Influence of<i>Helicobacter pylori</i>infection on ghrelin levels in children

Deng, Zhongliang; Chu, Bo; Xu, Yongjin; Zhang, Bin; Jiang, Lirong

doi:10.3748/wjg.v18.i36.5096

Cited by 18 publications

(13 citation statements)

References 26 publications

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“…Similar results were also obtained by Yang et al [101] , who found lower serum ghrelin levels, reduced body weight and height and lower BMI and body weight gain in H. pylori-infected children, with restored ghrelin levels and increased growth observed one year after H. pylori eradication. Increased plasma and gastric mucosal ghrelin levels after H. pylori eradication were also shown by Deng et al [103] in 50 children with H. pylori-associated functional dyspepsia. However, a study reported by Choe et al [109] failed to show a relationship between H. pylori infection and stomach mucosal ghrelin levels, with no effect of eradication therapy.…”

Section: Weight Controlmentioning

confidence: 70%

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Brain-gut axis in the pathogenesis ofHelicobacter pyloriinfection

Budzyński¹

2014

WJG

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Helicobacter pylori (H. pylori) infection is the main pathogenic factor for upper digestive tract organic diseases. In addition to direct cytotoxic and proinflammatory effects, H. pylori infection may also induce abnormalities indirectly by affecting the brain-gut axis, similar to other microorganisms present in the alimentary tract. The brain-gut axis integrates the central, peripheral, enteric and autonomic nervous systems, as well as the endocrine and immunological systems, with gastrointestinal functions and environmental stimuli, including gastric and intestinal microbiota. The bidirectional relationship between H. pylori infection and the brain-gut axis influences both the contagion process and the host's neuroendocrine-immunological reaction to it, resulting in alterations in cognitive functions, food intake and appetite, immunological response, and modification of symptom sensitivity thresholds. Furthermore, disturbances in the upper and lower digestive tract permeability, motility and secretion can occur, mainly as a form of irritable bowel syndrome. Many of these abnormalities disappear following H. pylori eradication. H. pylori may have direct neurotoxic effects that lead to alteration of the brain-gut axis through the activation of neurogenic inflammatory processes, or by microelement deficiency secondary to functional and morphological changes in the digestive tract. In digestive tissue, H. pylori can alter signaling in the brain-gut axis by mast cells, the main brain-gut axis effector, as H. pylori infection is associated with decreased mast cell infiltration in the digestive tract. Nevertheless, unequivocal data concerning the direct and immediate effect of H. pylori infection on the brain-gut axis are still lacking. Therefore, further studies evaluating the clinical importance of these host-bacteria interactions will improve our understanding of H. pylori infection pathophysiology and suggest new therapeutic approaches.

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Section: Weight Controlmentioning

confidence: 70%

“…Moreover, H. pylori eradication has also been shown to normalize some of these alterations [55,95,[100][101][102][103] .…”

Section: Role Of the Brain-gut Axis In Chronic H Pylori Infectionmentioning

confidence: 96%

Brain-gut axis in the pathogenesis ofHelicobacter pyloriinfection

Budzyński¹

2014

WJG

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“…With similar action as motilin, it has been proposed that the increase in ghrelin level can affect LES pressure and decrease GERD (27). Ghrelin was found to be decreased in both the plasma and gastric cell in H. pylori infection and to be increased after eradication (5,(28)(29)(30). It has been reported that the decrease of ghrelin abolishes the control on LES and increases GERD development (27).…”

Section: Discussionmentioning

confidence: 99%

Effect of H. pylori infection on gastrin, ghrelin, motilin, and gastroesophageal reflux

Eren

Çolak²,

Işıksoy³

et al. 2015

Turk J Gastroenterol

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Background/Aims: To evaluate the occurrence of gastroesophageal reflux and possible mechanisms in Helicobacter pylori infection. Materials and Methods: Symptoms of H. pylori-infected children, their total gastroesophageal reflux episodes, acid exposure percentage, gastrin, ghrelin, and motilin levels were evaluated before and after H. pylori eradication. Results: Forty-two H. pylori-infected children were eligible for this study. Acid exposure % and total reflux episodes before and after H. pylori eradication were 10.2%±14.8% vs. 7.71%±5.0% and 94.7%±102.1% vs. 64.6%±55.0%, respectively (p=0.28, p=0.082). There was an insignificant change in the serum gastrin (93.4±153.8 pmol/L vs. 1.28±149.4 pmol/L, p=0.67), ghrelin (7.69±197.5 pg/mL vs. 8.36±299.5 pg/mL, p=0.274), and motilin (75.1±81.2 pg/mL vs. 97.2±80.5 pg/mL, p=0.206) levels after eradication. Gastrin and ghrelin levels were negatively correlated after H. pylori eradication (r=−0.38, p=0.031). There was no association between gastroesophageal reflux episodes and gastrin, ghrelin, and motilin levels (r=0.25 and p=0.11; r= 0.24 and p=0.13; r=-0.23 and p=0.14, respectively) Conclusion: H. pylori infection is neither protective nor harmful in the gastroesophageal reflux. Neither ghrelin nor motilin levels was associated with gastroesophageal reflux. None of gastrin, ghrelin, and motilin levels was affected by H. pylori infection. There is an inverse association between gastrin and ghrelin levels after H. pylori eradication.

