Objective To study the earlier and later clinic results of 64 chronic duodenal ulcer patients treated with high selective vagotomy and mucosal antrectomy (HSV+MA). Methods The clinic results of the patients and the changes of gastrin, motilin and somatostatin in the blood were prospectively investigated. Results Fifty nine (92.2%) patients after 3-6 months of follow-up and 26 (92.9%) patients after 5-8 years of follow-up achieved Visick grates Ⅰ-Ⅱ. No patients died. Gastric acid secretion and infection rate of helicobacter pylori in antral mucosa were significantly reduced after operation. No significant difference was showed in bile acids and total bacterial counts of gastric juice before and after operation. No ulcer recurrence was found by barium meal and endoscopy. There was no significant difference in serum gastrin and plasma motilin before and after operation. The level of somatostatin in the blood of patients after 5-8 years of follow-up was decreased. Conclusion HSV+MA is the better operative treatment for duodenal ulcer, since it can not only effectively and lastingly decrease acid secretion and rates of ulcer recurrence, but also preserve the function of the antrum and pylorus and keep the gastric milieu interne relatively stable.
To explain how to treat common gastric diseases like chronic gastritis, peptic ulcer, functional dyspepsia and gastric oesophageal reflux disease (GORD) based on evidence-based medicine. Through this paper, we try to help readers find and use clinical evidence to solve clinical problems.
Objective To investigate the expressions of monocyte chemoattractant protein-1 (MCP-1) and vascular endothelial growth factor (VEGF) in gastric cancer tissues and normal gastirc mucosa tissues and the situation of helicobacter pylori (HP) infection, and detect their relationships and clinicopathologic significances. Methods Expressions of MCP-1 and VEGF were detected by immunohistochemistry in gastric cancer tissues and normal gastric mucosa tissues (5-10 cm from the mass), and HP was detected in specimen from gastric antrum by Giemsa dyeing method. Results MCP-1 and VEGF expressions in gastric cancer tissues were significantly higher than those in normal gastric mucosa tissues (P＜0.05), but there was no difference in HP positive and negative tissues included the cancer and the normal tissues （P＞0.05）. The expressions of MCP-1 and VEGF in carcinoma with tumordiameter ＞5 cm, poorly differentiated， lymph node metastasis， distant metastasis and Ⅲ+Ⅳ stage of TNM were significantly higher than those with tumor diameter ≤5 cm, well and moderately differentiated， non-lymph node metastasis， non-distant metastasis and Ⅰ+Ⅱ stage of TNM (P＜0.05). Conclusion The high expressions of MCP-1 and VEGF in gastric cancer may relate to tumor angiogenesis and metastasis, but HP infection may be irrelevant.
Objective To evaluate the clinical effectiveness of helicobacter pylori (HP) eradication in treating functional dyspepsia (FD) patients with HP infection. Methods The randomized controlled trials (RCTs) about HP eradication vs. general treatment for FD patients published by April, 2012 were searched in the following databases: CBM, CNKI, WanFang Data, PubMed, Ovid, EMbase and The Cochrane Library (Issue 1, 2012). According to the inclusion and exclusion criteria, two reviewers independently screened studies, extracted data, and evaluated the methodological quality. Then the meta-analysis was conducted using RevMan 5.1 software. Results The total 14 RCTs were included. Among all 2 665 patients involved in, 1 339 were in the treatment group, while the other 1 326 were in the control group. The results of meta-analysis showed that HP eradication was superior to general treatment for FD patients in clinical effects (RR=3.90, 95%CI 3.08 to 4.94, Plt;0.000 01), symptomatic score (WMD=−1.68, 95%CI −1.88 to −1.47, Plt;0.000 01), and improvement of upper abdominal pain (RR=2.84, 95%CI 2.02 to 3.99, Plt;0.000 01). Conclusion With obviously clinical effects, HP eradication can decrease the symptomatic score of dyspepsia, and especially improve upper abdominal pain. For the quality and quantity limitations of the included studies, more well-designed and double blind RCTs are required to further prove this conclusion.
