Abstract
Background - Vitamin E (α-tocopherol) is an important endogenous antioxidant and may also act as an anticarcinogen. Aim - To determine the vitamin E status of subjects with, and without, gastroduodenal inflammation and Helicobacter pylori infection. Subjects - 36 patients undergoing routine gastroscopy for investigation of dyspepsia. Methods - High performance liquid chromatography with fluorometric detection was used to determine α- tocopherol values. Results - In H pylori negative subjects with normal gastroduodenal histology (n=11) median α-tocopherol values (ng/mg tissue weight) were significantly higher in the corpus (16.4, interquartile range (IQR) 8.9-22.6) than in the antrum (3.0, IQR 2.6-6.7, p=0.001) or duodenum (6.7, IQR 2.5-8.4, p=0.001). H pylori infection (n = 19) was associated with a reduction in the corpus α-tocopherol values (median 8.3, IQR 4.9-13.7, p<0.05) but there was no significant change in the antral concentrations although this was the main site of inflammation and neutrophil activity. Duodenal α-tocopherol values were not significantly changed in the presence of duodenitis or gastric H pylori infection. α-Tacopherol was not detected in the gastric juice of any of the subjects. Plasma α-tocopherol concentrations in the H pylori negative subjects (median 10.4 mg/l, IQR 7.2- 11.9) were not significantly different to the values in the H pylori positive subjects (median 11.1 mg/l, IQR 7.6-12.7). Conclusions - Concentrations of α-tocopherol in H pylori negative subjects are higher in the corpus than in the antrum or duodenum. In the presence of predominantly antral H pylori infection and neutrophil activity the major change seen is a reduction in corpus α-tocopherol values while antral concentrations are maintained. These findings may reflect a mobilisation of antioxidant defences to the sites of maximal inflammation in the stomach.
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Phull, P. S., Price, A. B., Thorniley, M. S., Green, C. J., & Jacyna, M. R. (1996). Vitamin E concentrations in the human stomach and duodenum - Correlation with Helicobacter pylori infection. Gut, 39(1), 31–35. https://doi.org/10.1136/gut.39.1.31
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