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“…Deng et al. evaluated plasma and gastric ghrelin and body mass index (BMI) before and after H. pylori eradication in 50 children. The authors found that plasma and tissue ghrelin levels significantly increased after successful eradication, although the BMI in the two groups did not differ significantly.…”

Section: Clinical Presentationmentioning

confidence: 99%

“…The gastrointestinal hormone ghrelin regulates food intake in humans and a decreased appetite in H. pylori-infected children has been related to lowplasma ghrelin levels, which returned to normal after H. pylori eradication. Deng et al [33] evaluated plasma and gastric ghrelin and body mass index (BMI) before and after H. pylori eradication in 50 children. The authors found that plasma and tissue ghrelin levels significantly increased after successful eradication, although the BMI in the two groups did not differ significantly.…”

Section: Growth Retardationmentioning

confidence: 99%

Helicobacter pylori Infection in Pediatrics

Iwańczak

Francavailla

2014

Helicobacter

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This review concerns important pediatric studies published from April 2013 to March 2014. New data on pathogenesis have demonstrated that Th1 type cytokine secretion at the gastric level is less intense in children compared with adults. They have also shown that the most significant risk factor for Helicobacter pylori infection is the parents' origin and frequency of childcare in settings with a high prevalence of infection. A new hypothesis on the positive relationship between childhood H. pylori infection and the risk of gastric cancer in adults has been suggested which calls for an implementation of preventive programs to reduce the burden of childhood H. pylori infection in endemic areas. Several studies have investigated the role of H. pylori infection in iron-deficiency anemia, and results support the role of the bacterium in this condition. Antibiotic resistance is an area of intense research with data confirming an increase in antibiotic resistance, and the effect of CYP2C19 genetic polymorphism on proton-pump inhibitor metabolism should be further investigated as cure rates are lower in extensive metabolizers. Studies confirmed that probiotic supplementation may have beneficial effects on eradication and therapy-related side effects, particularly diarrhea in children. PathophysiologyIn numerous studies, the influence of Helicobacter pylori virulence on the development of various diseases has been studied. Alvarez et al. [1,2] studied methylation of some genes predisposing to gastric cancer. They observed that THBS1 and GATA-4 were methylated already in the early stage of infection and are downregulated. HIC-1 demonstrated the lowest level of methylation and therefore, the main mechanism of downregulation has to be different. On the other hand, methylation of promotor regions of MGMT and MLH 1 depended on the duration of the infection. Nodular gastritis was very frequently associated with H. pylori infection in childhood. Nodular gastritis associated with H. pylori infection can commonly occur in childhood and is regarded as benign with no clinical significance. Yang et al. [3] analyzed gastric mucosa-associated lymphoid tissue (MALT) to clarify the significance of nodular gastritis in 80 H. pylori-infected children; histopathologic grading of MALT and immunohistochemistry were evaluated by CD3, CD20, cytokeratin, and Ki-67. On endoscopy, severe nodular gastritis was observed in 47% of the cases and mild gastritis in 34%; gastritis was absent in 19%. Density of H. pylori and lymphocyte infiltration differed among the 3 groups (p = .022 and .025, respectively) and histologic grading for gastric lymphoid infiltrates was compatible, with grade 1 in 59%, grade 2 in 26%, grade 3 in 9%, and grade 4-5 in 5%. The degree of nodular gastritis, density of H. pylori, neutrophil activity, and gastritis score in the antrum varied with MALT grades (p = .003, p = .042, p = .028, and p = .006, respectively). This study suggests that nodular gastritis may present as a significant gastric manifestation and that tho...

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Influence ofHelicobacter pyloriinfection on ghrelin levels in children

Abstract: H. pylori eradication increases the plasma and tissue ghrelin levels in children with H. pylori-associated functional dyspepsia.

Cited by 18 publications

References 26 publications

Brain-gut axis in the pathogenesis ofHelicobacter pyloriinfection

Brain-gut axis in the pathogenesis ofHelicobacter pyloriinfection

Effect of H. pylori infection on gastrin, ghrelin, motilin, and gastroesophageal reflux

Helicobacter pylori Infection in Pediatrics

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