Evaluation of the Ez-HBT Helicobacter blood test to establish Helicobacter pylori eradication

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73012/1/j.1365-2036.2005.02655.x.pd

13C-Urea breath test: Reproducibility and association with the severity of Helicobacter pylori-associated antral gastritis

BackgroundThe purpose of the present paper was to assess the reproducibility of the (13)C-urea breath test ((13)C-UBT) and its ability to reflect the level of Helicobacter pylori-associated inflammation.MethodsAsymptomatic H. pylori-positive subjects (n = 21) performed the (13)C-UBT six times. The H. pylori-positive symptomatic subjects (n = 55) performed the (13)C-UBT and had antral biopsies taken for histopathology, culture, urease activity assay and myeloperoxidase activity assay.ResultsNo significant intraindividual variation in (13)C-UBT results were observed for the asymptomatic subjects. The (13)C-UBT results were significantly higher in symptomatic subjects with a moderate to severe gastritis compared to a mild gastritis and to no inflammation (34.5 +/- 4.4 vs 17.7 +/- 2.8 vs 1.7 +/- 0.1, respectively, P < 0.01). The (13)C-UBT results significantly correlated with urease (r = 0.55) and myeloperoxidase activity (r = 0.82) but not with bacterial load. conclusion: The (13)C-UBT is a reproducible determinant of H. pylori infection and non-invasively assesses the severity of antral inflammation.Matthews, Geoffrey M; Cummins, Adrian G; Lawrence, Andrew; Johnson, Bruce; Campbell, Fiona; Butler, Ross

Cellular mucosal defense during Helicobacter pylori infection: A review of the role of glutathione and the oxidative pentose pathway

Helicobacter pylori is the primary cause of gastritis and peptic ulcer disease and is known to infect greater than 50% of the world's population. It is also known to lead to the onset of gastric cancer and unless treated, lasts throughout life in most individuals. Mouse models of H. pylori infection have improved our ability to study this organism and can be used to investigate the host mucosal response to the infection, particularly the early events postinoculation. Previous studies have shown that H. pylori infection leads to an increased production of reactive oxygen species within the gastric mucosa which are thought to play a major role in the mediation of associated disease. Recent studies have shown differences in the availability of an important antioxidant, glutathione, during chronic H. pylori infection. The availability of glutathione is primarily controlled by the activity of the oxidative pentose pathway. This review proposes that the severity of inflammation and damage associated with H. pylori infection is dependent on the ability of mucosal cells to counteract the increased load of reactive oxygen species. It is hypothesized that the oxidative pentose pathway and glutathione availability are important factors modulating this response. It is suggested that the therapeutic regulation of glutathione availability could provide a novel method for preventing or reducing the damage caused during H. pylori infection