Electrogastrography Abnormalities in Pediatric Gastroduodenal Disorders

2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Sameer Bhat ◽  
Chris Varghese ◽  
Daniel A. Carson ◽  
Tommy C.L. Hayes ◽  
Christopher N. Andrews ◽  
...  
2016 ◽  
Vol 4 (3) ◽  
pp. 364-373
Author(s):  
Ali Ibrahim Ali Al-Ezzy

AIM: To evaluate the Immunomodulatory effects of CagA expression; pepsinogen I, II & gastrin-17 on PMNs and lymphocytes Fas expression in inflammatory and gastric cells; demographic distribution of Fas molecule in gastric tissue and inflammatory cells.METHODS: Gastroduodenal biopsies were taken from 80 patients for histopathology and H. pylori diagnosis. Serum samples were used for evaluation of pepsinogen I (PGI); (PGII); gastrin-17 (G-17).RESULTS: Significant difference (p < 0.001) in lymphocytes & PMNs Fas expression; epithelial & lamina propria Fas localization among H. pylori associated gastric disorders. No correlation between grade of lymphocytes & PMNs Fas expression in gastric epithelia; lamina propria and types of gastric disorder. Significant difference (p < 0.001) in total gastric Fas expression, epithelial Fas; lamina propria and gastric gland Fas expression according to CagA, PGI; PGII; PGI/PGII; Gastrin-17. Total gastric Fas expression has significant correlation with CagA, PGII levels. Gastric epithelial and gastric lamina propria Fas expression have significant correlation with CagA, PGI; PGII levels. Significant difference (p < 0.001) was found in lymphocytes & PMNs Fas expression; epithelial & lamina propria localization of lymphocytes & PMNs Fas expression according to CagA, PGI; PGII; PGI/PGII; Gastrin-17. Lymphocytes Fas expression have correlation with PGI, PGII, PGI/PGII. PMNs Fas expression have correlation with PGI, PGII.CONCLUSION: Fas gene expression and localization on gastric and inflammatory cells affected directly by H. pylori CagA and indirectly by gastric hormones. This contributes to progression of various gastric disorders according to severity of CagA induced gastric pathology and gastric hormones disturbance throughout the course of infection and disease.


1998 ◽  
Vol 14 (6) ◽  
pp. 467-472 ◽  
Author(s):  
Jay A. Perman ◽  
Barbara Dudley

2013 ◽  
Vol 1 (1) ◽  
pp. 29-34 ◽  
Author(s):  
Abolghasem Ajami ◽  
Mojtaba Shadman ◽  
Alireza Rafiei ◽  
Vahid Hosseini ◽  
Amin TalebiBezmin Abadi ◽  
...  

2018 ◽  
Vol 7 (30) ◽  
pp. 3385-3389
Author(s):  
Tejaswini C. J ◽  
Madhu Srinath ◽  
Shilpa Avarebeel ◽  
Shivanand Shivanand

Pathogens ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 104 ◽  
Author(s):  
Ramsés Dávila-Collado ◽  
Oscar Jarquín-Durán ◽  
Le Thanh Dong ◽  
J. Luis Espinoza

Epstein–Barr virus (EBV) and Helicobacter pylori (H. pylori) are two pathogens associated with the development of various human cancers. The coexistence of both microorganisms in gastric cancer specimens has been increasingly reported, suggesting that crosstalk of both pathogens may be implicated in the carcinogenesis process. Considering that chronic inflammation is an initial step in the development of several cancers, including gastric cancer, we conducted a systematic review to comprehensively evaluate publications in which EBV and H. pylori co-infection has been documented in patients with non-malignant gastroduodenal disorders (NMGDs), including gastritis, peptic ulcer disease (PUD), and dyspepsia. We searched the PubMed database up to August 2019, as well as publication references and, among the nine studies that met the inclusion criteria, we identified six studies assessing EBV infection directly in gastric tissues (total 949 patients) and three studies in which EBV infection status was determined by serological methods (total 662 patients). Due to the substantial methodological and clinical heterogeneity among studies identified, we could not conduct a meta-analysis. The overall prevalence of EBV + H. pylori co-infection in NMGDs was 34% (range 1.8% to 60%). A higher co-infection rate (EBV + H. pylori) was reported in studies in which EBV was documented by serological methods in comparison with studies in which EBV infection was directly assessed in gastric specimens. The majority of these studies were conducted in Latin-America and India, with most of them comparing NMGDs with gastric cancer, but there were no studies comparing the co-infection rate in NMGDs with that in asymptomatic individuals. In comparison with gastritis caused by only one of these pathogens, EBV + H. pylori co-infection was associated with increased severity of gastric inflammation. In conclusion, only relatively small studies testing EBV and H. pylori co-infection in NMGDs have been published to date and the variable report results are likely influenced by geographic factors and detection methods.


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