Effect of <Emphasis Type="Italic">Helicobacter bilis</Emphasis> Infection on Human Bile Duct Cancer Cells

Background  

Helicobacter pylori infection is known to be associated with chronic atrophic gastritis, peptic ulcers, and gastric malignancies. However, the effects of other Helicobacter species have not been investigated extensively. In mice, a close relationship is observed between Helicobacter hepaticus and hepatocellular carcinoma, and Helicobacter species can be found in humans, most commonly in extragastric organs. There have also been reports that H. bilis may be associated with biliary malignancies in humans. The effect of H. bilis infection on a human bile duct cancer cell line was investigated in this study.     

Helicobacter pylori in gallbladder mucosa in patients with gallbladder disease

Background

Helicobacter species have been found to be associated with biliary tract diseases. This prospective study was done to determine the prevalence of H. pylori in the biliary tract of patients suffering from gallbladder disease.

Methods

Forty-nine patients undergoing laparoscopic/open cholecystectomy for benign biliary tract diseases were investigated with urea breath test for H. pylori infection of gastric antrum. Bile and gallbladder tissues were studied for presence of H. pylori by rapid urease test, histopathological examination, culture and PCR analysis. Gallbladder specimens from two patients who underwent Whipple??s operation and from 10 cadavers were studied as controls.

Results

The mean (SD) age of patients was 42.4 (11.1) years. Urea breath test was positive in 17 (34.6%) cases. Rapid urease test was negative in all the cases. There was no evidence of H. pylori infection of gallbladder on histopathological examination using H&;E, Giemsa and Warthin Starry stains. H. pylori DNA were detected in 16 patients (32.6%) and none of the 12 controls by PCR analysis (p?=?0.025). The presence of H. pylori DNA in bile and/or gallbladder was associated with positive urea breath test, (p?H. pylori infection of bile and gallbladder.

Conclusions

Nearly three quarters of patients with positive urea breath test have detectable H. pylori DNA in gallbladder tissue. The significance of these findings needs to be further evaluated.     

Helicobacter pylori in Thai patients with cholangiocarcinoma and its association with biliary inflammation and proliferation

Objectives

To investigate whether Helicobacter spp. infection and the cagA of H. pylori are associated with hepatobiliary pathology, specifically biliary inflammation, cell proliferation and cholangiocarcinoma (CCA).

Methods

Helicobacter species including H. pylori, H. bilis and H. hepaticus were detected in the specimens using the polymerase chain reaction (PCR). Biliary inflammation of the liver and gallbladders was semi-quantitatively graded on hematoxylin and eosin (H&E)-stained slides. Biliary proliferation was evaluated by immunohistochemistry using the Ki-67-labelling index.

Results

Helicobacter pylori was found in 66.7%, 41.5% and 25.0% of the patients in the CCA, cholelithiasis and control groups (P < 0.05), respectively. By comparison, H. bilis was found in 14.9% and 9.4% of the patients with CCA and cholelithiasis, respectively (P > 0.05), and was absent in the control group. The cagA gene of H. pylori was detected in 36.2% and 9.1% of the patients with CCA and cholelithiasis, respectively (P < 0.05). Among patients with CCA, cell inflammation and proliferation in the liver and gallbladder were significantly higher among those DNA H. pylori positive than negative.

Conclusions

The present findings suggest that H. pylori, especially the cagA-positive strains, may be involved in the pathogenesis of hepatobiliary diseases, especially CCA through enhanced biliary cell inflammation and proliferation.     

<Emphasis Type="Italic">Helicobacter pylori</Emphasis> May Play a Contributory Role in the Pathogenesis of Primary Sclerosing Cholangitis

Helicobacter pylori (H. pylori) DNA has been identified in human livers and has been implicated in chronic liver disease and liver cancer. To better understand the role of H pylori in primary sclerosing cholangitis (PSC), 25 patients with end-stage PSC and 31 controls were studied. Genomic DNA was extracted from microdissected hilar hepatic ducts of liver explants and was amplified for H pylori DNA. Serum was tested for H pylori antibodies. Helicobacter DNA was detected in 9 of the 56 (16%) patients by 16SrRNA PCR (an additional case [for a total of 18%] was antibody positive). Seven of the 9 cases identified by polymerase chain reaction were positive for the CagA gene, confirming they were H pylori. Seven of the 25 (28%) patients with PSC and 3 of the 31 (9.7%) controls were positive for Helicobacter (P=.087). H pylori DNA was detected in microdissected hilar biliary epithelium in more PSC patients than controls, supporting the hypothesis that bile reflux from the duodenum into the biliary tract might carry H pylori organisms into the proximal biliary system, possibly contributing to PSC development and/or progression in some patients.     

