Abstract
The gram-negative bacterium, Helicobacter pylori (H. pylori), infection is predominantly known for its strong association with development of gastric diseases, including gastritis, peptic ulcers, and stomach cancer. Numerous clinical reports show that ascorbic acid deficiency has been connect with gastritis. Vitamin C levels both in gastric acid and serum have constantly been affirmed to be low in subjects with H. pylori infected gastritis and peptic ulcers. Ascorbic acid supplementation likely relates to reduced incidences of bleeding from peptic ulcers and gastric cancer. H. pylori eradication is shown to increase vitamin C levels, while the benefits of ascorbic acid oral intake to increase the effectiveness of H. pylori-eradication therapy are controversial. Recent studies suggest that ascorbate intake intravenously, but not orally; pharmacologic ascorbate concentrations up to 30 mmol/L in blood, several millimolar in tissues as well as in interstitial fluid, are easily and safely achieved. Pharmacologic ascorbate can exert pro-oxidant effects locally as a drug by mediating hydrogen peroxide (H2O2) formation, which was applied to animal and clinical trials of cancer, sepsis, and severe burns etc. In this review, we summarize current understanding of the associations of vitamin C and H. pylori infection, and outline some potential strategies for H. pylori intervention from emerging advances on ascorbic acid physiology and pharmacology.
Highlights
Since Helicobacter pylori (H. pylori) was first identified in 1982 by Robin Warren and Barry Marshall, gastritis and peptic ulcer disease have been gradually approached as an infectious disease (Warren and Marshall, 1983; Suerbaum and Michetti, 2002)
Eradication of H. pylori is an effective treatment for gastritis, peptic ulcer disease, and early lymphoma of mucosal-associated lymphoid tissue (MALT); it has the potential to reduce the risk of gastric cancer development (Parsonnet et al, 1991; Ito et al, 2002; Wong et al, 2004; Wündisch et al, 2005)
Vitamin C protects the body from various deleterious effects of free radicals and reactive oxygen species (ROS) that are produced during normal metabolic processes, via active immune cells, as well as by exposure to toxins and contaminants (Carr and Frei, 1999)
Summary
Since Helicobacter pylori (H. pylori) was first identified in 1982 by Robin Warren and Barry Marshall, gastritis and peptic ulcer disease have been gradually approached as an infectious disease (Warren and Marshall, 1983; Suerbaum and Michetti, 2002). Eradication of H. pylori is an effective treatment for gastritis, peptic ulcer disease, and early lymphoma of mucosal-associated lymphoid tissue (MALT); it has the potential to reduce the risk of gastric cancer development (Parsonnet et al, 1991; Ito et al, 2002; Wong et al, 2004; Wündisch et al, 2005). Lower vitamin C levels, both in gastric juice and serum, have repeatedly been linked to patients with H. pylori infected gastritis and peptic ulcers (Ruiz et al, 1994; Zhang et al, 1998; Annibale et al, 2003). H. pylori eradication can reverse the negative effect and increase vitamin C levels in serum and gastric juice; studies of ascorbic acid oral intake on H. pylori-eradication therapy reported ambiguous results (Sobala et al, 1993; Banerjee et al, 1994; Jarosz et al, 1998; Koçkar et al, 2001; Sezikli et al, 2012; Demirci et al, 2015)
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