BACKGROUND: Helicobacter pylori (H. pylori) has been considered a definitive carcinogen in gastric cancer. Telomerase is activated in gastric cancer and some premalignant gastric lesions, including intestinal metaplasia (IM). In this study, we evaluated the relationships of both H. pylori infection and telomerase activity with endoscopic and histologic features in IM. The effects of H. pylori eradication on endoscopic, histologic and biochemical changes were evaluated. METHODS: Endoscopic biopsies were obtained from 43 patients with IM for rapid urease, histologic and telomerase tests. The endoscopic and histologic features, H. pylori infection and telomerase were assessed. After H. pylori eradication, 15 patients were re-evaluated and compared after 4 months. RESULTS: Thirty-four (79.1%) patients were infected with H. pylori. The incidence of H. pylori infection was borderline correlated to the severity of IM (p=0.076). Telomerase was elevated in eight (18.6%) patients. Telomerase tends to be high in subtype III and endoscopic grade III of IM. After H. pylori eradication, endoscopic extent (p=0.039) and histologic severity (p=0.074) showed improvements, and telomerase decreased significantly (p=0.0001). CONCLUSION: Our data suggest that telomerase is associated with the severity and extent of IM and that H. pylori eradication improves the endoscopic and histologic features in IM, and decreases telomerase activity. H. pylori eradication can be considered one of the methods to prevent gastric cancer in patients with H. pylori-infected IM. Further long-term and large-scaled study will be needed.
Female ; Helicobacter Infections/*enzymology ; *Helicobacter pylori ; Human ; Intestinal Mucosa/enzymology/microbiology/*pathology ; Male ; Metaplasia/enzymology/microbiology ; Middle Aged ; Precancerous Conditions/enzymology/microbiology ; Stomach Neoplasms/*enzymology/microbiology ; Telomerase/*metabolism

OBJECTIVETo investigate the protein expression of cyclooxygenase 2 (COX-2) and nuclear factor kappa B (NF-kappaB) in gastric mucosa-associated lymphoid tissue (MALT) lymphoma and its clinical significance.

METHODSProtein expression of COX-2 and NF-kappaB in gastric MALT lymphoma were examined by immunohistochemistry of Envision two-step method. The correlations of COX-2 and NF-kappaB expression with Helicobacter pylori (Hp) infection, clinical stage, depth of tumor invasion, tumor size, recurrent rate and treatment were analyzed by univariate, multivariate and Pearson analysis.

RESULTSThe positive expression of COX-2 and NF-kappaB in gastric MALT lymphoma were 48.9%(23/47) and 36.2% (17/47) respectively, and a positive correlation was found between these two factors(r=0.326,P<0.05). Moreover, COX-2 expression was positively correlated with Hp infection,clinical stage, depth of invasion and tumor size (P<0.05). Univariate analysis showed that the overall survival of gastric MALT lymphoma patients with positive COX-2 protein (59.9 months) was shorter than that of patients with negative COX-2 protein (77.8 months), but the difference was not significant (P>0.05). The survival was significantly shorter in gastric MALT lymphoma patients with positive NF-kappaB protein (26 months) than that of patients with negative NF-kappaB protein (123.2 months)(P<0.05). Multivariate Cox regression analysis revealed that clinicopathological stage was independent prognostic factor, and associated with short survival.

CONCLUSIONUp-regulated expression of COX-2 and activation of NF-kappaB are associated with Hp infection in gastric MALT lymphoma, and their protein expression is correlated with the development of tumor and prognosis.

Cyclooxygenase 2 ; metabolism ; Female ; Gastric Mucosa ; metabolism ; microbiology ; Helicobacter Infections ; metabolism ; Helicobacter pylori ; Humans ; Lymphoma, B-Cell, Marginal Zone ; metabolism ; microbiology ; pathology ; Male ; Middle Aged ; NF-kappa B ; metabolism ; Neoplasm Staging ; Prognosis ; Stomach Neoplasms ; metabolism ; microbiology ; pathology

OBJECTIVETo determine the influence of Helicobacter pylori (H. pylori) on gastric cancer-related antigen MG7 expression.

METHODSThe H. pylori infection and the expression level of antigen MG7 in gastric mucosa were determined by HE stain, PCR, ELISA and immunohistochemistry in 291 patients with H. pylori-related conditions, among whom 34 were followed-up.

