Effect of Eradication of Helicobacter pylori and Iron Supplementation on the Iron Status of Children with Iron Deficiency

Duque, Ximena; Morán, Segundo; Mera, Robertino; Medina, Mayela; Martı́nez, Homero; Mendoza, Eugenia; Torres, Javier; Correa, Pelayo

doi:10.1016/j.arcmed.2009.11.006

Cited by 35 publications

(35 citation statements)

References 26 publications

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“…Indeed, in a subsequent study, high salt diets promoted gastric adenocarcinomas in Mongolian gerbils infected with H. pylori strains with a functional CagA, but not with H. pylori lacking CagA. 114 Iron is another important dietary factor, as iron deficiency has been associated with the presence of H. pylori 158,159 and hypochlorhydria. 49,56 Animal models have demonstrated that Helicobacter infection results in iron deficiency, 158 while reduced dietary iron coupled with H. pylori infection promoted gastric cancer.…”

Section: Other Infectionsmentioning

confidence: 97%

The role of the gastrointestinal microbiome inHelicobacter pyloripathogenesis

Sheh¹,

2013

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The discovery of Helicobacter pylori overturned the conventional dogma that the stomach was a sterile organ and that pH values<4 were capable of sterilizing the stomach. H. pylori are an etiological agent associated with gastritis, hypochlorhydria, duodenal ulcers, and gastric cancer. It is now appreciated that the human stomach supports a bacterial community with possibly 100s of bacterial species that influence stomach homeostasis. Other bacteria colonizing the stomach may also influence H. pylori-associated gastric pathogenesis by creating reactive oxygen and nitrogen species and modulating inflammatory responses. In this review, we summarize the available literature concerning the gastric microbiota in humans, mice, and Mongolian gerbils. We also discuss the gastric perturbations, many involving H. pylori, that facilitate the colonization by bacteria from other compartments of the gastrointestinal tract, and identify risk factors known to affect gastric homeostasis that contribute to changes in the microbiota.

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Section: Other Infectionsmentioning

confidence: 97%

The role of the gastrointestinal microbiome inHelicobacter pyloripathogenesis

Sheh¹,

2013

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“…Chronic Hp infection is a major cause of gastric and duodenal ulcer disease, a risk factor for gastric cancer [2], and recently has also been associated with iron deficiency anemia [3], [4]. During colonization of the stomach, a significant number of Hp (∼20%) adhere to the host cell surface via various adhesins [5]–[7].…”

Section: Introductionmentioning

confidence: 99%

Helicobacter pylori Perturbs Iron Trafficking in the Epithelium to Grow on the Cell Surface

et al. 2011

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Helicobacter pylori (Hp) injects the CagA effector protein into host epithelial cells and induces growth factor-like signaling, perturbs cell-cell junctions, and alters host cell polarity. This enables Hp to grow as microcolonies adhered to the host cell surface even in conditions that do not support growth of free-swimming bacteria. We hypothesized that CagA alters host cell physiology to allow Hp to obtain specific nutrients from or across the epithelial barrier. Using a polarized epithelium model system, we find that isogenic ΔcagA mutants are defective in cell surface microcolony formation, but exogenous addition of iron to the apical medium partially rescues this defect, suggesting that one of CagA's effects on host cells is to facilitate iron acquisition from the host. Hp adhered to the apical epithelial surface increase basolateral uptake of transferrin and induce its transcytosis in a CagA-dependent manner. Both CagA and VacA contribute to the perturbation of transferrin recycling, since VacA is involved in apical mislocalization of the transferrin receptor to sites of bacterial attachment. To determine if the transferrin recycling pathway is involved in Hp colonization of the cell surface, we silenced transferrin receptor expression during infection. This resulted in a reduced ability of Hp to colonize the polarized epithelium. To test whether CagA is important in promoting iron acquisition in vivo, we compared colonization of Hp in iron-replete vs. iron-deficient Mongolian gerbils. While wild type Hp and ΔcagA mutants colonized iron-replete gerbils at similar levels, ΔcagA mutants are markedly impaired in colonizing iron-deficient gerbils. Our study indicates that CagA and VacA act in concert to usurp the polarized process of host cell iron uptake, allowing Hp to use the cell surface as a replicative niche.

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“…In the study of Duque et al [40], iron deficiency anemia and HP infection have been found in 1 Giardia trophozoites and their toxic proteins damage the microvillus brush border, reduce the intestinal surface area, and cause iron malabsorption [7,[42][43][44]. In one report [45], iron deficiency anemia was found in one quarter of the Giardia-infected children.…”

Section: Anemic Children and Upper Gastrointestinal System mentioning

confidence: 98%

Diagnostic Yield of Upper Gastrointestinal Endoscopy in the Evaluation of Iron Deficiency Anemia in Older Children and Adolescents

Gülen

Kasırga

Yildirim

et al. 2011

Pediatric Hematology and Oncology

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Iron deficiency anemia (IDA) is frequent in childhood. Inadequate nutrition and gastrointestinal malabsorption are the frequent causes of IDA in children. But reduced iron absorption and insidious blood loss from the gastrointestinal tract has been identified as the most frequent causes of IDA in older children and adolescents. Therefore the authors evaluated the frequency and etiologies of the upper gastrointestinal system pathologies causing IDA in older pediatric population. Patients with known hematological or chronic diseases, heavy menstrual flow, and obvious blood loss were excluded from the study. Forty-four children between the ages of 9.5 and 17.5 years and diagnosed with IDA were enrolled. They underwent upper gastrointestinal endoscopy and biopsy from esophagus, stomach, and duodenum. Mean age and hemoglobin (Hb) levels of study group (32 boys, and 12 girls) were 14.6 ± 2.0 years and 7.9 ± 1.8 g/dL, respectively. Only 1 patient had a positive serology testing with anti-tissue transglutaminase and small bowel biopsy correlating with celiac disease. Endoscopy revealed abnormal findings in 25 (56.8%) patients (21 endoscopic antral gastritis, 2 active duodenal ulcers, and 2 duodenal polyps). Helicobacter pylori (HP) infection was identified by using antral histopathological evaluation in 19 of 44 children (43.2%). In 2 of duodenal samples, one patient had celiac disease, and the other one was diagnosed as giardiasis. In conclusion, there are different etiologies resulting in IDA in older children and adolescents. When older children and adolescents are found to have iron deficiency, HP infection and other gastrointestinal pathologies should be ruled out before iron deficiency treatment.

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Effect of Eradication of Helicobacter pylori and Iron Supplementation on the Iron Status of Children with Iron Deficiency

Cited by 35 publications

References 26 publications

The role of the gastrointestinal microbiome inHelicobacter pyloripathogenesis

The role of the gastrointestinal microbiome inHelicobacter pyloripathogenesis

Helicobacter pylori Perturbs Iron Trafficking in the Epithelium to Grow on the Cell Surface

Diagnostic Yield of Upper Gastrointestinal Endoscopy in the Evaluation of Iron Deficiency Anemia in Older Children and Adolescents

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