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Abstracts

LE Magazine January 2008
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Correlation between Helicobacter pylori infection, gastric diseases and life habits among patients treated at a university hospital in Southeast Brazil.

Helicobacter pylori is considered a significant agent in the development of various gastric diseases. However, the diseases caused by this bacterium are known as being multi-factorial, with the genotype, immune system and life habits of the host playing important roles in the establishment of the clinical outcome. Also, H. pylori exhibit a high degree of genetic variability, contributing to the complexity of the host-pathogen relationship. These observations, considered together with the widely-varying origins and social habits of the Brazilian population, lead us to speculate about the influence of these life habits on H. pylori infection and the clinical outcome. Therefore, in this study we evaluated the relationship between H. pylori infection and certain diseases in 172 patients treated at the Hospital das Clínicas of Ribeirão Preto (HCRP), Brazil, taking into account their different life habits, such as non-steroidal anti-inflammatory drugs and alcohol ingestion, and smoking habit. Our analysis indicated that H. pylori infection is not affected by any of the life habits evaluated but is associated with the development of peptic ulcers (gastric and duodenal ulcer) and inverse correlate with gastroesophageal reflux disease (GERD). No correlation was found between the infection with this bacterium and gastritis or intestinal metaplasia. However, gastritis and erosive gastritis were directly correlated with non-steroidal anti-inflammatory drugs (NSAID) ingestion. Moreover, ingestion of alcohol beverages exhibited a protective effect on gastritis development in men. Our data also indicated that to achieve reliable detection of this bacterium in biopsies, two or three detection methods should be used.

Braz J Infect Dis. 2007 Feb;11(1):89-95

H pylori infection and other risk factors associated with peptic ulcers in Turkish patients: a retrospective study.

AIM: To identify and evaluate the relative impact of H pylori infection and other risk factors on the occurrence of gastric ulcer (GU), duodenal ulcer (DU) and gastritis in Turkish patients. METHODS: A total of 4,471 patients (48.3% female) out of 4863 attended the Samatya hospital in Istanbul (June 1999-October 2003) were included. The records of H pylori status (CLO-test), endoscopic findings of GU, DU and gastritis, personal habits (smoking, alcohol intake) and medication [non-steroidal anti-inflammatory drugs (NSAIDs), aspirin intake] were analyzed using multi-way frequency analysis. RESULTS: We have found that GU in the presence of H pylori had significant association with aspirin (P=0.0001), alcohol (P=0.0090) and NSAIDs (P=0.0372). DU on the other hand had significant association with aspirin/smoking/NSAIDs (P=0.0259), aspirin/alcohol (P=0.0002) and aspirin/smoking (P=0.0233), also in the presence of H pylori. In the absence of H pylori GU had significant association with alcohol/NSAIDs (P=0.0431), and NSAIDs (P=0.0436). While DU in the absence of H pylori had significant association with smoking/alcohol/ NSAIDs (P=0.0013), aspirin/NSAIDs (P=0.0334), aspirin/alcohol (P=0.0360). CONCLUSION: In the presence of H pylori, aspirin, alcohol and NSAIDs intake act as an independent risk factors that had an augmenting impact on the occurrence of GU and only together on the occurrence of DU in Turkish patients.

World J Gastroenterol. 2007 Jun 21;13(23):3245-8

New Molecular Mechanisms of Duodenal Ulceration.

Stress is a major etiologic factor in the pathogenesis of gastric & duodenal ulceration, as first described in rats by Hans Selye. In patients with “peptic ulcers” duodenal ulcers (DU) are more frequent than gastric ulcers (except in Japan). Thus, our research during the last 3 decades focused on the molecular mechanisms of DU in rodent models of chemically induced DU, and here we review our 3 recent findings: Endothelins (ET-1), the immediate early gene egr-1 & imbalance of angiogenic/anti-angiogenic molecules. Namely, we found an enhanced expression & release of ET-1 within 15-30 min after the administration of duodenal ulcerogen cysteamine, resulting in local ischemia that triggers the expression of hypoxia-inducible factors (HIF-1α). Our gene expression studies also revealed an early (0.5-2 hr) increase in the expression of egr-1 that is followed (12-24 hr) by upregulation of angiogenic growth factors (e.g., VEGF, bFGF, PDGF). Surprisingly, this event is also associated with an enhanced production of angiostatin & endostatin that probably counteract the beneficial effect of angiogenic molecules. Thus, the initial injury to endothelial & epithelial cells in DU seems to be aggravated (& not initiated) by HCl & proteolytic enzymes. The resulting mucosal necrosis does not rapidly heal because of the imbalance of VEGF & angiostatin/endostatin, hence duodenal ulcers develop. The experimental ulcers Selye described morphologically are now characterized at the molecular & genome level, involving unexpected mediators like ET-1, egr-1 & angiogenesis-related molecules.

