• Pediatric Gastroenterology, Hepatology & Nutrition
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• 제11권sup1호
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• pp.83-92
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• 2008

Helicobacter pylori is the causative agent of chronic gastritis and has a role in the pathogenesis of peptic ulcer diseases, and gastric cancer. There have been reports suggesting a close link between these gastroduodenal disorders and a state of vitamin C deficiency. In this paper, the past, present and future perspectives on H. pylori infection and vitamin C will be discussed under the following view points. Since the ecological niche of H. pylori is the mucus layer and intercellular junctions of the gastric epithelium, the various kinds of host inflammatory cells motivated by the local and systemic immune responses cannot eliminate the microorganisms. When the invading foreign body is not removed, despite full activation of defense mechanisms, adverse consequences of the immune responses develop on the host gastric mucosa. The reasons for the body vitamin C depletion could be explained as follows; 1) the increased vitamin C consumption by increased oxygen free radical production through the prolonged hypersensitivity reactions in the gastric mucosa, 2) the increased vitamin C oxidation by the nitrite which is formed from nitrate reduction by the intragastric bacteria proliferated in the hypochlorhydric gastric cavity, 3) the strong ${\gamma}$-glutamyltranspeptidase activity of H. pylori which depletes the glutathiones in gastric mucosa. Depletion of glutathiones in the stomach favors irreversible oxidative destruction of ascorbic acid. Both persistent inflammatory burdens in the stomach by H. pylori and resultant vitamin C depletions synergistically and uninhibitedly might aggravate the hypothetical sequence of gastric carcinogenesis: atrophic gastritis${\rightarrow}$intestinal metaplasia${\rightarrow}$dysplasia${\rightarrow}$gastric adenocarcinoma. High intake of vitamin C could reverse the hypothetical sequence of the gastric carcinogenesis via direct and indirect effects on H. pylori and host-parasite relationships.

• 자원환경지질
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• 제48권3호
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• pp.241-246
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• 2015

Helicobacter pylori는 사람의 위점막에서 발견되는 전염성이 있는 중요한 병원균이다. 장기간 기생하면서 만성위염, 소화성궤양, 위 변연부 B세포 림프종, 그리고 위암을 일으키는 세균으로 알려져 있다. 국내에서는 프로톤펌프 억제제(proton pump inhibitor, PPI)와 두 가지 항생제(amoxicillin, clarithromycin)를 포함하는 표준 삼제 요법을 1차 치료로 사용하여 왔으나, 점점 증가하고 있는 항생제 내성으로 인해 제균율은 점차 감소하고 있다. 여기서는 H. pylori의 현재의 치료법들과 이들 치료법들의 문제점들을 검토하고, 표적치료의 필요성과 표적치료에 활용할 수 있는 약물전달체로서의 점토광물의 가능성에 대해 알아보고, 이들을 이용한 새로운 치료 방향에 대한 향후 연구계획 등에 대해서 논하고자 한다.

• 대한한의학원전학회지
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• 제37권1호
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• pp.25-39
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• 2024

Objectives : This paper focuses on recent research related to the relationship between 'Pizhuweiwei(脾主爲衛)' and intestinal flora, and suggests Korean Medical treatment methods that can treat and prevent diseases related to Spleen Deficiency(脾虛) such as ulcerative colitis, atrophic gastritis, diabetes, and obesity that is prevalent today. Methods : This study summarizes recent research results based on various literature on the relationship between the spleen and intestinal flora. Results : Polysaccharides contained in Jianpi herbs(健脾藥) have the effect of increasing beneficial bacteria and maintaining the diversity of intestinal microorganisms to improve intestinal function, managing intestinal metabolites to improve the body's immune function, and regulating the intestinal immune defense system. Therefore, based on the theory of 'Pizhuweiwei(脾主爲衛)', if the symptoms are treated through the spleen with Spleen-strengthening herbal medicinals, it could provide a substantial starting point for improving immunity. Conclusions : Polysaccharides contained in Jianpi herbs(健脾藥) could be considered as potential probiotics based on research findings which show that polysaccharides can regulate the intestinal flora and strengthen weak spleen, playing an important role.

