• Asian Pacific Journal of Cancer Prevention
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• v.13 no.10
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• pp.5043-5046
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• 2012

The role of Helicobacter pylori status and serum zinc value in gastric disease patients and healthy controls were investigated. Cases used in this work were 45 gastric cancer patients, 44 with peptic ulcers, 52 suffering gastritis and 64 healthy controls, all diagnosed histologically with the controls undergoing medical checkups. Helicobacter pylori status and serum levels of Zn were determined by 13C-urea breath test and flame atomic absorption spectrophotometer, respectively. Our study showed that Helicobacter pylori infection has no change in gastritis, peptic ulcer and gastric cancer group, on the contrast, serum levels of Zn were significantly reduced in gastritis, peptic ulcer and gastric cancer group, compared with healthy controls, and the higher the Zn levels are, the more increased risk of gastric cancer. Helicobacter pylori infection is a cause of gastritis, peptic ulcers and even gastric cancer, while serum zinc level is an indicator of protection of gastric membranes against damage.

• The Journal of Pediatrics of Korean Medicine
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• v.30 no.3
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• pp.42-51
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• 2016

Objectives The purpose of this study is to report a case of iron deficiency anemia in a child with repetitive bleeding in the upper gastrointestinal tract caused by Helicobacter pylori infection, and summarize review of a western literature. Methods A 13-year-old patient, who were suffering from iron deficiency anemia from repetitive bleeding in the upper gastrointestinal tract, was administered by Ikwiseungyang-tang gamibang (益胃升陽湯加味方) and Samchulgeonbitang (蔘出健脾湯). After several tests, we realized that an iron deficiency anemia was related to Helicobacter pylori. Results By herb medication, the patient's symptoms were alleviated. Conclusions Helicobacter pylori infection is one of the reasons of refractory iron-deficiency anemia which is unresponsiveness to oral iron therapy. We report the findings of herb medication along with summarization of a western literature.

• KSBB Journal
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• v.19 no.3
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• pp.187-191
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• 2004

Among 14 medicinal plants selected for the study ethanol (70%) extract of Coptis japonica Makino showed the highest anti-microbial activity against Helicobacter pylori followed by Perilla frutescens var. acuta KUDO, Caesalpinia sappan L. and Schizonepeta tenuifolia Briq. However, anti-urease activity of methanol (80％) extracts was best for Forsythiae Fructus followed by Caesaipinia sappan L. and Schizonepeta tenuifolia Briq. In the second fractionation using water, ethyl acetate and butanol more than 90％ of the anti-urease activity was detected in the ethyl acetate fraction.

• Natural Product Sciences
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• v.23 no.3
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• pp.175-182
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• 2017

This study evaluated the anti-Helicobacter and anti-inflammatory effects of Sohamhyungtang (SHHT). The minimum inhibitory concentration (MIC) of SHHT against Helicobacter pylori (H. pylori) was determined by the agar dilution method. Expression of the H. pylori cagA gene in the presence of SHHT was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Inhibition of H. pylori urease by SHHT was determined by the phenol-hypochlorite assay. Antiadhesion activity of SHHT was measured by urea-phenol red reagent. Inhibition of nitric oxide (NO) production in AGS cells was measured with Griess reagent. Inducible nitric oxide synthase (iNOS) and IL-8 mRNA expression in AGS cells which were infected with H. pylori was determined by qRT-PCR. IL-8 level was measured by enzyme-linked immunosorbent assay (ELISA). The MIC of SHHT was $100{\mu}g/mL$ and the expression of cagA gene was decreased about 25 folds in the presence of SHHT. H. pylori urease was inhibited 90% by SHHT. SHHT inhibited H. pylori adhesion on AGS cell in a concentration dependent manner. mRNA expression of iNOS and IL-8 and the production of NO and IL-8 were significantly decreased in the presence of SHHT. In conclusion, SHHT showed anti-Helicobacter activity and has potent anti-inflammatory effect on H. pylori-induced inflammation in human gastric epithelial AGS cells.

• Korean Journal of Veterinary Pathology
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• v.5 no.1
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• pp.5-8
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• 2001

Prevalence of Helicobacter infection in pet dogs and positive relations between the presence of Helicobacter app. and gastritis were studied. Twenty-one dogs, which died of various disease, were referred from three animal hospitals and necropsied. Upon histopathological examination, Helicobacter-like organisms (HLO) were observed only in the gastric mucosa of 5 (23.5%) out of the 21 stomachs. The bacteria mainly colonized in the mucus, gastric pits, and the lumen of gastric glands. Regardless of HLO infection, there was mild to moderate lymphocytic infiltration in fundic and pyloric mucosa. Average gastritis scores of the group infected with HLO were 1.250${\pm}$0.214 and 1.833${\pm}$0.167 in the fundic and pyloric mucosa, whereas those of uninfected group were 1.000${\pm}$0.165 and 1.625${\pm}$0.239, respectively. Accordingly, we concluded that no association exists between HLO infection and gastritis.