Ann N Y Acad Sci. 2007 Jul 26

Inflammation, atrophy, and gastric cancer.

The association between chronic inflammation and cancer is now well established. This association has recently received renewed interest with the recognition that microbial pathogens can be responsible for the chronic inflammation observed in many cancers, particularly those originating in the gastrointestinal system. A prime example is Helicobacter pylori, which infects 50% of the world’s population and is now known to be responsible for inducing chronic gastric inflammation that progresses to atrophy, metaplasia, dysplasia, and gastric cancer. This Review provides an overview of recent progress in elucidating the bacterial properties responsible for colonization of the stomach, persistence in the stomach, and triggering of inflammation, as well as the host factors that have a role in determining whether gastritis progresses to gastric cancer. We also discuss how the increased understanding of the relationship between inflammation and gastric cancer still leaves many questions unanswered regarding recommendations for prevention and treatment.

J Clin Invest. 2007 Jan;117(1):60-9

Helicobacter pylori and benign upper digestive disease.

Acute infection with Helicobacter pylori causes hypo-chlorhydria and gastrointestinal upset. As the infection persists, patients develop chronic antral-predominant or pangastritis. Gastric and duodenal ulcers arise from chronic mucosal inflammation and disordered acid secretion in the stomach. With successful eradication of H. pylori, non-NSAID-related gastric and duodenal ulcers heal even without long-term acid suppression. More importantly, peptic ulcers and their complications rarely recur. Clearing H. pylori infection also reduces the risk of mucosal injury in NSAID and aspirin users; the protective effects are more pronounced in NSAID-naïve and aspirin users. H. pylori is unlikely to be the cause of gastro-oesophageal reflux disease. However, a patient’s reflux symptoms may be more difficult to control after clearing the infection. Although there is little evidence to support a causal relationship between H. pylori and non-ulcer dyspepsia, treatment of the infection gives a modest improvement of symptoms.

Best Pract Res Clin Gastroenterol. 2007;21(2):261-79

The inflammatory and immune response to Helicobacter pylori infection.

Lifelong Helicobacter pylori infection and its associated gastric inflammation underlie peptic ulceration and gastric carcinogenesis. The immune and inflammatory responses to H. pylori are doubly responsible: gastric inflammation is the main mediator of pathology, and the immune and inflammatory response is ineffective, allowing lifelong bacterial persistence. However, despite inducing gastric inflammation, most infections do not cause disease, and bacterial, host and environmental factors determine individual disease risk. Although H. pylori avoids many innate immune receptors, specific virulence factors (including those encoded on the cag pathogenicity island) stimulate innate immunity to increase gastric inflammation and increase disease risk. An acquired T helper 1 response upregulates local immune effectors. The extent to which environmental factors (including parasite infection), host factors and H. pylori itself influence T-helper differentiation and regulatory T-cell responses remains controversial. Finally, effective vaccines have still not been developed: a better understanding of the immune response to H. pylori may help.

Best Pract Res Clin Gastroenterol. 2007;21(2):237-59

Helicobacter pylori infection and gastric cancer.

Gastric cancer remains a major health burden on many societies claiming hundreds of thousands of lives every year. The discovery of Helicobacter pylori has no doubt revolutionised our understanding of this malignancy, which is now regarded as a paradigm for infection-induced chronic inflammation-mediated cancer. In this paper, we discuss the evidence for the association between H. pylori and gastric adenocarcinoma and MALT lymphoma. We also discuss the pathogenesis of these two forms of cancer and the factors that determine their outcome. There is no doubt that the knowledge accumulated over the past two decades will be translated into eventual victory over this killer cancer, largely because we now appreciate that the best way to prevent the cancer is by preventing acquisition of the infection in the first place, or by eradicating the infection in infected subjects. Defining the optimal timing of intervention is going to be the challenge facing us over the next two decades.