RESULTSNo significant difference was found between H. pylori-negative and H. pylori-positive intestinal metaplasia, atrophic gastritis and dysplasia of gastric epithelium in positive rate of antigen MG7 expression. There was significant difference between H. pylori-negative and H. pylori-positive superficial gastritis in the positive rate of MG7 expression (P < 0.05). During follow-up, one of 3 H. pylori-negative cases turned to be H. pylori-positive, and its MG7 expression turned to be higher at the same time. Three of 31 H. pylori-positive patients were discovered as having early gastric cancer, among whom one with antigen MG7 expression (+ + +) was found to have a reduced Mg7 expression accompanied with H. pylori eliminutied after operation.

CONCLUSIONThere is correlationship between H. pylori infection and MG7 expression in superficial gastritis. Although the MG7-positive lesions with H. pylori infection shows a benign nature in morphology, they also have the potential risk of developing into gastric cancer. Therefore, they should be followed up, during which special attention should be paid to patients with increased MG7 expression.

Antibodies, Bacterial ; blood ; Antigens, Neoplasm ; biosynthesis ; DNA, Bacterial ; genetics ; Enzyme-Linked Immunosorbent Assay ; Gastric Mucosa ; metabolism ; microbiology ; pathology ; Gastritis ; metabolism ; microbiology ; Helicobacter Infections ; metabolism ; microbiology ; Helicobacter pylori ; genetics ; growth & development ; immunology ; Humans ; Immunohistochemistry ; Polymerase Chain Reaction ; Stomach Diseases ; metabolism ; microbiology ; Stomach Ulcer ; metabolism ; microbiology

OBJECTIVE: To observe the change in expressions of connexin 32 and connexin 43 after the eradication of Helicobacter pylori (H.pylori) in patients with gastric precancerous lesion. METHODS: The expressions of connexin 32 and connexin 43 in gastric mucosa specimens biopsy under endoscopy were detected by immunohistochemistry. The expressions of connexin 32 and connexin 43 were detected before and after the eradication of H.pylori in 88 patients with gastric precancerous lesion, and in 33 patients with chronic superficial gastritis (CSG). RESULTS: The positive expression rates and the expressional intensity of connexin 32 and connexin 43 in patients with gastric precancerous lesions (51.1% and 54.5%) were lower than those in patients with CSG (100% and 93.9%, P < 0.05).In patients with gastric precancerous lesions,the positive expression rates and the expressional intensity of connexin 32 and connexin 43 in H.pylori positive group (41.4% and 44.8%) were lower than those in H.pylori negative group (70% and 73.3%, P < 0.05). In gastric precancerous lesions group, the positive expression rates of connexin 32 and connexin 43 in H.pylori positive group before the eradication therapy (41.4% and 44.8%, respectively) was lower than those after the eradication of H.pylori (97.9% and 91.7%, P < 0.05); in the eradication failure group, the positive expression rates of connexin 32 and connexin 43 were 40% and 50%. The eradication failure group before the treatment and after the treatment had no statistical significance(P > 0.05). CONCLUSION The expressions of connexin 32 and connexin 43 in patients with gastric precancerous lesions are low, and the eradication of H.pylori can upregulate their expressions.
Adult ; Aged ; Connexin 43 ; biosynthesis ; Connexins ; biosynthesis ; Female ; Gastritis ; metabolism ; microbiology ; Helicobacter Infections ; drug therapy ; metabolism ; Helicobacter pylori ; Humans ; Male ; Middle Aged ; Precancerous Conditions ; metabolism ; microbiology ; Stomach Neoplasms ; metabolism ; microbiology

Although it is difficult to define the term "aging" consensually, in medical fields, usually it means the progressive accumulation of irreversible degenerative changes leading to loss of homeostasis. It is supposable that there is also modest decline in the structure and function of several digestive organs. However, data about this subject are not enough. Main problem in studying aging digestive organ is that discrimination of primary senile change of the organ with secondary one from other senile diseases is not easy. That is, the prevalence of many non-digestive disorders which can badly affect the digestive functions is increasing by aging; for example, diabetes, malignancy, etc. To prove that some phenomenon is as result of pure senile change, it is necessary to exclude secondary one, but, the process is very complicated and difficult. In spite of this limitation, here, I will discuss the senile change of several digestive organs by aging, especially at the view of the gastrointestinal functions, with review of literatures.
*Aging ; Digestive System Diseases/*physiopathology ; Esophageal Diseases/physiopathology ; Humans ; Intestinal Diseases/metabolism/physiopathology ; Stomach Diseases/metabolism/microbiology/physiopathology