Detection of Helicobacter pylori in paraffin-embedded specimens from patients with chronic liver diseases, using the amplification method

Helicobacter DNA has been detected in the liver specimens of patients with various hepato-biliary diseases. The aim of this study was to investigate the presence of H. pylori DNA in the liver tissue of Iranian patients with chronic liver diseases (CLD). Genomic DNA was extracted from the paraffin sections of 46 liver biopsies of patients with CLD and 13 from patients with metastatic adenocarcinoma as a control group. Polymerase chain reaction (PCR) analysis was carried out using primers for H. pylori 16S rRNA and cagA genes. On analysis, 17 of the 46 patient samples were positive in H. pylori 16S rRNA PCR and 2 of the 13 were positive from the control group. None of the samples were positive for the cagA gene. This study showed the greater presence of H. pylori-like DNA in the liver samples from patients with CLD than in controls.     

Identification of Helicobacter spp. in bile and gallbladder tissue of patients with symptomatic gallbladder disease

Background:

This experimental study was designed to determine if Helicobacter spp. contribute to benign gallbladder disease using polymerase chain reaction (PCR) methods.

Methods:

Patients with benign gallbladder disease scheduled for elective cholecystectomy at New York University Langone Medical Center were recruited from February to May 2008. Bile, gallbladder tissue and gallstones were collected. DNA was isolated from these specimens and amplified via PCR using C97F and C98R primers specific for Helicobacter spp. Appropriate positive and negative controls were used. Products were analysed with agarose gel electrophoresis, sequenced and results aligned using sequencher. Plasma was collected for detection of anti-Helicobacter pylori antibodies via enzyme-linked immunosorbent assay.

Results:

Of 36 patients, 12 patients'' bile and/or tissue were positive for Helicobacter spp. by PCR. Species were most homologous with H. pylori, although other Helicobacter spp. were suggested. Six of 12 patients demonstrated anti-Helicobacter antibodies in plasma, suggesting that the remaining six might have demonstrated other species besides H. pylori. Four of six plasma samples with anti-Helicobacter antibodies were anti-CagA (cytotoxin associated gene) negative.

Discussion:

Helicobacter spp. can be detected in bile and gallbladder tissue of patients with benign gallbladder disease. The contribution of these bacteria to the pathophysiology of gallbladder disease and gallstone formation requires further study.     

Detection of Helicobacter pylori DNA in Human Biliary Tree and Its Association with Hepatolithiasis

Recently, several authors have reported that Helicobacter pylori DNA has been found in human bile. The aim of this study is to investigate the presence of H. pylori in the biliary tree of Koreans, including the bile, biliary epithelium, and gallstones. This study analyzed intrahepatic bile, bile duct tissue, and gallstones from 43 patients with hepatobiliary disease (PTCS group), gallbladder bile and tissue from 23 patients with gallbladder disease (CCT group), and eight patients without hepatobiliary disease (control group). H. pylori was examined by PCR with two different primers. PCR was positive in 4/43 (9.3%) by 26 kDa protein antigen primer and in 5/43 (11.6%) by urease A gene primer in bile from the PTCS group. However, in intrahepatic duct tissue, PCR was positive in only one case. PCR of gallbladder bile, tissue, and intrahepatic duct stones was negative. Upon intrahepatic bile analysis, the pH was significantly lower in PCR-positive than in negative cases (P < 0.05). In conclusion, H. pylori DNA may be present in the bile when there are certain environmental changes, such as lowered pH; however, H. pylori does not colonize the bile duct epithelium. We could find no pathogenetic role for H. pylori in the formation of hepatolithiasis.     

