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AIM To investigate the changes of gastricmucosal ascorbic acid secretion in patients withnonulcer dyspepsia and the effect of gastrin onit,and to relate any observed changes to H.pylori infection and mucosal histology.METHODS Ascorbic acid secretions in patientswere examined by collecting continuouslygastric juice for one hour after having aspiratedand discarded fasting gastric juice.Using theclearance rate(mL/min)of ascorbic acid fromblood to gastric juice represented ascorbic acidsecretion in the gastric mucosa.Ascorbic acidconcentrations in plasma and juice weremeasured by ferric reduced method.RESULTS Gastric ascorbic acid secretions inH.pylori-positive patients(1.46 mL/min,range0.27-3.78)did not significantly differ fromthose in H.pylori-negative patients(1.25 mL/min,0.47-3.14)(P>0.05).There were nosignificant differences in ascorbic acidsecretions between patients with mild(1.56 mL/min,0.50-3.30),moderate(1.34 mL/min,0.27-2.93)and severe(1.36 mL/min,0.47-3.78)inflammation(P>0.05).There were nosignificant differences in ascorbic acidsecretions between patients without activity(l.45mL/min,0.27-3.14)and with mild(1.32mL/min,0.61-2.93),moderate(1.49mL/min,0.50-3.78)and severe(1.43 mL/min,0.51-3.26)activity of chronic gastritis either(P>0.05).Ascorbic acid secretions in patientswith severe atrophy(0.56 mL/min,0.27-1.20)were markedly lower than those in patientswithout atrophy(1.51 mL/min,0.59-3.30)and with mild(1.43 mL/ min,0.53-3.78)andmoderate(1.31 mL/min,0.47-3.16)atrophy(P<0.005).There was a significant negativecorrelation between ascorbic acid secretion andseverity of atrophy(correlation coefficient=-0.43,P<0.005).After administration ofpentagastrin,ascorbic acid secretions weremarkedly elevated(from 1.39 mL/min,0.36-2.96 to 3.53mL/min,0.84-5.91)(P<0.001).CONCLUSION Ascorbic acid secretion ingastric mucosa is not affected by H.pyloriinfection.Gastric ascorbic acid secretion ismarkedly related to the severity of atrophy,whereas not related to the severity ofinflammation and activity.Gastrin may stimulategastric ascorbic acid secretion.A decreasedascorbic acid secretion may be an importantfactor in the link between atrophic gastritis andgastric carcinogenesis.
AIM To investigate the changes of gastric mucosal ascorbic acid secretion in patients with nonulcer dyspepsia and the effect of gastrin onit, and to relate any observed changes to H. pylori infection and mucosal histology. METHODS Ascorbic acid secretions in patients were monitored by collecting continuouslygastric juice for one hour After having aspirated and discarded fasting gastric juice. Using the scarance rate (mL / min) of ascorbic acid from blood to gastric juice as ascorbic acid secretion in the gastric mucosa. Ascorbic acid concentrations in plasma and juice were measurable by ferric reduced method. RESULTS Gastric ascorbic acid secretions inH. (P> 0.05). There were no significant differences in ascorbic (1.36 mL / min, 0.47-3.78) inflammation (P> 0.05), moderate (1.34 mL / min, 0.27-2.93) and severe . There were nosignificant differences in ascorbic acid secretion between patients without activity (1.45 mL / min, 0.27-3.14) and with mild (1.32 mL / min, 0.61-2.93), moderate (1.49 mL / min, 0.50-3.78) and severe (1.43 mL / min, 0.51-3.26) activity of chronic gastritis either (P> 0.05). Ascorbic acid secretions in patients with severe atrophy (0.56 mL / min, 0.27-1.20) were markedly lower than those in patients without atrophy min, 0.59-3.30) and with mild (1.43 mL / min, 0.53-3.78) and moderate (1.31 mL / min, 0.47-3.16) atrophy (P <0.005). There was a significant negative correlation between ascorbic acid secretion and severity of atrophy correlation coefficient = -0.43, P <0.005). After administration ofpentagastrin, ascorbic acid secretions were markedly elevated (from 1.39 mL / min, 0.36-2.96 to 3.53 mL / min, 0.84-5.91) (P <0.001) .CONCLUSION Ascorbic acid secretion ingastric mucosa is not affected by H. pylori infection. Gastric ascorbic acid secretion is markedly related to the severity of atrophy, not not related to the severity ofinflammation and activity. Gastrin may stimulategastric ascorbic acid secretion. A decreasedascorbic acid secretion may be an important factor in the link between atrophic gastritis andgastric carcinogenesis.