ObjectiveIron deficiency (ID) and iron deficiency anaemia (IDA) are global major public health problems, particularly in developing countries. Whilst an association between H. pylori infection and ID/IDA has been proposed in the literature, currently there is no consensus. We studied the effects of H. pylori infection on ID/IDA in a cohort of children undergoing upper gastrointestinal endoscopy for upper abdominal pain in two developing and one developed country.MethodsIn total 311 children (mean age 10.7±3.2 years) from Latin America - Belo Horizonte/Brazil (n = 125), Santiago/Chile (n = 105) - and London/UK (n = 81), were studied. Gastric and duodenal biopsies were obtained for evaluation of histology and H. pylori status and blood samples for parameters of ID/IDA.ResultsThe prevalence of H. pylori infection was 27.7% being significantly higher (p<0.001) in Latin America (35%) than in UK (7%). Multiple linear regression models revealed H. pylori infection as a significant predictor of low ferritin and haemoglobin concentrations in children from Latin-America. A negative correlation was observed between MCV (r = −0.26; p = 0.01) and MCH (r = −0.27; p = 0.01) values and the degree of antral chronic inflammation, and between MCH and the degree of corpus chronic (r = −0.29, p = 0.008) and active (r = −0.27, p = 0.002) inflammation.ConclusionsThis study demonstrates that H. pylori infection in children influences the serum ferritin and haemoglobin concentrations, markers of early depletion of iron stores and anaemia respectively.

The density of antral gastrin (G)- and somatostatin (D)-immunoreactive cells and the contents of antral gastrin and somatostatin were investigated in endoscopic antral biopsy specimens from patients with duodenal ulcer before and after eradication of Helicobacter pylori. After H. pylori eradication both antral somatostatin concentration (p = 0.0002) and antral D-cell density (p = 0.01) increased significantly. Conversely, although the number of G-cells was unchanged, antral (p = 0.0002) and serum (p = 0.001) gastrin contents decreased significantly. The number of oxyntic D-cells did not change significantly. These results strongly suggest that the hypergastrinaemia observed in H. pylori-positive patients may be due to a deficiency in antral somatostatin, which normally inhibits the synthesis and release of gastrin.

SUMMARYBackground: Helicobacter pylori treatment failure is a growing problem in daily practice. Aim: To determine the efficacy of the combination of rabeprazole, levofloxacin and furazolidone as a rescue therapy. Methods: Duodenal ulcer patients previously submitted, without success, to at least two H. pylori treatment regimens were included. Gastroscopy (urease test, histological examination and culture) and 13 C-urea

Although our results suggest an association between the presence of H. pylori in the intestine and ulcerative colitis-like phenotype of Crohn's disease, H. pylori infection in the actual causality of Crohn's disease is still to be determined.

Our results demonstrate that clarithromycin and furazolidone in combination with omeprazole are a good alternative for H. pylori eradication in Brazilian patients with duodenal ulcer.

Th17 cells seem to have an important role in the efficacy of vaccines against Helicobacter pylori. Because children are a target group for human vaccination and Th17/T(reg) cells have intrinsically linked and antagonic commitments, we compared the gastric levels of Th17- and T(reg)-associated cytokines of children and adults. IL-6, IL-10 and TGF-β1 levels and Foxp3(+) cell numbers were higher, but IL-1β, IL-17A and IL-23 were lower in infected children than in infected adults. In conclusion T(reg) instead of Th17 cell response to H. pylori-infection predominates in children.

In a search for Helicobacter species in the intestinal mucosae of 42 patients with ulcerative colitis (UC) and 74 without UC, only H. pylori was found. Although the bacterium was detected in UC patients by culture (7.1%) and nested PCR (19.0%), its presence was not associated with the disease (P ‫؍‬ 0.13).Ulcerative colitis (UC) is an inflammatory bowel disease (IBD) of unknown etiology that is confined to the large bowel mucosa. It seems to be a multifactorial disorder involving both genetic and environmental components, particularly the bacterial gut microbiota (13). However, no specific pathogenic or commensal bacterium has been convincingly implicated as the etiologic agent (4). Numerous studies have demonstrated that indigenous Helicobacter species of the gut of mice-Helicobacter hepaticus and Helicobacter bilis-are able to induce a persistent inflammation of the colon and cecum in some immunocompromised mouse models (1,5,8,15). Moreover, other Helicobacter species have been isolated from the gut of cottontop tamarins (14) and rhesus monkeys (7) with IBD-like disease. We hypothesize that species of the genus Helicobacter may also be associated with the pathogenesis of UC in human beings. Therefore, we investigated the presence of Helicobacter species in the intestinal mucosa of patients with UC and controls, by culture and PCR.We studied prospectively 42 patients with UC and 74 without IBD (controls) who were undergoing colonoscopy. Prior consent of all patients and approval of the institutional ethics committee were obtained. The UC diagnosis was established by standard clinic, radiologic, endoscopic, and histologic criteria. The extent of ulcerative colitis was determined by histology. The gastric H. pylori status was assessed by serology (Cobas-Core EIA; Roche Diagnostic Systems, Basel, Switzerland) (12) and 13 C urea breath test ( 13 C-UBT; NDIRIS; Wagner Analysen Technik, Bremen, Germany) (13). Patients' characteristics, including gastric H. pylori status, are shown in Table 1.Colonoscopic biopsy fragments were taken from the rectum, the sigmoid, descending, transverse, and ascending colon, the cecum, and the terminal ileum of each patient for culture and PCR. For culture, one fragment from each region was ground separately in a glass tissue grinder and plated onto Belo Horizonte medium (11) supplemented with polymyxin B plus bacitracin (Sigma Chemical Co., St. Louis, Mo.). The culture conditions and detailed characterization of the isolates were as previously described (10).DNA from bacteria and mucosal fragments was extracted with a QIAamp DNA minikit (Qiagen GmbH, Hilden, Germany).Primers C70 and B37 were used to amplify a product of ϳ1.5 kb from the 16S rRNA gene of the isolated strains (10). The amplicons were then purified and directly sequenced as described by Queiroz et al. (10). The sequences were aligned and compared with those in the GenBank database.For the detection of Helicobacter DNA in fragments of the intestinal mucosa, the 16S rRNA gene was amplified by nested PCR using an outer prime...

Association between H. pylori infection, iron deficiency and iron deficiency anaemia has been described, but the mechanisms involved have not been established. We hypothesized that in H. pylori infected children increased gastric concentrations of IL-1β and/or TNF-α, both potent inhibitors of gastric acid secretion that is essential for iron absorption, are predictors for low blood concentrations of ferritin and haemoglobin, markers of early depletion of iron stores and anaemia, respectively. We evaluated 125 children undergoing endoscopy to clarify the origin of gastrointestinal symptoms. Gastric specimens were obtained for H. pylori status and cytokine evaluation and blood samples for determination of iron deficiency/iron deficiency anaemia parameters and IL1 cluster and TNFA polymorphisms that are associated with increased cytokine secretions. Higher IL-1β and TNF-α gastric concentrations were observed in H. pylori-positive (n = 47) than in -negative (n = 78) children. Multiple linear regression models revealed gastric IL-1β, but not TNF-α, as a significant predictor of low ferritin and haemoglobin concentrations; results were reproduced in young children in whom IL1RN polymorphic genotypes associated with higher gastric IL-1β expression and lower blood ferritin and haemoglobin concentrations. In conclusion, high gastric levels of IL-1β can be the link between H. pylori infection and iron deficiency/iron deficiency anaemia in childhood.