Background: ‘Helicobacter pylori' “H. pylori” is one of the most common infections
that colonizes human gastric mucosa and generates reactive oxygen and nitrogen
species. The aim of this study was to evaluate the oxidative stress markers in the gastric
mucosa of “H. pylori”– infected children.
Patients and Methods: The present study was carried out on 60 children infected with “H.
pylori” including 28 males, 32 females with their age ranging from 7-10 years and mean
age value of 8.5 ± 1.65 years (Group I). This study included also 60 healthy children as a
control group including 26 males and 34 females with their age ranging from 7-11 years
and mean age value of 8.99 ± 1.63 years (Group II). All children were subjected to full
history taking, thorough clinical examination, diagnosis of “H. pylori” infection through
“H. pylori” stool antigen testing using enzyme immunoassay kit (Group I and II) and gastric
antrum mucosal biopsies which were tested for urease activity using Campylobacter
like organism test (CLO test) (Group I only) and measurement of gastric mucosal oxidative
stress markers including Malondialdehyde (MDA), Superoxide dismutase (SOD), reduced
glutathione (GSH), Catalase and nitric oxide (NO) [The sum of Nitrite (NO2
Results: The main clinical presentations in studied patients and controls were recurrent
abdominal pain, recurrent vomiting, dyspepsia and hematemesis with no significant difference
between patients and controls as regard abdominal pain, vomiting or dyspepsia
but hematemesis was found only in patients. There were significant differences between
patients and controls as regard site and duration of abdominal pain with epigastrium being
the most common site of pain in patients versus diffuse abdominal pain in control group
with significantly longer duration of abdominal pain in patients compared with controls.
“H. pylori” infected children has significantly lower gastric mucosal nitric oxide and
reduced glutathione and significantly higher gastric mucosal MDA, catalase and SOD
compared to controls (nitric oxide was 85.68 ± 23.16 nmol/gm in patients versus
106.423±2.111 nmol/gm in controls, reduced glutathione in patients was 1.83 ± 0.16
nmol/gm versus 2.44 ± 0.07 nmol/gm in controls, MDA in patients was 189.15 ± 6.14
nmol/gm versus 166.21 ± 3.13 nmol/gm in controls, catalase was 57.38 ± 19.85 unit/gm
in patients versus 36.51 ± 2.34 unit/gm in controls and SOD in patients was 375.52 ±
26.51 unit/gm versus 318.51 ± 32.06 unit/gm in controls.
Conclusion: “H. pylori” infection is associated with gastric mucosal oxidative stress with
significantly lower gastric mucosal nitric oxide and reduced glutathione and significantly
higher gastric mucosal MDA, Catalase and SOD in patients compared to controls.
Recommendations: Antioxidants may be an important adjuvant therapy for “H. pylori”
infection as this infection is associated with gastric mucosal oxidative stress.