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Long-term effects of clearing Helicobacter pylori on growth in school-age children.

ABSTRACT: A new Helicobacter pylori infection affects growth velocity negatively, and clearing the infection produces a small significant rebound, but it is not known whether height and weight in children are impacted over the long term.We investigated 295 school-age children followed in 2 cohorts, treated (150) and untreated (145), from 2004 for 3.7 years with 1105 child-years of observation. Follow-up intervals were 3 months for anthropometry measurements and 6 months for H. pylori status ascertained by urea breath test. Height in centimeters and weight in kilograms were analyzed using growth models.A multivariate mixed model that adjusted for age, sex, father's education, and number of siblings found no significant differences in height or weight at baseline by H. pylori status. The same model showed a significant impact of clearing H. pylori across time, with increasing significant differences in average height and weight as the follow-up progressed.Children who were always negative or who cleared the infection grew significantly faster than those who stayed positive after adjusting for other covariates. This study suggests that school-age children's growth benefits from being treated for H. pylori infection.

SUBMITTER: Mera RM

PROVIDER: S-EPMC3415984 | biostudies-literature | 2012 Mar

REPOSITORIES: biostudies-literature

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Long-term effects of clearing Helicobacter pylori on growth in school-age children.

Mera Robertino M RM Bravo Luis E LE Goodman Karen J KJ Yepez Maria C MC Correa Pelayo P

The Pediatric infectious disease journal 20120301 3

<h4>Background</h4>A new Helicobacter pylori infection affects growth velocity negatively, and clearing the infection produces a small significant rebound, but it is not known whether height and weight in children are impacted over the long term.<h4>Methods</h4>We investigated 295 school-age children followed in 2 cohorts, treated (150) and untreated (145), from 2004 for 3.7 years with 1105 child-years of observation. Follow-up intervals were 3 months for anthropometry measurements and 6 months ...[more]

PMID: 22315005

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Project description:Helicobacter pylori (H. pylori) classified as a class I carcinogen by the World Health Organization (WHO) plays an important role in the progression of chronic gastritis and the development of gastric cancer. A major bioactive component of Evodia rutaecarpa, evodiamine, has been known for its anti-bacterial effect and anti-cancer effects. However, the inhibitory effect of evodiamine against H. pylori is not yet known and the inhibitory mechanisms of evodiamine against gastric cancer cells are yet to be elucidated concretely. In this study, therefore, anti-bacterial effect of evodiamine on H. pylori growth and its inhibitory mechanisms as well as anti-inflammatory effects and its mechanisms of evodiamine on H. pylori-induced inflammation were investigated in vitr. Results of this study showed the growth of the H. pylori reference strains and clinical isolates were inhibited by evodiamine. It was considered one of the inhibitory mechanisms that evodiamine downregulated both gene expressions of replication and transcription machineries of H. pylori. Treatment of evodiamine also induced downregulation of urease and diminished translocation of cytotoxin-associated antigen A (CagA) and vacuolating cytotoxin A (VacA) proteins into gastric adenocarcinoma (AGS) cells. This may be resulted from the reduction of CagA and VacA expressions as well as the type IV secretion system (T4SS) components and secretion system subunit protein A (SecA) protein which are involved in translocation of CagA and VacA into host cells, respectively. In particular, evodiamine inhibited the activation of signaling proteins such as the nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) and the mitogen-activated protein kinase (MAPK) pathway induced by H. pylori infection. It consequently might contribute to reduction of interleukin (IL)-8 production in AGS cells. Collectively, these results suggest anti-bacterial and anti-inflammatory effects of evodiamine against H. pylori.

Project description:Helicobacter pylori infection changes gastric microbiota profiles. However, it is not clear whether H. pylori eradication can restore the healthy gastric microbiota. Moreover, there has been no study regarding the changes in gastric microbiota with aging. The objective of this study was to investigate the changes in gastric corpus microbiota with age and following H. pylori eradication. Changes in corpus mucosa-associated microbiota were evaluated in 43 individuals with endoscopic follow-up > 1 year, including 8 H. pylori-uninfected and 15 H. pylori-infected subjects with no atrophy/metaplasia by histology and pepsinogen I/II ratio > 4.0; 17 H. pylori-infected subjects with atrophy/metaplasia and pepsinogen I/II ratio < 2.5; and 3 subjects with atrophy/metaplasia, no evidence of active H. pylori infection, negative for anti-H. pylori immunoglobulin G (IgG) antibody testing, and no previous history of H. pylori eradication. Successful H. pylori eradication was achieved in 21 patients. The gastric microbiota was characterized using an Illumina MiSeq platform targeting 16S ribosomal DNA (rDNA). The mean follow-up duration was 57.4 months (range, 12-145 months), and median follow-up visit was 1 (range, 1-3). Relative abundance of Lactobacillales and Streptococcus was increased with atrophy/metaplasia. In H. pylori-uninfected subjects (n = 8), an increase in Proteobacteria (Enhydrobacter, Comamonadaceae, Sphingobium); a decrease in Firmicutes (Streptococcus, Veillonella), Fusobacteria (Fusobacterium), Nocardioidaceae, Rothia, and Prevotella; and a decrease in microbial diversity were observed during the follow-up (p trend < 0.05). In 10 of 21 subjects (47.6%), H. pylori eradication induced restoration of microbial diversity; however, a predominance of Acinetobacter with a decrease in microbial diversity occurred in 11 subjects (52.3%). The presence of atrophy/metaplasia at baseline and higher neutrophil infiltration in the corpus were associated with the restoration of gastric microbiota after successful eradication, whereas a higher relative abundance of Acinetobacter at baseline was associated with the predominance of Acinetobacter after H. pylori eradication (p < 0.05). To conclude, in H. pylori-uninfected stomach, relative abundance of Proteobacteria increases, relative abundance of Firmicutes and Fusobacteria decreases, and microbial diversity decreases with aging. H. pylori eradication does not always restore gastric microbiota; in some individuals, gastric colonization by Acinetobacter species occurs after anti-Helicobacter treatment.

Dataset Information

Long-term effects of clearing Helicobacter pylori on growth in school-age children.

Publications

Long-term effects of clearing Helicobacter pylori on growth in school-age children.

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