Helicobacter pylori (H. pylori) is a helical Gram-negative bacterium having 4-6 flagella on one end, and was known to the world in 1983 when Barry Marshall and Robin Warren succeeded in culturing H. pylori in human gastric mucosa [1,2]. H. pylori is the pathogen of chronic active gastritis, and is closely connected to the occurrence of duodenal ulcer, gastric ulcer, stomach cancer, MALT (mucosa-associated lymphoid tissue) lymphoma, etc. Moreover, it has been reported to be associated with non-gastrointestinal general symptoms such as iron deficiency anemia, protein losing enteropathy, chronic idiopathic thombocytopenic purpura, and malabsorption [3-7].

On the other hand, interest in gastroduodenal ulcer in children has been relatively low because the disease is rarer in children than in adults and there were restrictions in the application of endoscopy to children, but the recent development of pediatric endoscopy is activating research on pediatric gastroduodenal ulcer [8]. It has already been known that duodenal ulcer is in close connection to H. pylori infection, and it was reported that among Korean pediatric patients 65% of duodenal ulcer cases and 32% of gastric ulcer cases were H. pylori positive [9].

Considering that if H. pylori infection occurs at a young age and is not treated, the infection may last throughout the lifetime, it is important to diagnose and treat the disease properly during childhood [10].

Thus the authors compared clinical and endoscopic findings according to the presence of infection with H. pylori in pediatric patients with gastroduodenal ulcer diagnosed through upper gastrointestinal endoscopy.

H. pylori is a helical Gram-negative bacterium having motile flagella, and is differentiated from Campylobacter mycetoma by fatty acid and the structural characteristics of 16s ribosome RNA sequence. Human is known to be the only host of this bacterium, and its infection route has not been explained clearly yet. There is evidence suggesting human-human transmission, but it is not clear whether the transmission is through the oral-oral route or through the fecal-oral route [11]. If H. pylori infects gastric mucosa, in most cases it causes an immune response and forms an antibody but this does not mean the removal of bacteria or the acquisition of immunity [12].

H. pylori is considered one of crucial factors causing chronic active gastritis and peptic ulcer not only adults but also in children [13], and with regard to the mechanism that H. pylori infection develops from an asymptomatic state to various diseases including peptic ulcer and gastric adenocarcinoma, there have been reports on the virulence factor of H. pylori and the host's immune response [14].

As criteria for determining H. pylori infection, several different 'gold standards' are being used and it is hard to say definitely which is most accurate, but common methods using biopsy tissue obtained through endoscopy are urease test (CLO test), histological methods such as H&E staining, Giemsa staining and Warthin Starry Silver staining, and the culture of H. pylori in a special medium [15].

Because these methods require biopsy tissue obtained through endoscopy, however, they have restrictions in diagnosis and treatment effect evaluation for children as it is not easy to apply endoscopy to children. Thus, mass screening, epidemiological investigation, etc. use H. pylori-specific IgG antibody test or non-invasive methods such as C¹³ or C¹⁴ breath test (UBT) and stool antigen test [16].

The criterion for H. pylori infection used in this study was that H. pylori was detected in endoscopic biopsy tissue treated through Giemsa stain or that the results of UBT and CLO were both positive.

The prevalence of H. pylori in children was reported to increase with aging. Egharia et al. [17] reported that H. pylori positive cases were found among children aged over 7, and among domestic studies Jung et al. [12] divided children into three age groups (10-11, 12-13 and 14-15), compared them and found that the prevalence of infection increased significantly with aging from 10.3% to 15.9% and 20.7%, respectively. In our study, children aged over 2 showed H. pylori infection and the prevalence showed a significant correlation with age.

According to the cause, pediatric peptic ulcer can be divided into primary ulcer associated with H. pylori infection, and secondary ulcer induced by other systemic diseases or drugs like NSAIDS [18]. Kim [19] reported that gastroduodenal ulcer was diagnosed in 22.5% of pediatric patients who received upper gastrointestinal endoscopy for acute abdominal pain, but our study showed relatively low prevalence of 8.2% probably because we included not only those with acute abdominal pain but also pediatric patients complaining of chronic symptoms.

Peptic ulcer may result in complications such as gastrointestinal bleeding, obstruction, perforation, etc. In Lee et al. [20] and Park et al. [21], bleeding was observed most frequently as 43.5% and 57.7%, respectively, and in our study, 13.8% of the pediatric patients found to have bleeding as a complication.

In children, H. pylori gastritis has a close correlation with duodenal ulcer [22]. A study in Toronto [23] reported that all of 13 pediatric patients with duodenal ulcer had chronic antral gastritis associated with H. pylori, and Hassel and Dimmick [24] followed up 27 pediatric patients with duodenal ulcer for 6 years and found that 23 of them had H. pylori positive chronic antral gastritis. There are also other reports that 90-100% of duodenal ulcer patients showed evidence for H. pylori gastritis [25,26]. Accordingly, we can say that primary duodenal ulcer without evidence for H. pylori infection is very rare. In this study, however, only 66.7% of pediatric patients diagnosed with duodenal ulcer were H. pylori positive and this rate was lower than previous reports. This result is probably because we did not exclude pediatric patients administered with antibiotic, bismuth drug, histamine inhibitor or proton pump inhibitor within 4 weeks before endoscopy.

With regard to the association between H. pylori infection and gastroesophageal reflux, studies with adults reported that H. pylori inhibits reflux esophagitis by inducing atrophic gastritis, but the mechanism in children is not clear. Aeri et al. [27] reported that H. pylori infection in children was in a positive correlation with the incidence of reflux esophagitis, and in our study reflux esophagitis was observed in one patient with duodenal ulcer and the case was H. pylori positive but we could not determine the correlation between the two factors because the number of patients was too small.

As to other endoscopic findings accompanying duodenal ulcer, nodular gastritis was most frequent (48.5%) as reported by Kim et al. [28], which was followed by non-specific finding (18.2%) and superficial gastritis (15.1%).

As endoscopic findings accompanying gastric ulcer, nodular gastritis was most frequent (43.3%) and it was followed by erosive gastritis (16.7%) and hemorrhagic gastritis (11.7%) in Lee et al.8), but in our study, erosive gastritis was most frequent (40.0%) and was followed by superficial gastritis (32.0%) and hemorrhagic gastritis (16.0%).

Summing up these results, in pediatric patients with gastroduodenal ulcer, H. pylori infection was not correlated with clinical symptoms. Among endoscopic findings accompanying in duodenal ulcer pediatric patients infected with H. pylori, nodular gastritis showed a significant correlation with H. pylori infection, but the correlation was not observed in gastric ulcer patients. H. pylori infection was not in a statistically significant correlation with gastroduodenal ulcer, but the H. pylori positive rate showed a significant correlation with age.

Future research may need to examine prospectively the relation between H. pylori and gastroduodenal ulcer in the Incheon area.