• 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.

• The Korean Journal of Food And Nutrition
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• v.10 no.2
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• pp.186-192
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• 1997

Endoscopic diagnosis and medical management from K43 and C45 patients, whose sex, occupation, character and life patterns are quite different each other, were discussed. The K43 was patient with erosive gastritis, which may caused by maldietary habits and life stresses. Although the effective drugs such as H2-receptor antagonists with atacids, H+/K+-pump inhibitors, prokinetics, colloidal bismuth, and sucralfates, were administrated for long time, symptomatic relief of abdominal pain was not improved. The tests of clinical phathology and abdominal sonogram were normal, visceral hypersensitivity was appeared from barostat test of stomach. However C45 had taken headache during every day life, and endoscopically confirmed as a gastric·duodenal ulcer patiant, which may caused by chronic use of NSAIDs. The her ulceric symptoms were suppressed from active stage to healing stage by using combination therapy for H. pylori with traditional antipeptic ulcer drugs, where as amitriptyline was administrated to the K43 but not effective. Nonulcer dyspepsia and irritable bowel syndrome is pooly defined, and affect about 15% of the population annually in U. S. A. but don't seek medical care. Author would like to point out that statistics for visceral pains are absent in Korea.

• Journal of Gastric Cancer
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• v.14 no.3
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• pp.196-203
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• 2014

Purpose: Vascular endothelial growth factor (VEGF) is one of the most important growth factors for metastatic tumors. To clarify the role of VEGF-A and C in patients with peptic ulcer disease (PUD) or gastric cancer (GC), we evaluated the expression levels of these two molecules. We also analyzed the effect of Helicobacter pylori infection on VEGF-A and C expression levels. Materials and Methods: Patients with dyspepsia who needed diagnostic endoscopy were selected and divided into three groups: nonulcer dyspepsia (NUD), PUD, and GC, according to their endoscopic and histopathological results. Fifty-two patients with NUD, 50 with PUD, and 38 with GC were enrolled in this study. H. pylori infection was diagnosed by the rapid urease test. After RNA extraction and synthesis of cDNA, the expression levels of VEGF-A and C were determined by quantitative reverse transcriptase polymerase chain reaction. Results: The VEGF-C expression level in the PUD and GC groups was significantly higher than that in the NUD group. Moreover, the VEGF-A expression level in the PUD and GC groups was higher than in the NUD group, although the differences were not statistically significant. Significant positive correlations were also observed between the expression levels of these two molecules in the PUD and GC groups. In addition, the expression levels of these two molecules were higher in H. pylori positive patients with PUD or GC than in H. pylori negative patients of the same groups; however, these differences did not reach statistical significance. Conclusions: Up-regulation of VEGF-C expression during gastric mucosal inflammation may play a role in the development of peptic ulcers or GC.