to luminal heat or both luminal and serosal heat while mounted in Ussing chambers. Luminal heat, mimicking exposure to hot beverages, reduced potential difference (PD) and resistance ( R) when applied at ≥49°C and reduced short-circuit current ( I sc) at ≥60°C. At ≥60°C, subepithelial blisters developed. Higher temperatures reduced R only moderately and reversibly. In contrast, the I sc declined sharply and irreversibly once threshold was reached. Luminal and serosal heat also reduced PD, I sc, and R, although the threshold for reduction in I scwas now similar to that for R. Additionally, luminal and serosal heat reduced I sc more than R for any given temperature and resulted in blisters at lower temperatures (50°C) than luminal heat alone. The heat-induced decline in I sc was attributed in part to inactivation of Na-K-ATPase activity, although other transport systems could have been equally affected, and the decline in R to an increase in paracellular permeability. The latter effect on R also contributed to an increase in tissue sensitivity to luminal acid damage. Consumption of hot beverages exposes the esophagus to temperatures that can negatively impact epithelial structure and function. Impaired barrier function by heat increases the risk of esophageal damage by subsequent contact with (refluxed) gastric acid. These findings help explain in part the association between esophageal disease and consumption of hot beverages.

Chloride transport in rabbit esophageal epithelial cells

Epidemiological studies indicate a relationship between alcohol consumption and esophageal epithelial disease. We therefore sought the contribution of the direct effects of ethanol on esophageal epithelial structure and (transport and barrier) function. Epithelium from the rabbit was mounted in Ussing chambers and exposed luminally for 1 h to 1-40% ethanol. At concentrations of 1-5% potential difference (PD) increased, and at 10-40% PD decreased. The increase in PD with 1-5% ethanol was accompanied by an increase in short-circuit current (Isc), and this increase in Isc could be blocked by ouabain pretreatment. The decrease in PD with 10-40% ethanol was associated with a decrease in electrical resistance (R), and this decrease in R was paralleled by an increase in transepithelial [14C]mannitol flux. Reversibility of these changes was limited at ethanol concentrations > or = 10%, and these were associated morphologically by patchy or diffuse tissue edema. Moreover, as with ethanol exposure in vitro, exposure in vivo produced dose-dependent changes in PD, Isc, R, and morphology. These observations indicate that exposure to ethanol in concentrations and under conditions reflecting alcohol consumption in humans can alter and impair esophageal epithelial transport and barrier functions. Such impairments are likely to contribute to the observed increase in risk of esophageal disease with regular consumption of alcoholic beverages.Epidemiological studies indicate a relationship between alcohol consumption and esophageal epithelial disease. We therefore sought the contribution of the direct effects of ethanol on esophageal epithelial structure and (transport and barrier) function. Epithelium from the rabbit was mounted in Ussing chambers and exposed luminally for 1 h to 1-40% ethanol. At concentrations of 1-5% potential difference (PD) increased, and at 10-40% PD decreased. The increase in PD with 1-5% ethanol was accompanied by an increase in short-circuit current ( I sc), and this increase in I sccould be blocked by ouabain pretreatment. The decrease in PD with 10-40% ethanol was associated with a decrease in electrical resistance ( R), and this decrease in R was paralleled by an increase in transepithelial [14C]mannitol flux. Reversibility of these changes was limited at ethanol concentrations ≥10%, and these were associated morphologically by patchy or diffuse tissue edema. Moreover, as with ethanol exposure in vitro, exposure in vivo produced dose-dependent changes in PD, I sc, R, and morphology. These observations indicate that exposure to ethanol in concentrations and under conditions reflecting alcohol consumption in humans can alter and impair esophageal epithelial transport and barrier functions. Such impairments are likely to contribute to the observed increase in risk of esophageal disease with regular consumption of alcoholic beverages.

The role of pepsin in acid injury to esophageal epithelium.

We investigated Cl(-) transport pathways in the apical and basolateral membranes of rabbit esophageal epithelial cells (EEC) using conventional and ion-selective microelectrodes. Intact sections of esophageal epithelium were mounted serosal or luminal side up in a modified Ussing chamber, where transepithelial potential difference and transepithelial resistance could be determined. Microelectrodes were used to measure intracellular Cl(-) activity (a), basolateral or apical membrane potentials (V(mBL) or V(mC)), and the voltage divider ratio. When a basal cell was impaled, V(mBL) was -73 +/- 4.3 mV and a(i)(Cl) was 16.4 +/- 2.1 mM, which were similar in presence or absence of bicarbonate. Removal of serosal Cl(-) caused a transient depolarization of V(mBL) and a decrease in a(i)(Cl) of 6.5 +/- 0.9 mM. The depolarization and the rate of decrease of a(i)(Cl) were inhibited by approximately 60% in the presence of the Cl(-)-channel blocker flufenamate. Serosal bumetanide significantly decreased the rate of change of a(i)(Cl) on removal and readdition of serosal Cl(-). When a luminal cell was impaled, V(mC) was -65 +/- 3.6 mV and a was 16.3 +/- 2.2 mM. Removal of luminal Cl(-) depolarized V(mC) and decreased a by only 2.5 +/- 0.9 mM. Subsequent removal of Cl(-) from the serosal bath decreased a(i)(Cl) in the luminal cell by an additional 6.4 +/- 1.0 mM. A plot of V(mBL) measurements vs. log a(i)(Cl)/log a(o)(Cl) (a(o)(Cl) is the activity of Cl(-) in a luminal or serosal bath) yielded a straight line [slope (S) = 67.8 mV/decade of change in a(i)(Cl)/a(o)(Cl)]. In contrast, V(mC) correlated very poorly with log a/a (S = 18.9 mV/decade of change in a/a). These results indicate that 1) in rabbit EEC, a(i)(Cl) is higher than equilibrium across apical and basolateral membranes, and this process is independent of bicarbonate; 2) the basolateral cell membrane possesses a conductive Cl(-) pathway sensitive to flufenamate; and 3) the apical membrane has limited permeability to Cl(-), which is consistent with the limited capacity for transepithelial Cl(-) transport. Transport of Cl(-) at the basolateral membrane is likely the dominant pathway for regulation of intracellular Cl(-).