ObjectiveTo summarize the recent advances in the pathogenic mechanism of microorganisms and pancreatic cancer.MethodThrough the retrieval of relevant literatures, the recent progresses in the study of microorganism and pathogenesis of pancreatic cancer were reviewed.ResultsIn recent years, the potential role of intestinal microbiota in the pathogenic mechanism of pancreatic cancer had been studied. The studies found that the microbiome played an important role in the development of pancreatic cancer. Among them, the infections of Helicobacter pylori, oral pathogenic bacteria such as the Porphyromonas ginggivalis, Aggregatibacter actinomycetemcomitans and Phylum fusobacteria, and the changes of composition and diversity of intestinal microflora were closely related to the pancreatic cancer. The microorganisms induced the chronic inflammation and immune response through multiple pathways. The bacterial lipopolysaccharide stimulated the mutations in the KARS gene and mediated the inflammatory response by activating the nuclear factor-κB signaling pathway through Toll like receptor. The oral pathogenic microorganisms and Helicobacter pylori could also promote the cancer progression by secreting toxins that activated cancer-related signaling pathways.ConclusionsBacteria might be important carcinogens. These microorganisms promote development of cancer by causing chronic inflammation, activating cancer-related pathways, activating immune response, oxidative stress, and damaging DNA double strands.
Serum tumor markers CEA, CA19-9, CA72-4 and Helicobacter pylori (H.pylori) antibodies were measured in 162 patients with gastric cancer. CEA, CA19-9 and CA72-4 had sensitivities of 24.0%, 35.5% and 21.9% respectively. CA72-4 provided 100% specifity, compared to 77% and 93% for CA19-9 and CEA. The positive predictive value (PV) in CEA, CA19-9 and CA72-4 was higher than negative PV. Serum CA19-9 and CA72-4 levels rose in tumor of ＞5.0cm in diameter. The CA19-9 increased remarkably when the deeper stomach wall was invased. The significantly elevated CEA, CA72-4 and CA19-9 levels were found in patients who had nodal involvement in more than 50% and distant metastasis. However, the increase of CEA, CA19-9 and CA72-4 were found in undifferentiated tumor. Antibodies to H.pylori were detected in 54% of patients but in only 22% control subjects. A significant association was found between H.pylori infection and gastric cancer (odds ratio=3.75; 95% confidence interval=2.11-5.41, Ｐ＜0.01). Conclusions: CEA, CA19-9 and CA72-4 have higher specifity but lower sensitivity in diagnosis of the gastric cancer. The levels of CEA, CA19-9 and CA72-4 are significantly associated with the diameter, the depth of invasion, nodal involvement, distant metastasis and cell differention. Infection with H.pylori may be an important cause of gastric cancer.
Objective To investigate the efficacy of pantoprazole and omeprazole as part of triple therapy in treatment of duodenal ulcer. Methods Seventy-eight patients with duodenal ulcer and HP-positive were randomized to two groups. A random number table was used to generate random sequence. The sequence was not concealed. No blinding was used. Thirty-nine patients received pantoprazole 40 mg + amoxicillin 1.0 g + clarithromycin 0.5 g (PAC group) and 39 patients received omeprazole 20 mg + amoxicillin 1.0 g + clarithromycin 0.5 g (OAC group), twice daily with duration of 7 days. The follow-up time was 4 to 6 weeks. Results At the end of the treatment, 38 patients completed the study, and 1 patient lost to follow-up in the PAC group; thirty-seven patients completed the study, two patients lost to followup in the OAC group. The results of intention-to-treat analysis and per-protocol analysis showed that the HP eradication rates were 87.2%/89.5% in the PAC group and 87.2%/91.9% in the OAC group (P＞0.05); the clinical improvement rates were 79.4%/81.6% in the PAC group and 82.0%/86.5% in the OAC group (P＞0.05). The side effect rates were 10.6% in the PAC group and 8.1% in the OAC group (P＞0.05). No significant difference was found between the two groups (P＞0.05). Conclusions The PAC group is therapeutically effective for eradication of HP and improves symptoms and has an equivalent effect to OAC group for patients with HP-positive duodenal ulcer. Both drugs are well tolerated.