Helicobacter infection in patients with HCV-related chronic hepatitis,cirrhosis, and hepatocellular carcinoma

Chronic hepatitis may progress to cirrhosis and hepatocellular carcinoma (HCC). HCC represents one of the most common human cancers. Incidence rates for this tumor vary widely on a worldwide, suggesting that environmental factors such as infectious microorganisms, carcinogens, or nutrition play a role in its pathogenesis. Several Helicobacter spp. colonize the liver of animals and induce hepatitis. The aim of this study was to determine whether Helicobacter infection was associated with HCV-related liver diseases in humans. Liver tissue samples, including biopsy and surgically excised tissues, were collected from patients positive for hepatitis C viruses (HCV) RNA in the serum. Genomic DNA was extracted from sections of formalin-fixed paraffin-embedded tissues by using the QIAamp Tissue Kit and subjected to polymerase chain reaction (PCR) analysis using two sets of Helicobacter-specific 16S ribosomal RNA primers. To identify positive samples for H. pylori, a set of primers specific for a conserved region in the H. pylori vacA gene were also used. The patients' H. pylori status was determined by ELISA. Forty-one patients (mean age 54.9, range 19–78 years; 24 men) were studied. Thirty patients had chronic viral hepatitis (CH) without (N = 18) or with (N = 12) cirrhosis (CIR), and 11 patients had HCC. Anti-H. pylori IgG was detected in 54%. The expected 422- and 210-bp fragments of Helicobacter 16S rRNA were amplified from 27% of liver samples, including 17% of CH-CIR and 55% of HCC (P = 0.004). The vacA sequence was amplified in 10 of 41(24%) samples (27% of those with HCC).: These data confirm the presence of H. pylori DNA sequences in human liver and suggest an association of Helicobacter spp. with HCV-related chronic liver diseases. Further studies are needed to ascertain whether Helicobacter spp. infection plays a role in the development of HCC.     

Different Expression of S100A8 in Malignant and Benign Gallbladder Diseases

Background

Proteomic analysis is a powerful tool for complete establishment of protein expression. Comparative proteomic analysis of human bile from malignant and benign gallbladder diseases may be helpful in research into gallbladder cancer.

Aims

Our objective was to establish biliary protein content for gallbladder cancer, gallbladder adenoma, and chronic calculous cholecystitis for comparative proteomic analysis.

Methods

Bile samples were collected from patients with gallbladder cancer, gallbladder adenoma, and chronic calculous cholecystitis. Peptides of biliary proteins were separated by two-dimensional liquid chromatography then identified by tandem mass spectrometry.

Results

Up to 544, 221, and 495 unique proteins were identified in bile samples from gallbladder cancer, gallbladder adenoma, and chronic calculous cholecystitis. Forty-three, 16, and 28 proteins with more than one unique peptide, respectively, were identified in the three groups. Among these, 30 proteins including S100A8 were overexpressed in gallbladder cancer, compared with benign gallbladder diseases. We also confirmed, by immunohistochemical analysis, that S100A8 is more abundant in tumor-infiltrating immune cells in cancerous tissue.

Conclusions

Compared with benign gallbladder diseases, consistently elevated S100A8 levels in malignant gallbladder bile and tissue indicate that gallbladder cancer is an inflammation-associated cancer. S100A8 may be a biomarker for gallbladder cancer.     

Detection of Helicobacter species in liver and stomach tissues of patients with chronic liver diseases using polymerase chain reaction-denaturing gradient gel electrophoresis and immunohistochemistry

Objective.Helicobacter DNA has been detected in the hepatobiliary tree of patients with chronic liver diseases (CLD). The presence of H. pylori in the stomach compared with in the liver of the same patients with CLD has not been studied, therefore to the aim of this study was to investigate the presence of Helicobacter DNA and antigens in the liver and stomach of Polish patients with chronic liver diseases using molecular and immunological methods. Material and methods. Gastric mucosa and liver tissue samples and sera were collected from 97 Polish patients with CLD. Anti-H. pylori antibodies were detected by enzyme immunoassay (EIA), and H. pylori-like antigens detected by immunohistochemistry. Helicobacter DNA was detected in stomach and liver samples using a semi-nested Helicobacter genus-specific polymerase chain reaction (PCR) assay, and Helicobacter species identified by denaturing gradient gel electrophoresis (DGGE) and sequencing analysis of amplified PCR products. Results.H. pylori was identified by DGGE and sequence analysis in 60/62 (97%) and 25/25 (100%) of the gastric and liver Helicobacter genus-positive samples, respectively, whereas DNA of H. heilmannii was detected in 2/62 (3%) of the Helicobacter genus-positive gastric samples. H. pyloricagA gene was detected in 23/62 (36%) and 3/25 (12%) gastric and liver tissue samples, respectively. H. pylori-like antigens were detected in 61/97 (63%) gastric mucosa and in 40/97 (41%) liver tissue samples. Conclusions.H. pylori-like organisms appeared to dominate the gastric mucosa and liver tissue of Polish patients with CLD. The prevalence of the cagA gene was higher in stomach compared with liver samples, which suggests a possible role of cagA negative H. pylori-like organisms in CLD. On the other hand, no significant correlation was found between the presence of H. pylori-like DNA and antigens in the liver and liver function tests.     