• Journal of Gastric Cancer
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• 제2권3호
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• pp.163-167
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• 2002

Purpose: Interleukin 1$\beta$ (IL-1$\beta$) polymorphisms are associated with hypochlorhydria, atrophic gastritis, and increased risk of gastric cancer in Caucasians. We tried to determine whether the IL-1.. and IL-1 receptor antagonist (IL-1 RN) genetic polymorphisms contribute to the development of gastric cancer and the specific type of gastritis in Korean. Materials and Methods: The study population was comprised of 128 gastric cancer patients with histologically proven carcinoma and 63 normal healthy individuals. Sixty-eight carcinomas were of intestinal-type and sixty tumors were of diffuse-type. No patient had a familial gastric cancer history. The 511 bp and 31 bp polymorphisms in the IL-1.. were genotyped by polymerase chain reaction (PCR)-restriction fragment length polymorphism. The polymorphism of the IL-1 RN was analyzed with variable number tandem repeat after PCR. Results: The genotype of 511C/-31T of IL-1$\beta$ and allele 1 of IL-1 RN was dominant in the present subjects. The allelic frequencies of the C allele IL-1$\beta$, which is a high risk genotype for gastric cancer, were 0.551 and 0.429 in gastric cancer and normal controls, respectively. Statistically, significant difference in allelic frequencies of three polymorphic sites between gastric cancer patients and normal controls, and between intestinal-type and diffuse-type was not observed. Conclusions: These results suggest that the polymorphisms of IL-1$\beta$ and IL-1 RN may not contribute to the development of Korean gastric caner and that other endogenous or exogenous factors will be important for gastric carcinogenesis.

• Asian Pacific Journal of Cancer Prevention
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• 제15권1호
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• pp.215-220
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• 2014

Objective: To determine the expression of E-cadherin, ${\beta}$-catenin, and transcription factor 4 (TCF4) proteins in gastric diseases with relation to Helicobacter pylori infection. Methods: A total of 309 patients including 60 with superficial gastritis (SG), 57 with atrophic gastritis (AG) and 192 with gastric cancer (GC), were enrolled. The expression of E-cadherin, ${\beta}$-catenin, TCF4 proteins in the gastric mucosa was detected by immunohistochemistry and H. pylori infection by immunohistochemistry and PCR. Results: The expression rates of E-cadherin were significantly higher in SG and AG than in GC (P<0.01), while those of ${\beta}$-catenin in the nucleus were significantly lower in SG and AG than in GC (P<0.05). In GC cases, the expression rates of E-cadherin, ${\beta}$-catenin and TCF4 were significantly higher in the intestinal type than in the diffuse type (P<0.05). In GC patients, the expression rate of E-cadherin was significantly higher in the presence of H. pylori than in the absence of infection (P=0.011). Moreover, the expression level of TCF4 and ${\beta}$-catenin protein was significantly higher in the nucleus and cytoplasm in H. pylori positive than in H. pylori negative GC patients, especially in those with the intestinal type (all P < 0.05). Conclusion: The expression of E-cadherin and ${\beta}$-catenin progressively decreases during the process of GC tumorigenesis, while overexpression of TCF4 occurs. H. pylori infection is associated with a significant increase in the expression of E-cadherin and ${\beta}$-catenin in the cytoplasm and nucleus in GC patients, especially those with the intestinal type.