• Journal of Preventive Medicine and Public Health
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• v.32 no.4
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• pp.427-434
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• 1999

Objectives: This study was conducted to determine, by reviewing the literature, whether treatment of Helicobacter pylori infection in patients with non-ulcer dyspepsia affects symptoms. Methods: We retrieved the literature using MEDLINE search, with nonulcer dyspepsia and Hericobacter pylori and treatment as key words, which were reported from 1984 to 1998, and manual literature search. The criteria for inclusion was as follows; 1) The paper should have confirmed nonulcer dyspepsia as case definition. 2) The paper should have peformed a randomized, blind trial. 3) Confirmation of Helicobacter pylori eradication should be done 4 weeks after treatment. 4) studies with no information on measurement of symptoms after treatment were not accepted. The percentage of patients with symptom improvement after eradication therapy for Helicobacter pylori infection was calculated. Cumulative odds ratio was compared by fixed effect model and random effect model as sensitivity and funnel plot was used to evaluate publication bias. Results: The overall effect size of symptom improvement was calculated by cumulative odds ratio. Cumulative odds ratio of random effect model was 4.16(95% CI: 1.55-11.19). Before integrating each effect sizes into common effect size, the homogeneity test was conducted and random effect model was selected(Cochran's Q=41.08 (d.f=10, p<0.001)). The heterogeneity across studies was evaluated and the different methodological aspects of studies led to differences between study results Conclusions: The results suggest that the eradication of Helicobacter pylori in patients with non-ulcer dyspepsia results more symptom improvement. In studios that shows the opposite results there are methodological aspects explaining the heterogeneity.

• Journal of Veterinary Clinics
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• v.25 no.6
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• pp.447-451
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• 2008

This study was aimed to determine the prevalence of Helicobacter spp. in privately owned pet dog's oral cavity samples (saliva, dental plaque, vomitus) and fecal samples in Korea and to evaluate the potential route for transmission. Total 100 patients dogs attending one Veterinary Medical Teaching Hospital were examined by Helicobacter genus-specific PCR assay and these dogs were divided into two groups whether they had gastrointestinal signs (vomiting, nausea and diarrhea) or not. The total detection rate of Helicobacter spp. by PCR in saliva, dental plaque and fecal samples was 23%, 1% and 68% respectively. The difference of prevalence with regarding the gastrointestinal sings was not significant. In vomitus, two of seven samples had positive results. These results suggested that Helicobacter spp. are present in the oral cavity although they were present in very low number and are not like to be normal oral flora of the oral cavity and Helicobacter spp. in dogs could be transmitted through oral-oral, gastrooral and fecal-oral route.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1996.04a
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• pp.197-197
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• 1996

Helicobacter pylori (H. pylori) is a microaerophilic spiral bacterium and infection by it in the human stomach causes gastritis, furthermore, it is considered to be involved in the pathogenesis of peptic ulcers and the development of gastric carcinoma. We assessed the inhibitory activity of new antiulcer drugs against Helicobacter pylori. The activities of new antiulcer agents against Helicobacter pylori strains were determined by the standard agar dilution method with blood agar base #2, supplemented with 5% sheep blood and 4 antibiotics to support growth of these organisms. They were inoculated by multipoint inoculator and incubated at 37$^{\circ}C$ for 3 days under microaerophilic atmosphere. The MIC of antiulcer agents was the lowest concentration that inhibited visible growth of these organisms. According to results of various biochemical tests, these bacteria were identified as Helicobacter pylori strains. And the MIC results showed that the strains were very susceptible to omeprazole and YJA20379s. Some of YJA20379s were more potent than omeprazole. These results suggest that our new antiulcer drugs have potent inhibitory activity against Helicobacter pylori, so that our new antiulcer drugs might be useful for the clinical eradication of gastrointestinal Helicobacter pylori.

• Journal of Gastric Cancer
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• v.2 no.2
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• pp.73-80
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• 2002

In spite the fact that H. pylori infection might be the causative organisms of acute and chronic gastritis, peptic ulcer diseases and the definition as the class I carcinogen by WHO IARC, still debates exist about the relationship between H. pylori and gastric carcinogenesis. Epidemiological and animal studies demonstrated a link between gastric cancer and chronic infection with H, pylori, but the exact mechanism responsible for the development of gastric cancer in H. pylori-infected patients still remain obscure. In order to declare the clear association, definate evidences like that decrement in the incidence of gastric cancer after the eradication of H. pylori in designated area compared to noneradicated region or the blockade of specific mechanism acting on the carcinogenesis by H. pylori infection. The other way is to identify the upregulating oncogenes or downregulating tumor suppressor genes specifically invovled in H. pylori-associated carcinogenesis. For that, we established the animal models using C57BL/6 mice strain. Already gastric carcinogenesis was developed in Mongolian gerbils infected with H. pylori, but there has been no development of gastric cancer in mice model infected with H. pylori after long-term evaluation. Significant changes such as atrophic gastritis were observed in mice model. However, we could observe the development of mucosal carcinoma in the stomach of transgenic mice featuring the loss of TGF-beta sig naling by the expressions of dominant negative forms of type II receptor specifically in the stomach. Moreover, the incidence of gastric adenocarcinoma was significantly increased in group administered with both MNU and H. pylori infection than MNU alone, signifying that H. pylori promoted the gastric carcinogenesis and there might be host susceptibility genes in H. pylori-associated gastric carcinogenesis. Based on the assumption that chronic, uncontrolled inflammation might predispose to carcinogenesis, there have been several evidences showing chronic atrophic gastritis predisposed to gastric carcinogenesis in H. pylori infection. Although definite outcome of chemoprevention was not drawn after the longterm administration of anti-inflammatory drug in H. pylori infection, the actual incidence of atrophic gastritis and molecular evidence of chemoprevention could be obtained. Selective COX-2 inhibitor was effective in decreasing the development of gastric carcinogenesis provoked by H. pylori infection and carcinogen like in chemoprevention of colon carcinogenesis.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.1 no.1
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• pp.9-18
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• 1998