1,721,184 research outputs found
Variability in the outcome of treatment of Helicobacter pylori infection: a critical analysis
No full textHelicobacter pylori therapy: a paradigm shift
No full textHelicobacter pylori (H. Pylori) is a leading cause of gastroduodenal disease,
including gastric cancer. H. pylori eradication therapies and their efficacy are
summarized. A number of current treatment regimens will reliably yield >90% or
95% cure rates with susceptible strains. None has proven to be superior. We show
how to predict the efficacy of a regimen in any population provided one knows the
prevalence of antibiotic resistance. As with other infectious diseases, therapy
should always be susceptibility-based. Susceptibility testing should be demanded.
We provide recommendations for empiric therapies when that is the only option and
describe how to distinguish studies providing misinformation from those providing
reliable and interpretable data. When treated as an infectious disease, high H.
pylori cure rates are relatively simple to reliably achieve
Ulcers and gastritis
No full textComment on
High-risk population for gastric cancer development based on serum pepsinogen status and lifestyle factors. [Helicobacter. 2009]
Helicobacter pylori invades the gastric mucosa and translocates to the gastric lymph nodes. [Lab Invest. 2008]
H. pylori eradication prevents the progression of gastric intestinal metaplasia in reflux esophagitis patients using long-term esomeprazole. [Am J Gastroenterol. 2009]
Re-evaluation of histogenesis of gastric carcinomas: a comparative histopathological study between Helicobacter pylori-negative and H. pylori-positive cases. [Dig Dis Sci. 2009
Epidemiology of Helicobacter pylori Infection
No full textThis review summarizes epidemiologic studies published between April 2004 and March 2005. DNA of Helicobacter pylori was detected in river water, but the culture was unsuccessful. H. pylori infection was associated with Shigella infection. Despite many studies, predominant infection routes of H. pylori have not yet been clearly identified. In some limited populations in developing countries, H. pylori infection was rare or with strange distributions. Trials to reduce the H. pylori infection rate were performed including H. pylori eradication in total family units and fly control. The hypothesis of a causal role of Helicobacter species and H. pylori infection in cancer of the hepatobiliary tract was indeed confirmed
Perturbations in gastric physiology in Helicobacter pylori duodenal ulcer: are they all epiphenomena?
No full textBACKGROUND:
The Holy Grail of physiological studies in acid secretion has been to identify a specific abnormality in gastroduodenal physiology responsible for the development of duodenal ulcer disease.
METHODS:
We review the available data relating duodenal ulcer and Helicobacter pylori infection to perturbations in gastric physiology, especially acid secretion.
RESULTS:
It is known now that elevated serum pepsinogen levels, reduced inhibition of acid secretion with antral acidification or distention, exaggerated gastrin response to meals or infusion of bombesin or gastric-releasing peptide, exaggerated acid output in response to gastric-releasing peptide, and abnormalities in duodenal bicarbonate secretion in response to instillation of acid are reversible epiphenomena related to the H. pylori infection and are not in themselves responsible for duodenal ulcer disease. H. pylori is inhibited by bile, yet can thrive in the duodenal bulb of duodenal ulcer patients. Glycine-conjugated bile acids are precipitated by acid; thus, any mechanism that would increase the duodenal acid load may remove the inhibitory bile and allow unrestrained growth of H. pylori.
CONCLUSION:
These data and speculations offer one possible explanation for why duodenal ulcer occurs in only some people--those with high acid secretion--and suggest that the combination of high duodenal acid load and H. pylori infection is sufficient to result in duodenal ulcer disease
The QUADRATE study: a proposal for a change in the reporting of pharmaceutical supported trials.
No full textPathogenesis of Duodenal Ulcer Disease: the rest of the story.
No full textAlthough several duodenal ulcer disease-specific abnormalities in gastric function have been described (e.g. exaggerated gastrin releasing peptide-stimulated acid secretion and an abnormal sensitivity of the parietal cells to gastrin), none has withstood careful examination. We describe here the critical nature of the duodenal acid load in precipitating and washing out bile salts, which inhibit the growth of Helicobacter pylori (H. pylori) in the development of duodenal ulcer disease. The risk of duodenal ulcer is enhanced by infection with proinflammatory H. pylori (e.g. with an intact cag pathogenicity island). Progressive damage to the duodenum promotes gastric metaplasia, resulting in sites for H. pylori growth and more inflammation. This cycle results in an increasing inability of the duodenal bulb to neutralize acid entering from the stomach until changes in duodenal bulb structure and function are sufficient for an ulcer to develop. Cure of the H. pylori infection results in a sustained fall in duodenal acid load as well as a marked (and continuing) reduction in inflammation, which results in the cure of chronic ulcer disease
Ulcers and gastritis
No full textAbstract
Significant advances continue to be made in the area of gastritis and ulcer disease. Studies to identify the most appropriate use of capsule endoscopy have now confirmed that it is superior to other methods for identifying small-bowel mucosal pathology and sites of obscure gastrointestinal bleeding. It has increasingly been recognized that the complications of ulcer disease are secondary to the use of nonsteroidal anti-inflammatory drugs (NSAIDs) and to interactions between NSAlDs and Helicobacter pylori. Effective prophylaxis for NSA1D ulcers in H. pylori-negative individuals continues to be a challenge, as it has become clear that conclusions from studies focusing on "endoscopic ulcers" in patients whose H. pylori status was unknown provided a false sense of security. The concept of multifocal atrophic gastritis has been challenged. The precursor lesion to gastric cancer now appears to be a sheet of pseudopyloric metaplasia advancing into the gastric body with islands of intestinal metaplasia embedded within it. Multifactorial models such as those proposed for understanding periodontal disease, including the organism, environmental factors, and host factors, appear particularly applicable to understanding the pathogenesis of H. pylori-associated gastric cancer
Gastritis, dyspepsia and peptic ulcer disease.
No full textPeptic ulcer disease remains a common problem and it most frequently due to the presence of an Helicobacter pylori infection or use of non-steroidal anti-inflammatory drugs (NSAIDs). Dyspepsia is neither sensitive or specific for diagnosing peptic ulcer disease. The approach to patients with dyspepsia is to arrive at a definitive diagnosis without unnecessary exposure to invasive or costly diagnostic procedures. Non-invasive testing is preferred with endoscopy being reserved for those with alarm markers or above a specified age (e.g., 55 years in Western countries). Patients negative for H. pylori infection should receive an empiric trial of acid suppression for 4 to 8 weeks and if beneficial it can be continued
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