BACKGROUND/AIMS: Peroxisome proliferator-activated receptorgamma (PPARgamma), a nuclear transcription factor, plays a critical role in the regulation of gene expression associated with inflammation and cancer. PPARgamma is expressed in human gastric cancer as well as in colon cancer. Activation of PPARgamma by ligand produces pro-apoptotic effect and ameliorate growing of cancer cells. Helicobacter pylori (H. pylori) is a main etiologic agent for gastric inflammation, and raises cell turnover in gastric epithelium. Longstanding infection with this organism is related with the development of non-cardiac gastric cancer. The aim of this study was to investigate the effect of H. pylori on the expression of PPARgamma protein and mRNA in chronic gastritis. METHODS: Gastric biopsy samples were taken from H. pylori infected (n=18) and non-infected (n=21) patients during endoscopic examination. PPARgamma expressions were assessed by real time polymerase chain reaction and immunohistochemistry. RESULTS: PPARgamma was localized to the nuclei of the foveolar epithelial cells in both infected and non-infected mucosa. PPARgamma protein expression was higher in H. pylori infected patients than in non-infected patients (3.8+/-0.4 vs. 2.6+/-1.0, H. pylori infected and non-infected, respectively; p<0.05). However, PPARgamma mRNA levels were not significantly different between the two groups (24+/-18 vs. 29+/-25, H. pylori infected and noninfected, respectively). CONCLUSIONS: PPARgamma expression is increased in the gastric mucosa of H. pylori infected chronic gastritis, which suggests a certain role of PPARgamma in the mucosal inflammatory reaction to H. pylori infection.
Adult ; Colonic Neoplasms/metabolism/microbiology/pathology ; Computer Systems ; Female ; Gastric Mucosa/*metabolism/microbiology/pathology ; Gastritis/*metabolism/microbiology/pathology ; Helicobacter Infections/*metabolism/microbiology ; *Helicobacter pylori ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; PPAR gamma/*metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Stomach Neoplasms/metabolism/microbiology/pathology

This study was carried out to evaluate the prevalence and clinical characterizations of gastric Helicobacter spp. infection of dogs and cats in Korea. The prevalence of Helicobacter spp. infection of dogs and cats determined by urease test was 78.4% and 64%, respectively, although Helicobacter genus-specific PCR assay showed that it was 82.3% and 84%. Urease mapping results based on urease test showed that total positive rate of tested tissues from clinically abnormal dogs was significantly higher than that from clinically normal dogs (p=0.0018; Odds ratio = 6.118; 95% Confidence Interval = 1.96~19.103). These findings were consistent with the results of Helicobacter genus-specific PCR assay which showed that positive rate of the fundus (100%) and the antrum (100%) of clinically abnormal dogs was significantly higher than that of same gastric regions of clinically normal dogs (77.5 and 67.5% respectively). In comparison of gastric regions between clinically normal dogs and abnormal dogs, positive rate of urease test for the fundus (100%) and body (90.9%) in clinically abnormal dogs was significantly higher than that of abnormal dogs (72.5% and 57.5% respectively; p<0.05). The results of urease mapping in dogs and cats also indicated that Helicobacter colonization in the fundus was more dense compared with the density in the body and antrum. In Helicobacter species-specific PCR assay for dogs, 32 of 42 fundic tissues (76.2%) were positive for H. heilmannii and two (4.8%) were positive for H. felis. In cats, 18 of 21 fundic tissues (85.7%) were positive for H. heilmannii and 2 (9.5%) were positive for H. felis. Gastritis scores of fundic tissues from clinically abnormal infected dogs were similar to that from noninfected dogs and evidence of upregulation of IL-1beta, IL-8, and TNF-alpha mRNA was not detected in gastric fundic tissues from clinically abnormal infected dogs. This study suggested that Helicobacter spp. infection in domestic dogs including private owned pet dogs and cats is highly prevalent usually with no clinical sign but high density of colonization can be related to gastrointestinal signs
Animals ; Cat Diseases/enzymology/*epidemiology/microbiology ; Cats ; Cytokines/genetics ; DNA, Bacterial/analysis/genetics ; Dog Diseases/enzymology/*epidemiology/microbiology/pathology ; Dogs ; Gene Expression Regulation ; Helicobacter/classification/genetics/isolation&purification ; Helicobacter Infections/*epidemiology/microbiology/pathology/*veterinary ; Korea/epidemiology ; Polymerase Chain Reaction ; Prevalence ; RNA, Messenger/genetics/metabolism ; Species Specificity ; Stomach/microbiology ; Stomach Diseases/enzymology/*epidemiology/microbiology/*veterinary ; Urease/metabolism

