1,721,147 research outputs found
Clinical Practice: Diagnosis and Evaluation of Dyspepsia
Full text linkThe main issue regarding the approach to the patient with uninvestigated dyspepsia is whether the symptoms are the result of an important clinical illness, which then determines the appropriate management strategy for the treatment of the symptoms. An initial trial of empiric antisecretory drugs is recommended for those without Helicobacter pylori infection and no alarm symptoms, whereas H. pylori eradication is recommended for those with an active H. pylori infection. Treatment expectations for H. pylori infections should theoretically be similar to other common infectious diseases. In most regions, clarithromycin resistance has undermined traditional triple therapy so that it is no longer a suitable choice as an empiric therapy. Four drug therapies, such as sequential, concomitant, and bismuth-quadruple therapy are generally still acceptable choices as empiric therapies. Posteradication testing is highly recommended to provide early identification of otherwise unrecognized increasing antimicrobial resistance. However, despite the ability to successfully cure H. pylori infections, a symptomatic response can be expected in only a minority of those with dyspepsia not associated with ulcers (so called nonulcer dyspepsia). Overall, from the patients stand point, symptomatic relief is often difficult to achieve and physicians must rely on reassurance along with empiric and individualized care.
I.F.: 2.20
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
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 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
Variability in the outcome of treatment of Helicobacter pylori infection: a critical analysis
No full textA novel penicillin-binding protein(PBP-D) is involved in amoxicillin resistance in Helicobacter pylori
No full textUnderstanding treatment guidelines with bismuth and non-bismuth quadruple Helicobacter pylori eradication therapies.
No full textPBP-D, a novel penicillin-binding protein is involved in amoxicillin resistance in Helicobacter pylori.
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