• Journal of Gastric Cancer
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• v.17 no.2
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• pp.180-185
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• 2017

Despite the decreasing incidence and mortality from gastric cancer, it remains a major health problem worldwide. Ninety percent of cases are adenocarcinomas. Here, we report a case of gastric adenocarcinoma developed after successful treatment of prior primary gastric diffuse large B-cell lymphoma (DLBCL). Our patient was an elderly man with primary gastric DLBCL in whom complete remission was achieved after R-CHOP (cyclophosphamide, adriamycin, vincristine, prednisolone plus rituximab) chemotherapy. Helicobacter pylori infection persisted despite adequate treatment leading to sustained chronic gastritis. The mean time to diagnose metachronous gastric carcinoma was seven years. We believe that a combination of many risk factors, of which chronic H. pylori infection the most important, led to the development of gastric carcinoma following primary gastric lymphoma. In summary, patients who have been successfully treated for primary gastric lymphoma should be followed up at regular short intervals. H. pylori infection should be diagnosed promptly and treated aggressively.

• Journal of Microbiology and Biotechnology
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• v.26 no.10
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• pp.1817-1823
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• 2016

Areca nut (AN) chewing is a habit in many countries in Central, Southern, and Southeast Asia. It is strongly associated with the occurrence of oral, pharyngeal, and esophageal cancer as well as systemic inflammation. However, the association between AN intake and the development of gastric lesions has not yet been identified. The aim of this study was to investigate the effect of AN on gastric diseases using a mouse model for Helicobacter pylori infection. We studied four groups of mice: those fed a normal diet (ND), those fed a diet containing 2.5% AN (AD), those fed ND and infected with H. pylori PMSS1 strain (ND/HP), and those fed AD and infected with H. pylori PMSS1 strain (AD/HP). Food intake and body weight were monitored weekly during the experiments. At 10 weeks, the mice were sacrificed, and the stomach weight, H. pylori colonization, and gastric inflammation were evaluated. The stomach weight had increased significantly in the ND/HP and AD/HP groups along with increases in H. pylori colonization; however, there was no significant difference between these two groups with respect to stomach weight and colonization. On histological grading, mononuclear cell infiltration was severer in the AD/HP group than in the ND/HP group. These data suggest that chronic gastric inflammation was aggravated by AN treatment in the mice with H. pylori-induced gastric lesions. Furthermore, as previously suggested, this animal model is useful to determine the effect of potential carcinogens on gastric lesions induced by H. pylori infection.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.6 no.1
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• pp.1-9
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• 2003

Purpose: To investigate the relation of the gastric epithelial cell proliferation, apoptosis and genotypes of H. pylori in children. Methods: Histologic grading by updated Sydney system, PCNA immunostaining, TUNEL method and the genotypes (cagA, picB and iceA) by PCR were performed in H. pylori positive (N=20) and negative (N=20) gastric biopsy specimens. Results: PCNA index was significantly different between H. pylori positive children ($77.4{\pm}13.12$) and H. pylori negative children ($52.3{\pm}12.20$) (p=0.000). There were positive correlations between PCNA index and H. pylori density (r=0.624, p=0.000), polymorphonuclear neutrophil activity (r=0.460, p=0.005) and chronic inflammation (r=0.433, p=0.009). Apoptosis index of H. pylori positive children ($0.70{\pm}0.411$) was significantly higher than of H. pylori negative children ($0.14{\pm}0.201$) (p=0.000). Positive correlations between apoptosis index and H. pylori density (r=0.691, p=0.000), polymorphonuclear neutrophil activity (r=0.585, p=0.000) and chronic inflammation (r=0.535, p=0.001) were noted. As PCNA index increased, apoptosis index significantly increased (r=0.527, p=0.001). The positive rates of genotypes were cagA 90%, picB 75%, iceA1 60% and iceA2 15%, respectively. There were no significant correlations between the status of the genotypes and PCNA index, apoptosis index, the endoscopic findings and the histologic findings. Conclusion: PCNA index and apoptosis index in H. pylori positive children were higher than in H. pylori negative children but were not related to H. pylori genotypes. This study suggested that correlatively increased gastric epithelial cell proliferation and apoptosis are important to pathogenesis of H. pylori infection in children.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2003.11a
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• pp.95-95
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• 2003