Association of <Emphasis Type="Italic">Helicobacter pylori</Emphasis> with hepatobiliary stone disease,a prospective case control study

Background

Hepatobiliary stone disease is one of the most common surgical conditions worldwide. There are multiple causative agents responsible for the formation of hepatobiliary stones, and bacterial infection is one of them. The presence of Helicobacter DNA species has been investigated in the biliary epithelium of patients with biliary diseases. However, conflicting results have been observed that may have been due to the small number of subjects studied, difficulty in obtaining a healthy control group, absence of controlling for confounding factors, or ethical and regional differences among populations.

Methods

We investigated the presence of Helicobacter pylori species by PCR of 26-kDa surface antigen specific to H. pylori in bile samples from 50 cases with hepatobiliary stones and 25 controls without hepatobiliary stones. The control group comprised of 20 patients of hydatid cyst disease of liver and 5 patients of right colonic growth.

Result

H. pylori was present in 20 bile samples among cases and was absent in 30 bile samples among cases. Among controls, H. pylori could not be detected. A significant association of the presence of H. pylori with hepatobiliary stone disease was seen (p < 0.001).

Conclusion

There is an association between bile infection with H. pylori and hepatobiliary stone disease.

     

Occult pancreaticobiliary reflux is a pathogenic factor of some benign biliary diseases and gallbladder cancer

Background: Pancreaticobiliary maljunction(PBM) is a well-known high-risk factor for biliary malignant tumors because of constant pancreaticobiliary reflux(PBR). However, the impact of occult pancreaticobiliary reflux(OPR), which is characterized by high bile amylase levels in individuals with anatomically normal pancreaticobiliary junction, on biliary diseases remains unclear. The aim of this study was to assess the correlation between OPR and biliary diseases. Methods: We enrolled 94 consecuti...     

Serodiagnosis of <Emphasis Type="Italic">Helicobacter hepaticus</Emphasis> infection in patients with liver and gastrointestinal diseases: western blot analysis and ELISA using a highly specific monoclonal antibody for <Emphasis Type="Italic">H. hepaticus</Emphasis> antigen

Background  

Helicobacter hepaticus infection might be associated with liver and biliary tract diseases. To investigate its pathogenic role, the properties of anti-H. hepaticus serum antibody in patients with liver and diseases were elucidated.     

Study on the association of helicobacter species with viral hepatitis-induced hepatocellular carcinoma

Helicobacter species are important pathogens and previous studies in mice suggested a link between colonization by Helicobacter hepaticus (H. hepaticus) and hepatocellular carcinoma (HCC). This study aimed at corroborating this potential link in human patients. We used a sensitive and specific Helicobacter ssp PCR assay to screen stool samples from a collective of patients with viral-induced HCC (hepatitis B or hepatitis C) and a control group for presence of Helicobacter ssp DNA. Although retrieving DNA of H. pylori and H. canadensis from stool samples of non-HCC patients, we found no evidence indicating the presence of H. hepaticus in HCC-patients with chronic hepatitis B or hepatitis C. Interestingly we found H. canadensis in a stool sample of a patient presenting with diarrhea. Taken together, our data argue against a pathogenic role of H. hepaticus in viral-induced HCC. Yet, our results do not exclude a role of H. hepaticus in those HCC cases caused by other carcinogens, such as aflatoxin. Moreover, we speculate that H. canadensis might be a novel gastrointestinal pathogen.     

Helicobacter pylori infection is associated with greater impairment of cytochrome P-450 liver metabolic activity in anti-HCV positive cirrhotic patients

