Evidence map›Paper›PMID 14723839›Full record

ArticleCurrent treatment options in gastroenterology2004

Helicobacter pylori and Gastroesophageal Reflux Disease.

Richard M. Peek

Abstract read
PubMed Publisher
In one paragraph

Article in Current treatment options in gastroenterology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.4field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Curcumin Oxidation Is Required for Inhibition ofFrontiers in cellular and infection microbiology · 2021
    Article
  4. Article
  5. Article
  6. Approach to GERD.Canadian family physician Medecin de famille canadien · 2017
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Richard M. PeekDivision of Gastroenterology, Vanderbilt University School of Medicine, C-2104 Medical Center North, Nashville, TN 37232-2279, USA. richard.peek@vanderbilt.edu
Vanderbilt University Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Since the rediscovery of Helicobacter pylori two decades ago, it has become increasingly clear that the true relationships between this organism and diseases of the upper gastrointestinal tract are highly complex. H. pylori colonization is a strong risk factor for peptic ulceration and distal gastric cancer; however, gastritis has no adverse consequences for most hosts, and the prevalence of H. pylori is inversely related to gastroesophageal reflux disease (GERD) and its sequelae, which include Barrett's esophagus and esophageal adenocarcinoma. One clinical implication stemming from these data is that H. pylori eradication may not be appropriate in certain human populations due to potential beneficial effects conferred by persistent gastric inflammation. However, the majority of published intervention trials indicate that H. pylori treatment neither leads to the development of clinically significant de novo esophagitis nor exacerbates existing reflux disease. Superimposed upon these observations are reports that long-term acid suppression induced by proton-pump inhibitors (PPIs) in conjunction with H. pylori colonization may enhance the development of atrophic gastritis, a well-recognized histologic step in the progression to intestinal-type gastric cancer. Therefore, current evidence-based recommendations regarding management of H. pylori-positive individuals with GERD include the following. H. pylori should not be treated with the intent to either improve reflux symptoms or prevent the development of reflux complications. However, if patients are to receive long-term acid suppressive therapy, they should be tested for H. pylori and treated if positive, due to the potential for PPIs to accelerate atrophy within H. pylori-infected mucosa. Optimal first-line regimens in this country consist of a PPI in combination with clarithromycin and either amoxicillin or metronidazole (triple therapy) for at least 7, but preferably 10, days. Because the most effective second-line regimens contain metronidazole, it is advisable to use amoxicillin instead of metronidazole as first-line therapy in order to optimize results should subsequent therapy be required. If first-line regimens fail to eliminate H. pylori, patients should receive quadruple therapy consisting of a PPI, bismuth subsalicylate, metronidazole, and tetracycline for 14 days. Due to the availability and accuracy of noninvasive diagnostic tests for H. pylori, it is recommended that successful cure be confirmed after intervention.

Identifiers

PMID14723839
OpenAlexW1977726847

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.