Search

Aim: The association between Helicobacter pylori infection and gastrointestinal symptoms is debatable in childhood. We examined the potential relationship between H. pylori infection and gastrointestinal symptoms in Brazilian children with nonulcer dyspepsia., Methods: This prospective observational study analysed 240 Brazilian children and adolescents (68.7% girls) with chronic nonulcer dyspepsia, who underwent upper gastrointestinal endoscopy and biopsy. Their mean age was 9.8 years (range 4-17). Upper gastrointestinal symptoms, including abdominal pain, nausea, burning, early satiety, belching and weigh loss, were evaluated by a questionnaire and H. pylori infection was determined by histopathology of gastric biopsies., Results: H. pylori infection was identified in 123/240 patients (52%). There was no significant association between the H. pylori infection and gastrointestinal symptoms and no relationship between the infection and abdominal pain or pain characteristics. However, nausea was significantly associated with the H. pylori infection, with an odds ratio of 1.76 and 95% confidence interval of 1.1-2.94 p < 0.03. Symptoms lasting longer than 12 months were significantly more frequent in children with pangastritis than in those with antral gastritis (p < 0.05)., Conclusion: The prevalence of H. pylori infection was high in Brazilian children with nonulcer dyspepsia, but was not associated with specific signs and symptoms, except for nausea., (©2016 Foundation Acta Paediatrica. Published by John Wiley & Sons Ltd.)

The aim of this study was to investigate the role of TLR2, TLR4 and MyD88 in sepsis-induced AKI. C57BL/6 TLR2(-/-), TLR4(-/-) and MyD88(-/-) male mice were subjected to sepsis by cecal ligation and puncture (CLP). Twenty four hours later, kidney tissue and blood samples were collected for analysis. The TLR2(-/-), TLR4(-/-) and MyD88(-/-) mice that were subjected to CLP had preserved renal morphology, and fewer areas of hypoxia and apoptosis compared with the wild-type C57BL/6 mice (WT). MyD88(-/-) mice were completely protected compared with the WT mice. We also observed reduced expression of proinflammatory cytokines in the kidneys of the knockout mice compared with those of the WT mice and subsequent inhibition of increased vascular permeability in the kidneys of the knockout mice. The WT mice had increased GR1(+low) cells migration compared with the knockout mice and decreased in GR1(+high) cells migration into the peritoneal cavity. The TLR2(-/-), TLR4(-/-), and MyD88(-/-) mice had lower neutrophil infiltration in the kidneys. Depletion of neutrophils in the WT mice led to protection of renal function and less inflammation in the kidneys of these mice. Innate immunity participates in polymicrobial sepsis-induced AKI, mainly through the MyD88 pathway, by leading to an increased migration of neutrophils to the kidney, increased production of proinflammatory cytokines, vascular permeability, hypoxia and apoptosis of tubular cells.