Helicobacter pylori gastric infection has been associated with various digestive and extradigestive diseases. In liver disease bacterial infections have been associated with impairment of cytochrome P-450 liver metabolic activity. Moreover, infection by Helicobacter spp. seems to be linked with the development of hepatocellular carcinoma (HCC) in mice. Our aims were to evaluate the influence of H. pylori infection on cytochrome P-450 liver metabolic activity as assessed by means of monoethylglycinexylidide (MEGX) test and to assess the prevalence of H. pylori infection in patients with HCC. Ninety-six hepatitis C virus (HCV) -positive cirrhotic patients, 36 of whom had HCC, were tested for H. pylori infection by means of anti-H. pylori IgG. Patients underwent the MEGX test. Characteristics of the patients were then analyzed on the basis of the presence of H. pylori infection. Seroprevalence of H. pylori infection was similar between cirrhotic patients without (68%) or with (63.8%) HCC. Mean MEGX values were significantly (P < 0.0001) lower in H. pylori infected patients (18.2±13.9 ng/ml) as compared to the noninfected ones (46.9±17.1 ng/ml), independently of Child-Pugh's classification. These differences persisted even after subdividing patients according to the presence of HCC. In conclusion, in anti-HCV positive cirrhotic patients H. pylori infection is associated to an impairment of cytochrome P-450 liver metabolic activity. Seroprevalence of H. pylori infection in HCC patients is similar to that observed in tumor-free cirrhotics.     

Helicobacter pylori in Autoimmune Pancreatitis and Pancreatic Carcinoma

Background:Helicobacter pylori has been suggested to be involved in pancreatic diseases, namely autoimmune pancreatitis and pancreatic carcinoma. We investigated the presence of conserved sequences of Helicobacter in pancreatic tissue and pancreatic juice from patients with chronic nonautoimmune and autoimmune pancreatitis as well as pancreatic ductal adenocarcinoma (PDAC). Methods: 35 pancreatic juices collected during routine endoscopic retrograde cholangiopancreatography and 30 pancreatic tissues were studied. Nested PCR was used to detect H. pylori in the isolated DNA samples. In order to exclude a methodological bias, the samples were analyzed blindly in 2 different laboratories using either conventional or LightCycler PCR for H. pylori urease A and 16S ribosomal DNA. Results: In the pancreas of 11 patients with autoimmune pancreatitis, no H. pylori DNA could be detected. Further, in none of the other tissue samples of chronic pancreatitis or PDAC could we detect any Helicobacter sequences. Out of the pancreatic juice samples, none demonstrated either of the 2 Helicobacter gene sequences investigated. Conclusion: Despite good scientific reasoning for an involvement of Helicobacter in pancreatic diseases, a direct infection of the microbial agent seems unlikely. Rather, the pathomechanism must involve molecular mimicry in autoimmune pancreatitis, or the transformation of nitric food constituents to nitrosamines in pancreatic cancer.     

Helicobacter pylori cagA Status and Peptic Ulcer Disease in Iran

Helicobacter pylori contributes to the development of peptic ulcers and atrophic gastritis. Furthermore, H. pylori strains carrying the cagA gene are more virulent than cagA -negative strains and are associated with the development of gastric adenocarcinoma. The cagA gene is a putative H. pylori virulence factor of unknown function. The aim of this study was to determine the prevalence of the cagA gene among H. pylori isolates and its relationship with peptic ulcer disease in 128 Iranian patients. A total of 107 (83.6%) samples were positive, including 40 (95%) of the 42 patients with duodenal ulcer, 43 (86%) of the 50 patients with gastric ulcer, and 24 (66.6%) of the 36 patients with gastritis. cagA was present in 32 (80%) of 40 strains from duodenal ulcer patients, 33 (77%) of 43 strains from gastric ulcer patients, and 11 (46%) of 24 from gastritis patients. We also attempted to investigate the subtypes of 3′ region of cagA gene in H. pylori strains isolated from Iranian patients and their relation to H. pylori-associated gastroduodenal diseases. The PCR product of cagA positive strains obtained with primer set CAG1/CAG2 differed in size, varying from 642 to 651 bp (subtype A) in 33 isolates to 756 bp (subtype B/D) in 13 isolates. This does not support the view that subtypes of the 3′ region of cagA gene in H. pylori isolated from Iran correlate with the clinical outcomes of H. pylori, but colonization with cagA positive strains was significantly higher among duodenal ulcer than gastritis patients in Iran.     