Mycoplasmas resemble H. pylori in production of ammonia and induction of inflammatory cytokines from immune and non-immne cells. In Republic of Korea infection rate of H. pylori is relatively high but only a proportion of them invite additional inflammation and progress into gastric cancers. Therefore, additional risk factors cannot be excluded. The presence and identification of mycoplasma were confirmed by semi -nested PCR and sequencing and the results were compared with pathological data. Fifty-six samples collected from Korean chronic gastritis patients were used for the study. Twenty-three (41.1%) were positive to mycoplasmas and all of them were identified as human mycoplasmas, M. faucium, M. fermentans, M. orale, M. salivarium and M. spermatophilum. Mycoplasma-infected chronic gastritis samples showed more severe, additional infiltration of neutrophils than non-infected samples and the difference was significant (P < 0.05). In conclusion human mycoplasma infection may playa role in progression of chronic gastritis to metaplasia by inducing additional inflammation.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.17 no.3
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• pp.186-190
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• 2014

Lymphocytic gastritis (LG) is a rare subtype of chronic gastritis. It is defined as dense proliferation of intraepithelial lymphocytes (IELs) more than 25 lymphocytes per 100 epithelial cells. The known major causes of LG are celiac disease and Helicobacter pylori infection. H. pylori associated LG (HpLG) has more enhanced cytotoxic and apoptotic tendencies than chronic H. pylori gastritis. A 12-year-old girl with postprandial epigastric pain was diagnosed HpLG on endoscopic biopsy. After the 1st eradication therapy, H. pylori bacilli were still found, and urea breathing test was positive. Although the endoscopic finding was partially improved, clinical symptoms and histologic finding were persisted. We could achieve the improvement of clinical symptoms and disappearance of IELs after the 2nd eradication. The discordant of histopathologic and endoscopic improvement occurred after the 1st eradication therapy of HpLG. Therefore the clinical and histopathologic evaluation should be considered as well as endoscopic findings.

• Natural Product Sciences
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• v.21 no.1
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• pp.49-53
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• 2015

Eight isoflavonoid compounds were isolated from the EtOAc fraction of Maackia amurensis which had shown the highest anti-Helicobacter pylori activity among the fractions, using medium pressure liquid chromatography and recrystallization. Based on the spectroscopic data including $^1H$-NMR, $^{13}C$-NMR, HMBC and MS data, the chemical structures of the isolates were determined to be (-)-medicarpin (1), afromosin (2), formononetin (3), tectorigenin (4), prunetin (5), wistin (6), tectoridin (7) and ononin (8). Anti-H. pylori activity of each compound was evaluated with broth dilution assay. As a result, (-)-medicarpin (1), tectorigenin (4) and wistin (6) showed anti-H. pylori activity. (-)-Medicarpin (1) exhibited the most potent growth inhibitory activity against H. pylori with the minimal inhibitory concentration $(MIC)_{90}$ of $25{\mu}M$, and tectorigenin (4) with $MIC_{90}$ of $100{\mu}M$ ranked the second. This is the first study to show the anti-H. pylori activity of M. amurensis, and it is suggested that the stem bark of M. amurensis or the EtOAc fraction or the isolated compounds can be a new natural source for the treatment of H. pylori infection.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.5 no.1
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• pp.11-18
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• 2002

Purpose: It is known that lactoferrin serves as a source of iron for H. pylori in gastric mucosa. This study was undertaken to investigate the relationship between lactoferrin and H. pylori infection coexistent with iron-deficiency anemia by determining the lactoferrin levels in gastric biopsy specimens, and by locating the major sites of lactoferrin expression, according to the presence or absence of iron-deficiency anemia. Methods: Fifty-five adolescents that underwent gastroduodenoscopy were divided into three groups: NL (n=19) for normal controls, HP (n=15) for patients with H. pylori, and IDA (n=21) for patients with H. pylori gastritis and coexisting iron-deficiency anemia. Histopathologic features were graded from to marked on the basis of the Updated Sydney System. The gastric mucosal levels of lactoferrin were measured by immunoassay. Immunohistochemical technique was used to allow identification of the location and quantification of the lactoferrin expression. Results: Lactoferrin levels in the antrum increased significantly, in proportion to, H. pylori density, polymorphonuclear cell infiltration, and chronic inflammation in the histologic specimens. Patients in the HP and IDA groups showed significantly increased mucosal levels of lactoferrin compared with that observed in the normal group (p=0.0001). The lactoferrin level in IDA group tended to be higher than that in the HP group (p=0.2614). The major sites of lactoferrin expression by immunohistochemistry were in glands and neutrophils within epithelium. Lactoferrin was stained weakly in NL, and strongly in HP and IDA. Conclusion: The lactoferrin sequestration in the gastric mucosa of IDA was remarkable, and this finding seems to give a clue that leads to the clarification of the mechanism by which H. pylori infection contributes to iron-deficiency anemia.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.8 no.1
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• pp.1-11
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• 2005

