Helicobacter pylori: una causa no tradicional de deficiencia de hierro y anemia

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Date
2012
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Abstract
Helicobacter Pylori (H. pylori) is the most common cause for chronic gastritis, duodenal ulcers, MALT lymphoma and gastric cancer. H. pylori has also been associated with several extra gastric diseases such as iron deficiency (ID) and iron deficiency anemia (IDA). Several mechanisms by which H. pylori might contribute to the development of ID/IDA have been proposed. Alterations in the physiology of gastric mucosa and of iron metabolism as a consequence of the infection as well as direct competition for iron by H. pylori have been proposed as possible causes for ID/IDA development. H. pylori causes alterations in gastric pH as well as in the concentration of ascorbic acid in the stomach limiting the absorption of dietary iron in the gastrointestinal tract. In addition, pro-inflammatory cytokine secretion in response to the infection, in particular IL-1β are able to modulate acid secretion and stimulate the secretion of hepcidin from the liver inhibiting liberation of iron from iron stores. These results in less iron available for eritropoyesis, thus contributing to ID/IDA development. Several studies have suggested a direct relationship between the presence of the infection and the development of ID/IDA in children, adolescents and adults. H. pylori eradication has been associated to a better response to oral iron therapy in IDA patients. However some controversy still remains regarding the role of the infection in ID/IDA and the mechanisms involved. Studies aimed to evaluate the relationship between H. pylori and acid output in gastric mucosa, as well as studies to determine iron capture in strains isolated from IDA patients are still being conducted in order the shed some definitive light in the relationship between this bacterium and ID/IDA and their contributing mechanisms.
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Helicobacter pylori, Iron deficiency, Iron uptake
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