• Journal of Gastric Cancer
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• 제4권3호
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• pp.149-155
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• 2004

Purpose: According to the recent studies, it is shown that the polymorphism of Interleukin $1\beta$ gene is associated with the incidence of gastric cancer caused by the Helicobacter pylori infection. Interleukin $1\beta$ is a cytokine markedly inhibiting gastric acid secretion. Interleukin $1\beta$ production associated with Helicobacter pylori gastric infection may exacerbate mucosal damage including chronic gastritis and atrophic gastritis, may induce eventual neoplasia. Among these Interleukin $1\beta$ gene polymorphisms, polymorphisms at -31 portion and -511 portion may associated with these processes, eventually increase the risk of gastric cancer. We investigated the risk of gastric cancer according to the Helicobacter pylori infection and genetic polymorphism of Interleukin $1\beta$ in gastric cancer patients. Materials and Methods: 176 individuals with gastric cancer and 40 healthy controls were analyzed. Each group was divided into two groups whether they infected with Helicobacter pylori or not. DNA was extracted from the peripheral blood in all groups. The PCR-RFLP method was used for investigating the distribution of genotype of C/C, C/T, T/T at -31 portion and -511 portion. Results: T/T genotype at -511 portion was $19.3\%$ in gastric cancer cases and $10\%$ in controls, which was statistically significant. (P=0.0432) The risk of gastric cancer was increased 4.86 ($1.26\∼18.77$) in group which had T/T genotype. In gastric cancer cases, C/C genotype at 31 portion was $27.6\%$ in group with Helicobacter pylori infection and $12.8\%$ in group without infection, which was statistically significant. (P=0.0047) The risk of gastric cancer was increased 4.82 ($1.81\~12.81$) in group which had C/C genotype. Conclusion: T genotype at -511 portion among the Interleukin $1\beta$ genetic polymorphisms may be the risk factor of gastric cancer. And, with Helicobacter pylori infection, C genotype at -31 portion may be the risk factor of gastric cancer.

• Asian Pacific Journal of Cancer Prevention
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• 제17권2호
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• pp.733-738
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• 2016

Background: Ardabil, a Northwestern province of Iran, was found to have the highest rate of gastric cancer (GC) in the country (ASRs = 51.8/100,000 for males and 24.9/100,000 for females) and one of the highest gastric cardia cancer rates in the world. The aim of the present study was to assess the associations of the cagA and babA2 status of Helicobacter pylori with GC in the Ardabil population. Materials and Methods: A total of 103 patients with non-atrophic gastritis (56) and GC (47), who underwent endoscopy at the Imam Khomeini Hospital in Ardabil, were assessed. The status of 16S rDNA, cagA and babA2 genes was determined using PCR and histopathological assessment was performed. Results: The following genotypic frequency was observed: cagA+ (50.6%), cagA-(49.4%), babA2+ (26.5%), babA2- (73.5%) cagA+/babA2+ (19.3%), cagA-/babA2+ (7.2%), cagA+/babA2-(31.3%), cagA-/babA2-(42.2%). Although the frequency of the cagA+, cagA+/babA2+ and cagA-/babA2+ genotypes in patients with GC (55.6%, 25.9%, and 14.8%, respectively) was higher than in those with NAG (48.2%, 16.1%, and 3.6%, respectively), the difference did not reach significance. In contrast, the presence of the babA2 gene (40.7% vs 19.6%) significantly increased the risk of GC; the age-sex-adjusted odds ratio (95% confidence interval) was 5.068 (1.506-17.058; P=0.009), by multiple logistic regression. Conclusions: It is proposed that the H. pylori babA2 positivity might be considered as an important determinant of GC risk in Ardabil.

• Asian Pacific Journal of Cancer Prevention
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• 제17권3호
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• pp.917-921
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• 2016