BACKGROUND/AIMS: Oxidative stress may contribute to gastric epithelial damage and mutagenesis caused by Helicobacter pylori (H. pylori). H. pylori induces recruitment and activation of inflammatory cells, which produces reactive oxygen species. H. pylori extract directly induces the synthesis of reactive oxygen species in gastric epithelial cells and causes DNA damage. The aim of this study was to investigate the association between the levels of glutathione (GSH) and H. pylori density, histological findings, endoscopic findings, clinical variables, and virulence factors. METHODS: Gastric biopsy specimens were obtained from 73 consecutive patients. The 5,5'-dithiobis-(2-nitrobenzoic acid) reaction was used to determine GSH levels. RESULTS: The infection rate of H. pylori was 68.5%. The GSH level was not related to age, sex, alcohol intake, and endoscopic findings. The GSH level was lower in patients infected with H. pylori. GSH levels were not correlated significantly with the grades of neutrophil, intestinal metaplasia, and atrophy. However, the GSH levels were significantly correlated with H. pylori density (r=-0.296, p=0.01) and monocyte grade (r=-0.257, p=0.02). The GSH levels were not related to CagA, VacA, and UreA. CONCLUSIONS: This study suggests that H. pylori causes oxidative stresses which deplete GSH in gastric mucosa of patients infected with H. pylori.
Adolescent ; Adult ; Aged ; Female ; Gastric Mucosa/*metabolism/pathology ; Glutathione/*metabolism ; Helicobacter Infections/*metabolism/pathology ; *Helicobacter pylori ; Humans ; Male ; Middle Aged ; Oxidative Stress ; Stomach Diseases/*metabolism/microbiology/pathology

BACKGROUND/AIMS: Oxidative stress may contribute to gastric epithelial damage and mutagenesis caused by Helicobacter pylori (H. pylori). H. pylori induces recruitment and activation of inflammatory cells, which produces reactive oxygen species. H. pylori extract directly induces the synthesis of reactive oxygen species in gastric epithelial cells and causes DNA damage. The aim of this study was to investigate the association between the levels of glutathione (GSH) and H. pylori density, histological findings, endoscopic findings, clinical variables, and virulence factors. METHODS: Gastric biopsy specimens were obtained from 73 consecutive patients. The 5,5'-dithiobis-(2-nitrobenzoic acid) reaction was used to determine GSH levels. RESULTS: The infection rate of H. pylori was 68.5%. The GSH level was not related to age, sex, alcohol intake, and endoscopic findings. The GSH level was lower in patients infected with H. pylori. GSH levels were not correlated significantly with the grades of neutrophil, intestinal metaplasia, and atrophy. However, the GSH levels were significantly correlated with H. pylori density (r=-0.296, p=0.01) and monocyte grade (r=-0.257, p=0.02). The GSH levels were not related to CagA, VacA, and UreA. CONCLUSIONS: This study suggests that H. pylori causes oxidative stresses which deplete GSH in gastric mucosa of patients infected with H. pylori.
Adolescent ; Adult ; Aged ; Female ; Gastric Mucosa/*metabolism/pathology ; Glutathione/*metabolism ; Helicobacter Infections/*metabolism/pathology ; *Helicobacter pylori ; Humans ; Male ; Middle Aged ; Oxidative Stress ; Stomach Diseases/*metabolism/microbiology/pathology

Intestinal metaplasia (IM) has been regarded as a premalignant condition. However, the pathogenesis of IM is not fully understood. The aim of this study was to evaluate the role of CDX1 and CDX2 in the formation of IM and the progression to dysplasia and gastric cancer (GC). A total of 270 subjects included 90 with GC, dysplasia and age- and sex-matched controls. Real-time PCR (RT-PCR) was performed with body specimens for CDX1 and CDX2. The expression of CDX2 was significantly higher in H. pylori positive group than H. pylori negative group (P = 0.045). CDX1 and CDX2 expression increased proportional to the IM grade of the body (P < 0.001). CDX2 expression was significantly higher in incomplete type of IM than in complete type (P = 0.045). The expression of CDX1 in dysplasia group was significantly higher than in the control group (P = 0.001); in addition, CDX1 and CDX2 in cancer group was significantly higher than control group (P < 0.001, and P < 0.001, respectively). Aberrant expression of CDX1 and CDX2 correlated with H. pylori infection and grade of IM in the body. Furthermore, the results suggest that CDX1 and CDX2 play a role in the progression to GC and dysplasia.
Aged ; Female ; Helicobacter Infections/complications/microbiology ; Helicobacter pylori/isolation & purification ; Homeodomain Proteins/*genetics/metabolism ; Humans ; Intestinal Diseases/*genetics/microbiology/pathology ; Male ; Metaplasia/pathology ; Middle Aged ; Polymerase Chain Reaction ; Precancerous Conditions/metabolism/pathology ; Stomach Neoplasms/etiology/*genetics/microbiology