Best Pract Res Clin Gastroenterol. 2007;21(2):281-97

Correlation between Helicobacter pylori infection, gastric diseases and life habits among patients treated at a university hospital in Southeast Brazil.

Helicobacter pylori is considered a significant agent in the development of various gastric diseases. However, the diseases caused by this bacterium are known as being multi-factorial, with the genotype, immune system and life habits of the host playing important roles in the establishment of the clinical outcome. Also, H. pylori exhibit a high degree of genetic variability, contributing to the complexity of the host-pathogen relationship. These observations, considered together with the widely-varying origins and social habits of the Brazilian population, lead us to speculate about the influence of these life habits on H. pylori infection and the clinical outcome. Therefore, in this study we evaluated the relationship between H. pylori infection and certain diseases in 172 patients treated at the Hospital das Clínicas of Ribeirão Preto (HCRP), Brazil, taking into account their different life habits, such as non-steroidal anti-inflammatory drugs and alcohol ingestion, and smoking habit. Our analysis indicated that H. pylori infection is not affected by any of the life habits evaluated but is associated with the development of peptic ulcers (gastric and duodenal ulcer) and inverse correlate with gastroesophageal reflux disease (GERD). No correlation was found between the infection with this bacterium and gastritis or intestinal metaplasia. However, gastritis and erosive gastritis were directly correlated with non-steroidal anti-inflammatory drugs (NSAID) ingestion. Moreover, ingestion of alcohol beverages exhibited a protective effect on gastritis development in men. Our data also indicated that to achieve reliable detection of this bacterium in biopsies, two or three detection methods should be used.

Braz J Infect Dis. 2007 Feb;11(1):89-95

H pylori infection and other risk factors associated with peptic ulcers in Turkish patients: a retrospective study.

AIM: To identify and evaluate the relative impact of H pylori infection and other risk factors on the occurrence of gastric ulcer (GU), duodenal ulcer (DU) and gastritis in Turkish patients. METHODS: A total of 4,471 patients (48.3% female) out of 4863 attended the Samatya hospital in Istanbul (June 1999-October 2003) were included. The records of H pylori status (CLO-test), endoscopic findings of GU, DU and gastritis, personal habits (smoking, alcohol intake) and medication [non-steroidal anti-inflammatory drugs (NSAIDs), aspirin intake] were analyzed using multi-way frequency analysis. RESULTS: We have found that GU in the presence of H pylori had significant association with aspirin (P=0.0001), alcohol (P=0.0090) and NSAIDs (P=0.0372). DU on the other hand had significant association with aspirin/smoking/NSAIDs (P=0.0259), aspirin/alcohol (P=0.0002) and aspirin/smoking (P=0.0233), also in the presence of H pylori. In the absence of H pylori GU had significant association with alcohol/NSAIDs (P=0.0431), and NSAIDs (P=0.0436). While DU in the absence of H pylori had significant association with smoking/alcohol/ NSAIDs (P=0.0013), aspirin/NSAIDs (P=0.0334), aspirin/alcohol (P=0.0360). CONCLUSION: In the presence of H pylori, aspirin, alcohol and NSAIDs intake act as an independent risk factors that had an augmenting impact on the occurrence of GU and only together on the occurrence of DU in Turkish patients.

World J Gastroenterol. 2007 Jun 21;13(23):3245-8

New Molecular Mechanisms of Duodenal Ulceration.

Stress is a major etiologic factor in the pathogenesis of gastric & duodenal ulceration, as first described in rats by Hans Selye. In patients with “peptic ulcers” duodenal ulcers (DU) are more frequent than gastric ulcers (except in Japan). Thus, our research during the last 3 decades focused on the molecular mechanisms of DU in rodent models of chemically induced DU, and here we review our 3 recent findings: Endothelins (ET-1), the immediate early gene egr-1 & imbalance of angiogenic/anti-angiogenic molecules. Namely, we found an enhanced expression & release of ET-1 within 15-30 min after the administration of duodenal ulcerogen cysteamine, resulting in local ischemia that triggers the expression of hypoxia-inducible factors (HIF-1α). Our gene expression studies also revealed an early (0.5-2 hr) increase in the expression of egr-1 that is followed (12-24 hr) by upregulation of angiogenic growth factors (e.g., VEGF, bFGF, PDGF). Surprisingly, this event is also associated with an enhanced production of angiostatin & endostatin that probably counteract the beneficial effect of angiogenic molecules. Thus, the initial injury to endothelial & epithelial cells in DU seems to be aggravated (& not initiated) by HCl & proteolytic enzymes. The resulting mucosal necrosis does not rapidly heal because of the imbalance of VEGF & angiostatin/endostatin, hence duodenal ulcers develop. The experimental ulcers Selye described morphologically are now characterized at the molecular & genome level, involving unexpected mediators like ET-1, egr-1 & angiogenesis-related molecules.