Atrophic Corpus Gastritis and Helicobacter pylori Infection in Primary Biliary Cirrhosis

Chronic atrophic corpus gastritis, termed as autoimmune corpus gastritis or type A gastritis, and primary biliary cirrhosis (PBC) are characterized by a common immunological process against the exocrine glandular structures of both the stomach and bile duct. However, there has been controversy over whether atrophic corpus gastritis is associated with PBC. Recently, it has been suggested that Helicobacter pylori plays an important role in the early stage of atrophic corpus gastritis due to the induction of autoantibodies that are reactive with a protein in the gastric parietal cells. One hypothesis is that molecular mimicry, possibly resulting from H. pylori infection, might be responsible for initiating an autoimmune response in a predisposed host due to cross-reactivity among gastric mucosal, bile ductular, and bacterial antigens. The aim of this study is to assess whether atrophic changes of the gastric corpus could affect patients with PBC, and to determine the correlation with H. pylori infection. Sixteen patients with PBC were enrolled in this study. All patients were examined by serological studies of anti-pyruvate dehydrogenase (PDH) antibody, anti-H. pylori antibody, gastrin and vitamin B₁₂. Gastroscopy was performed on all patients in order to verify the histological findings and to microscopically identify H. pylori. Atrophic corpus gastritis was found in 2 of 16 patients with PBC (12.5%), one of whom was confirmed to have pernicious anemia, a developed stage of atrophic corpus gastritis. H. pylori infection in the gastric corpus and the anti-H. pylori antibody were found in 7 (43.8%) and 11 (68.8%) of 16 patients, respectively. Anti-H. pylori antibody was confirmed to be positive in both of the patients with atrophic corpus gastritis, although H. pylori was absent in the gastric biopsy specimen. There was a positive correlation between anti-PDH antibodies and anti-H. pylori antibodies in sera from patients with PBC. Atrophic corpus gastritis is not frequently involved in PBC. However, H. pylori is a possible pathogenic factor in atrophic corpus gastritis in PBC patients because of the presence of anti-H. pylori antibody. A positive correlation between the titer of anti-PDH antibodies and the titer of anti-H. pylori antibodies was confirmed. Consequently, H. pylori infection could induce autoimmune responses in the development of both PBC and atrophic corpus gastritis. H. pylori infection associated with PBC requires further study.     

Enterococcal Bactibilia in Patients with Malignant Biliary Obstruction

Biliary obstruction due to pancreaticobiliary malignancy is often accompanied by bactibilia. The aims of this study were to clarify the impact of preoperative antibiotic use on bile bacterial flora and to identify the bile bacteria responsible for postoperative septic complications in patients with malignant biliary obstruction. Eighty-four patients with malignant biliary obstruction underwent a biliary decompression procedure before definitive surgery. In 63 patients (75%), preoperative bile culture was positive, with nine species being detected. Only the incidence of enterococcal bactibilia increased after antibiotic use (P = 0.0009), with a 16% incidence before and 63% after antibiotic use. When analyzing the correlation between preoperative bile bacteria and postoperative complications, only the Enterococcus species was associated with the occurrence of complications (P = 0.037). In conclusion, bile bacterial flora changes after preoperative antibiotic use, with a significant increase in the incidence of enterococcal bactibilia. The Enterococcus species is most responsible for postoperative septic complications in patients with malignant biliary obstruction.     

The prevalence of <Emphasis Type="Italic">Helicobacter pylori</Emphasis> in Japanese children with gastritis or peptic ulcer disease

Background Although Helicobacter pylori infection is typically acquired in childhood, the role of H. pylori infection in gastroduodenal diseases in childhood remains to be defined. The purpose of this study was to evaluate the prevalence of H. pylori infection in children with gastritis, duodenal ulcer, and gastric ulcer.Methods This was a retrospective analysis of 283 Japanese children (mean age, 11.5 years) with non-nodular gastritis (n = 73), nodular gastritis (n = 67), duodenal ulcer (n = 100), and gastric ulcer (n = 43). H. pylori status was based on biopsy tests. Clinical symptoms at the time of endoscopy were analyzed with regard to a possible association with the infection.Results The prevalence of H. pylori in non-nodular gastritis, nodular gastritis, duodenal ulcer, and gastric ulcer was 28.8%, 98.5%, 83.0%, and 44.2%, respectively. H. pylori was significantly linked to duodenal ulcer and gastric ulcers in the age group of 10–16 years, but not in the age group of 9 years and under. In children with H. pylori infection, nodular gastritis was observed in 26.3% of gastric ulcer patients and in 74.7% of duodenal ulcer patients (P < 0.001). H. pylori infection was significantly associated with the prevalence of anemia (P < 0.05).Conclusions H. pylori is the most important causal factor for the development of duodenal ulcer in childhood. While H. pylori infection appears to be a risk factor in gastric ulcer, other causes are responsible for most cases. Nodular gastritis is the most common type of H. pylori gastritis in childhood. Chronic infection with H. pylori is associated with anemia.