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Related Concept Videos

Peptic Ulcer Disease IV: Management01:26

Peptic Ulcer Disease IV: Management

238
Medical treatment strategies for peptic ulcers encompass various methods. The primary goal of treatment is to diminish gastric acidity and strengthen mucosal defense mechanisms.
The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
Pharmacological management
The prevailing therapy for peptic ulcers involves a combination of managing the patient's current...
238
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents01:20

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents

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The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
818
Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors01:13

Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors

672
Peptic ulcers, often induced by H. pylori infections or NSAID usage, arise from disruptions in the delicate balance of gastric acid production. Peptic ulcers stem from heightened gastric acid levels due to H. pylori infections or NSAID use. The protective mucus layer diminishes in the presence of these factors, allowing gastric acid to erode the stomach lining and form ulcers.
Gastric acid, a potent cocktail of hydrogen and chloride ions, is produced in specialized parietal cells within the...
672
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

865
Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
865
Drugs for Peptic Ulcer Disease: Sucralfate as Mucosal Protective Agents01:24

Drugs for Peptic Ulcer Disease: Sucralfate as Mucosal Protective Agents

974
In the intricate landscape of the gastric lumen, excessive acid secretion disrupts the natural defense mechanisms, weakening the mucus-bicarbonate barrier. This vulnerability allows pepsin to infiltrate epithelial cells, digesting mucosal proteins and triggering erosion, leading to ulcer formation.
In this scenario, mucosal protective agents like sucralfate play an essential role. Sucralfate, a complex of sulfated sucrose and aluminum hydroxide, demonstrates its usefulness in acidic conditions,...
974
Gastroesophageal Reflux Disease II: Clinical Features and Management01:29

Gastroesophageal Reflux Disease II: Clinical Features and Management

394
Gastroesophageal reflux disease, or GERD, is a persistent medical condition that affects many individuals worldwide. Its clinical manifestations can vary greatly, making diagnosis and management challenging for healthcare professionals. The following is a comprehensive overview of the clinical manifestations, assessment, and management strategies for GERD.
Clinical Manifestations
GERD presents itself in a multitude of ways, with symptoms varying from person to person. The hallmark symptoms are...
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Related Experiment Video

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Reduced Procedure Time and Variability with Active Esophageal Cooling During Radiofrequency Ablation for Atrial Fibrillation
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Low-dose PPI to prevent bleeding after ESD: A multicenter randomized controlled study.

Li Yang1, Jian Qi2, Weiqing Chen3

  • 1Department of Gastroenterology, Xinqiao Hospital of Army Medical University, Chongqing, China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|January 15, 2021
PubMed
Summary
This summary is machine-generated.

Intermittent low-dose proton pump inhibitors (PPIs) effectively prevent bleeding after endoscopic submucosal dissection (ESD). This approach is sufficient for patients undergoing ESD and can reduce healthcare costs.

Keywords:
ESD-related ulcerEndoscopic submucosal dissection (ESD)Post ESD bleedingProton pump inhibitor (PPI)Randomized, controlled clinical trial

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Area of Science:

  • Gastroenterology
  • Endoscopy
  • Pharmacology

Background:

  • Proton pump inhibitors (PPIs) are standard for preventing gastric bleeding after endoscopic submucosal dissection (ESD).
  • Optimal PPI regimens for post-ESD bleeding prevention remain unclear.
  • This study evaluates intermittent low-dose PPIs for efficacy and safety.

Purpose of the Study:

  • To determine if intermittent low-dose PPIs are non-inferior to continuous high-dose PPIs in preventing post-ESD bleeding.
  • To assess the clinical effectiveness and cost-efficiency of different PPI dosing strategies.

Main Methods:

  • A multicenter, non-inferiority, randomized controlled trial involving 414 patients.
  • Patients received either intermittent low-dose or continuous high-dose esomeprazole for 8 weeks post-ESD.
  • The primary endpoint was bleeding within 7 days of ESD, analyzed by intention-to-treat.

Main Results:

  • No significant difference in post-ESD bleeding rates between groups (6.2% low-dose vs. 5.9% high-dose) within 7 days.
  • Similar rates of mucosal healing (scar stage) observed at one month.
  • The low-dose PPI group incurred significantly lower hospital costs.

Conclusions:

  • Intermittent low-dose PPIs are sufficient for preventing post-ESD bleeding.
  • This regimen offers a cost-effective alternative for clinical practice.
  • Further application in clinical practice may reduce PPI-related healthcare expenditures.