However, the incidence of gastric cancer (GC) has been decreased in past decades; GC is the second cause of cancer related death in the world. Evidence has illustrated that several factors including Helicobacter pylori (H. pylori) infection, host genetics, and environmental factors (smoking and particularly diet) may play a crucial role in gastric carcinogenesis. It has been demonstrated that high consumption of fresh fruits, vegetables, high level of selenium and zinc in drinking water, sufficient iron, and cholesterol protect against GC, while; smoked, pickled, and preserved foods in salt, and nitrites increase the risk of GC. Epidemiological studies have also proved that H. pylori infection and a high salt diet could independently induce atrophic gastritis and intestinal metaplasia. Recently, studies have been demonstrated that dietary factors directly influence H. pylori virulence. The use of appropriate diet could reduce levels of H. pylori colonization or virulence and prevent or delay development of peptic ulcers or gastric carcinoma. This is attractive from a number of perspectives including those of cost, treatment tolerability, and cultural acceptability. This review will describe new insights into the pathogenesis of H. pylori in relation to environmental factors, especially dietary, not only to find the developed means for preventing and treating GC, but also for understanding the role of chronic inflammation in the development of other malignancies.

• Journal of Ginseng Research
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• 제34권2호
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• pp.122-131
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• 2010

This clinical study was performed to evaluate whether supplementation of proton pump inhibitor (PPI)-based triple therapy with Korean red ginseng can enhance Helicobacter pylori (H. pylori) eradication and reduce levels of halitosis-associated volatile sulfur compounds (VSCs) in the stomach. Seventy-six patients were randomized into an eradication regimen-only group (n=45) or an eradication regimen plus 10 weeks of Korean red ginseng supplementation group (n=31). The eradication regimen consisted of PPI b.i.d., clarithromycin 500 mg b.i.d., and amoxicillin 1 g b.i.d.. for seven days. Korean red ginseng supplementation commenced on the last day of the eradication regimen. $^{13}C$-urea breath test and halimeter measurements were performed prior to protocol repetition. By intention-to-treat analysis, the H. pylori eradication rate in the Korean red ginseng group (77.4%, 24 of 31) was higher than that in the control group (45.0%, 26 of 45). However, by per protocol analysis, the eradication rate in the Korean red ginseng group was significantly higher than that in the control group (92.3%, 24/26 vs. 69.4%, 26/38; p<0.05). H. pylori infection was significantly associated with increased VSC levels. However, VSC levels decreased significantly in the Korean red ginseng group (p<0.05). In conclusion, supplementation of triple therapy with Korean red ginseng increased the H. pylori eradication rate and led to significant reductions in VSC levels, suggesting the usefulness of this substance in combating H. pylori infection.

• Journal of Preventive Medicine and Public Health
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• 제52권3호
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• pp.179-187
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• 2019

Objectives: In the USA, certain races and ethnicities have a disproportionately higher gastric cancer burden. Selective screening might allow for earlier detection and curative resection. Among a USA-based multiracial and ethnic cohort diagnosed with non-cardia gastric cancer (NCGC), we aimed to identify factors associated with curable stage disease at diagnosis. Methods: We retrospectively identified endoscopically diagnosed and histologically confirmed cases of NCGC at Mount Sinai Hospital in New York City. Demographic, clinical, endoscopic and histologic factors, as well as grade/stage of NCGC at diagnosis were documented. The primary outcome was the frequency of curable-stage NCGC (stage 0-1a) at diagnosis in patients with versus without an endoscopy negative for malignancy prior to their index exam diagnosing NCGC. Additional factors associated with curable-stage disease at diagnosis were determined. Results: A total of 103 racially and ethnically diverse patients were included. Nearly 38% of NCGC were stage 0-Ia, 34% stage Ib-III, and 20.3% stage IV at diagnosis. A significantly higher frequency of NCGC was diagnosed in curable stages among patients who had undergone an endoscopy that was negative for malignancy prior to their index endoscopy that diagnosed NCGC, compared to patients without a negative endoscopy prior to their index exam (69.6% vs. 28.6%, p=0.003). A prior negative endoscopy was associated with 94.0% higher likelihood of diagnosing curable-stage NCGC (p=0.003). No other factors analyzed were associated with curablestage NCGC at diagnosis. Conclusions: Endoscopic screening and surveillance in select high-risk populations might increase diagnoses of curable-stage NCGC. These findings warrant confirmation in larger, prospective studies.