Purpose: The aim of this study was to evaluate the relationship between H. pylori infection and recurrent abdominal pain (RAP) in children and to evaluate the effects of eradication therapy on RAP. Methods: From January 1998 to January 2005, 166 children with RAP (61 male, 105 female) aged $10.0{\pm}3.3$ years were included. Upper gastrointestinal endoscopies were performed for all the patients. All H. pylori infected children (n=70) received the eradication therapy and were divided into two groups: Group Ia (n=52); eradicated, Group Ib (n=18); non-eradicated. H. pylori-negative children (n=96) were divided into three groups according to the medication: Group IIa (n=67); no medication, Group IIb (n=13); acid-suppressant, Group IIc (n=16); both acid-suppressant and antibiotics. Questionnaire for symptoms were asked at the first, 6th, 12th, 24th, and 36th months following the treatment (grade 0; completely resolved, grade 1; definitely improved, but there are occasional episodes of mild abdominal pain, grade 2; no change in the frequency and intensity of abdominal pain). Results: In about 90% of H. pylori positive children, RAP improved in the both H. pylori-eradicated and non-eradicated children in a follow-up survey. In about 75% of H. pylori-negative children, RAP also improved among in the three groups of patients regardless of medication. Conclusion: These results suggest that there was no correlations between improvement of RAP and eradication of H. pylori, and between improvement of RAP and medication. Consequently the reassurance that the children with RAP have no serious organic cause was important to improvement of RAP.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.12
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• pp.5005-5006
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• 2015

Gastric cancer as one of the most common cancers worldwide has various genetic and environmental risk factors including Helicobacter pylori (H.pylori) infection. Recently, loss of a tumor suppressor gene named promyelocytic leukemia (PML) has been identified in gastric cancer. However, no mutation has been found in this gene in gastric cancer samples. Cag A H.pylori protein has been shown to exert post transcriptional regulation of some tumor suppressor genes. In order to assess such a mechanism for PML degradation, we performed in silico analyses to establish any interaction between PML and Cag A proteins. In silico interaction and docking studies showed that these two proteins may have stable interactions. In addition, we showed that imatinib kinase inhibitor can restore PML function by inhibition of casein kinase 2.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.23
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• pp.10489-10493
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• 2015

Background: Gastric cancer is the second most common gastrointestinal cancer and is largely attributed to Helicobacter pylori (H. pylori) infection. In addition, studies have also shown association with Epstein-Barr virus (EBV) in 10% of gastric cancers. This study assessed the characteristics of EBV associated gastric cancers (EBVaGC) in Brunei Darussalam. Materials and Methods: This study included gastric cancers diagnosed between 2008 and 2012, registered with the Department of Pathology RIPAS Hospital, Brunei Darussalam. Clinical case notes were systematically reviewed. Histology specimens were all stained for EBV and also assessed for intestinal metaplasia and H. pylori. Results: There were a total of 81 patients (54 male and 27 females) with a mean age of $65.8{\pm}14.8years$ included in the study. Intestinal metaplasia and active H. pylori infection were detected in 40.7% and 30.9% respectively. A majority of the tumors were proximally located (55.6%), most poorly differentiated (well differentiated 16%, moderately differentiated 30.9% and poorly differentiated 53.1%) and the stages at diagnosis were; stage I (44.4%), stage II (23.5%), stage III (8.6%) and stage IV (23.5%). EBV positivity (EBVaGC) was seen in 30.9%. Between EBVaGC and EBV negative gastric cancers, there were no significant differences (age, gender, ethnic group, presence of Intestinal metaplasia, tumor locations, stages of disease and degree of tumor differentiation). Conclusions: This study showed that a third of gastric cancers in Brunei Darussalam were positive for EBV, higher than what have been reported in the literature. However, there were no significant differences between EBVaGC and EBV negative gastric cancers. This suggests that the role of EBV in gastric cancer may be mostly incidental rather than any causal relation. However, further studies are required.