Ann N Y Acad Sci. 2007 Jul 26

Inflammation, atrophy, and gastric cancer.

The association between chronic inflammation and cancer is now well established. This association has recently received renewed interest with the recognition that microbial pathogens can be responsible for the chronic inflammation observed in many cancers, particularly those originating in the gastrointestinal system. A prime example is Helicobacter pylori, which infects 50% of the world’s population and is now known to be responsible for inducing chronic gastric inflammation that progresses to atrophy, metaplasia, dysplasia, and gastric cancer. This Review provides an overview of recent progress in elucidating the bacterial properties responsible for colonization of the stomach, persistence in the stomach, and triggering of inflammation, as well as the host factors that have a role in determining whether gastritis progresses to gastric cancer. We also discuss how the increased understanding of the relationship between inflammation and gastric cancer still leaves many questions unanswered regarding recommendations for prevention and treatment.

J Clin Invest. 2007 Jan;117(1):60-9

Helicobacter pylori and benign upper digestive disease.

Acute infection with Helicobacter pylori causes hypo-chlorhydria and gastrointestinal upset. As the infection persists, patients develop chronic antral-predominant or pangastritis. Gastric and duodenal ulcers arise from chronic mucosal inflammation and disordered acid secretion in the stomach. With successful eradication of H. pylori, non-NSAID-related gastric and duodenal ulcers heal even without long-term acid suppression. More importantly, peptic ulcers and their complications rarely recur. Clearing H. pylori infection also reduces the risk of mucosal injury in NSAID and aspirin users; the protective effects are more pronounced in NSAID-naïve and aspirin users. H. pylori is unlikely to be the cause of gastro-oesophageal reflux disease. However, a patient’s reflux symptoms may be more difficult to control after clearing the infection. Although there is little evidence to support a causal relationship between H. pylori and non-ulcer dyspepsia, treatment of the infection gives a modest improvement of symptoms.

Best Pract Res Clin Gastroenterol. 2007;21(2):261-79

The inflammatory and immune response to Helicobacter pylori infection.

Lifelong Helicobacter pylori infection and its associated gastric inflammation underlie peptic ulceration and gastric carcinogenesis. The immune and inflammatory responses to H. pylori are doubly responsible: gastric inflammation is the main mediator of pathology, and the immune and inflammatory response is ineffective, allowing lifelong bacterial persistence. However, despite inducing gastric inflammation, most infections do not cause disease, and bacterial, host and environmental factors determine individual disease risk. Although H. pylori avoids many innate immune receptors, specific virulence factors (including those encoded on the cag pathogenicity island) stimulate innate immunity to increase gastric inflammation and increase disease risk. An acquired T helper 1 response upregulates local immune effectors. The extent to which environmental factors (including parasite infection), host factors and H. pylori itself influence T-helper differentiation and regulatory T-cell responses remains controversial. Finally, effective vaccines have still not been developed: a better understanding of the immune response to H. pylori may help.

Best Pract Res Clin Gastroenterol. 2007;21(2):237-59

Helicobacter pylori infection and gastric cancer.

Gastric cancer remains a major health burden on many societies claiming hundreds of thousands of lives every year. The discovery of Helicobacter pylori has no doubt revolutionised our understanding of this malignancy, which is now regarded as a paradigm for infection-induced chronic inflammation-mediated cancer. In this paper, we discuss the evidence for the association between H. pylori and gastric adenocarcinoma and MALT lymphoma. We also discuss the pathogenesis of these two forms of cancer and the factors that determine their outcome. There is no doubt that the knowledge accumulated over the past two decades will be translated into eventual victory over this killer cancer, largely because we now appreciate that the best way to prevent the cancer is by preventing acquisition of the infection in the first place, or by eradicating the infection in infected subjects. Defining the optimal timing of intervention is going to be the challenge facing us over the next two decades.

Best Pract Res Clin Gastroenterol. 2007;21(2):281-97

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