Objective We aimed to evaluate the prevalence of H.pylori infection and the prevalence of cagA+ strains in patients with and without Barrett’s esophagus. Methods A full literature search to February 2008 was conducted in PubMed, MEDLINE and EMbase databases to identify case-control studies or cohort studies evaluating the prevalence of H.pylori in patients with or without Barrett’s esophagus. Summary odds ratios (OR) and 95% confidence interval (CI) were calculated by RevMan 4.2.8. Results Nineteen studies were identified (16 case-controlled studies and 3 cohort studies). In case controlled studies, the prevalence of H.pylori infection significantly decreased in patients with Barrett’s esophagus as compared subjects with normal endoscopic appearance, with a overall OR of 0.56 (95%CI 0.40 to 0.79). The prevalence of H.pylori infection was no statistically significant difference in patients with Barrett’s esophagus as compared to those with gastroesophageal reflux disease, with a overall OR of 0.86 (95% CI 0.74 to 1.00). In cohort studies, the prevalence of H. pylori was no statistically significant difference in patients with Barrett’s esophagus as compared to patients with normal endoscopic appearance or patients with gastroesophageal reflux disease, with a overall OR of 1.12 (95%CI 0.77 to 1.61) and 1.10 (95%CI 0.32 to 3.83). When the analysis was stratified by the status of cagA, the prevalence of cagA positive strains significantly decreased in patients with Barrett’s esophagus as compared both to subjects with normal endoscopic appearance with OR 0.30 and 95% CI 0.12 to 0.74, and to those with gastroesophageal reflux disease (OR 0.55; 95%CI 0.33 to 0.94). Irrespective of the presence of intestinal metaplasia, similar magnitude for the reduction of H.pylori infection was observed for patients with Barrett’s esophagus and those with normal endoscopic appearance. While accompared with the presence of intestinal metaplasia, Barrett’s esophagus was associated with a significantly reduction as compared to the patients with gastroesophageal reflux disease (OR 0.81, 95%CI 0.68 to 0.98). When stratified analyses were performed, a significant reduction of H.pylori infection was observed only in patients with long-segment Barrett’s esophagus (OR 0.54; 95%CI 0.35 to 0.82), but not in those with short-segment Barrett’s esophagus (OR 0.72; 95%CI 0.43 to 1.20). Conclusion This meta-analysis indicated that the prevalence of H.pylori infection, especially the prevalence of cagA positive strains was significantly lower in patients with Barrett’s esophagus than in subjects with normal endoscopic appearance. However, the prevalence of H. pylori infection was no statistical difference in patients with Barrett’s esophagus as compared to those with gastroesophageal reflux disease. Colonization with cagA positive strains may be protective against the formation of Barrett’s esophagus.
Objective To analyze the relationship between helicobacter pylori (HP) and gastric cancer. Methods We searched CNKI (Jan.1995-Dec.2005) and Wangfandatabase (Jan.1995-Dec.2005). Case-control studies on relationship of helicobacter pylori infection and gastric cancer were collected. Meta-analysis method was used to sum up the odds ratio (OR) and 95%CI of these studies.Results We identified 14 case-control studies with 11 studies of healthy adults versus gastric cancer patients and 4 studies of gastritis versus gastric cancer patients. The results of subgroup analyses based on patients resource showed: statistical difference was founded between healthy adults and gastric cancer patients with pooled OR 2.00 and 95%CI 1.25 to 3.20; no statistical difference was founded between gastritis patients and gastric cancer patients with pooled OR 1.54 and 95%CI 0.68 to 3.50. The results of subgroup analyses based on locations of gastric cancer showed: statistical difference was founded between the non-cardiac gastric cancer patients and the control with pooled OR 3.60 and 95%CI 1.25 to 10.36; no statistical difference was found between cardiac gastric cancer patients and control with pooled OR 0.88 and 95%CI 0.56 to 1.39.Conclusion HP infection can be associated with gastric cancer, and the different conclusions of the 14 reports may be attributed to the locations of gastric cancer and the selection of controls.
ObjectiveTo investigate the relation between colonic adenomatous polyps and Helicobacter pylori infection. MethodsA case-control study was conducted to collect clinical data of patients with colonic adenomatous polyps in People's Hospital of Zhongjiang County from February 2014 to September 2015. Patients with healthy colon of the corresponding period of the hospital were collected as a control group. The difference of positive rate of Hp infection was compared between the colonic adenomatous polyps group and the control group. According to the age, gender, living condition, location, type of pedicle, pathological type and number, the colonic adenomatous polyps group was divided into subgroups and the differences of positive rate of Hp infection were compared among the subgroups. ResultsA total of 219 patients involving 119 cases and 100 controls were included. The positive rate of Hp infection in the colonic adenomatous polyps group was significantly higher than that in the control group (69.7% vs. 52.0%) with a significant difference (χ2=7.239, P=0.007). Among 119 patients with colonic adenomatous polyps, no statistical differences were found in the positive rate of Hp infection among subgroups of different age, gender, living condition, location, type of pedicle, pathological type and number (all P values>0.05). ConclusionHp infection may increase the risk of developing colonic adenomatous polyps.