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Helicobacter pylori Infection Increases Serum Nitrate and Nitrite More Prominently Than Serum Pepsinogens
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AbstractBackground. Helicobacter pylori infection causes chronic gastritis and results in increased serum concentrations of pepsinogens I and II as well as gastrin, while the ratio of pepsinogen I to II (I : II) is decreased. Inducible nitric oxide synthase (iNOS) is induced in H. pylori‐associated gastritis and may modulate inflammation. However serum nitrate and nitrite (NOx) concentrations in patients with H. pylori‐induced chronic gastritis have not been reported. We examined differences in serum NOx between H. pylori‐negative and positive volunteers relative to differences in pepsinogens and gastrin.Materials and methods. Sera from 80 healthy asymptomatic volunteers younger than 36 years were analyzed for anti‐H. pylori antibody, NOx, gastrin and pepsinogens.Results. In H. pylori antibody‐positive subjects serum NOx concentrations were higher than in negative subjects (p < .005). In H. pylori‐negative subjects, NOx correlated with pepsinogen II (r = .405, p < .05). In subjects with low pepsinogen I or II, NOx was higher in H. pylori‐positive than negative subjects (p < .001). In subjects with high pepsinogen I : II (6 or higher), serum NOx was higher in H. pylori‐positive than in negative subjects.Conclusions. H. pylori‐induced gastritis increases serum NOx concentrations more prominently than those of pepsinogen. In H. pylori‐negative subjects, serum correlates with serum pepsinogen II.
Title: Helicobacter pylori Infection Increases Serum Nitrate and Nitrite More Prominently Than Serum Pepsinogens
Description:
AbstractBackground.
Helicobacter pylori infection causes chronic gastritis and results in increased serum concentrations of pepsinogens I and II as well as gastrin, while the ratio of pepsinogen I to II (I : II) is decreased.
Inducible nitric oxide synthase (iNOS) is induced in H.
pylori‐associated gastritis and may modulate inflammation.
However serum nitrate and nitrite (NOx) concentrations in patients with H.
pylori‐induced chronic gastritis have not been reported.
We examined differences in serum NOx between H.
pylori‐negative and positive volunteers relative to differences in pepsinogens and gastrin.
Materials and methods.
Sera from 80 healthy asymptomatic volunteers younger than 36 years were analyzed for anti‐H.
pylori antibody, NOx, gastrin and pepsinogens.
Results.
In H.
pylori antibody‐positive subjects serum NOx concentrations were higher than in negative subjects (p < .
005).
In H.
pylori‐negative subjects, NOx correlated with pepsinogen II (r = .
405, p < .
05).
In subjects with low pepsinogen I or II, NOx was higher in H.
pylori‐positive than negative subjects (p < .
001).
In subjects with high pepsinogen I : II (6 or higher), serum NOx was higher in H.
pylori‐positive than in negative subjects.
Conclusions.
H.
pylori‐induced gastritis increases serum NOx concentrations more prominently than those of pepsinogen.
In H.
pylori‐negative subjects, serum correlates with serum pepsinogen II.
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