Analysis of pathophysiological mechanisms of iron deficiency anemia in adult patients with chronic gastritis secondary to Helicobacter pylori infection

Introduction: Iron deficiency anemia (IDA) is the most prevalent nutritional deficiency worldwide, affecting approximately 1.2 to 2 billion people depending on the diagnostic criteria and reporting sources used. Chronic gastritis caused by Helicobacter pylori, present in more than 60% of the Mexican adult population, has been identified as a relevant and frequently underestimated etiopathogenic factor in the development and perpetuation of IDA. It acts through pathophysiological mechanisms that compromise both the absorption and systemic availability of iron.
Objective: To analyze the pathophysiological mechanisms that explain the development of iron deficiency anemia in patients with chronic gastritis caused by Helicobacter pylori, through a systematic review of the available scientific evidence, in order to establish a comprehensive theoretical basis to guide the etiological diagnosis and treatment of this association in clinical practice.
Methodology: A documentary, descriptive, and systematic bibliographic review with a qualitative approach was conducted. Searches were performed in PubMed/MEDLINE, Cochrane Library, SciELO, and LILACS databases using English and Spanish search terms combined with Boolean operators. Original scientific articles, systematic reviews, meta-analyses, and clinical practice guidelines published preferably between 2020 and 2025 were included, along with seminal publications of recognized scientific relevance.
Results: Three main pathophysiological pathways were identified through which chronic gastritis caused by H. pylorigenerates IDA: the inflammatory pathway mediated by hepcidin, in which IL-6 stimulates hepatic hepcidin synthesis via the JAK2/STAT3 pathway that blocks ferroportin and generates functional hypoferremia; the structural pathway mediated by hypochlorhydria, in which parietal cell atrophy raises the intragastric pH, compromising the reduction of ferric to ferrous iron necessary for duodenal absorption; and the direct bacterial competition pathway, in which H. pylori uses specialized molecular systems to capture iron from the host. H. pylori infection was identified as the most frequent etiology of malabsorption in patients with IDA, accounting for 54.1% of cases with demonstrated malabsorption. Furthermore, 70.3% of positive endoscopic findings in young patients with IDA corresponded to histopathologically confirmed H. pylori gastritis or duodenitis.
Conclusions: Chronic gastritis caused by H. pylori generates IDA through three synergistic pathophysiological pathways that mutually potentiate each other, explaining the frequent refractoriness to conventional oral iron treatment when the underlying infection is not identified and eradicated. Systematic investigation of H. pylori should be integrated into the diagnostic algorithm of every patient with unexplained or recurrent IDA, and its eradication should be considered an indispensable component of etiological treatment.