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Peptic ulcer disease (PUD) presents with diverse symptoms depending on the location and severity of the ulcer. Clinical manifestations of peptic ulcer include dull pain and a burning sensation in the mid-epigastric region.
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Peptic Ulcer Disease I: Introduction01:30

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Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
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Peptic ulcers can also be...
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Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
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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.
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Peptic Ulcer Disease IV: Management01:26

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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.
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Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

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Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
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  1. Home
  2. A Proton Pump Inhibitor Independently Elevates Gastrin Levels As A Marker For Metachronous Gastric Cancer After Endoscopic Submucosal Dissection.
  1. Home
  2. A Proton Pump Inhibitor Independently Elevates Gastrin Levels As A Marker For Metachronous Gastric Cancer After Endoscopic Submucosal Dissection.

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A Proton Pump Inhibitor Independently Elevates Gastrin Levels as a Marker for Metachronous Gastric Cancer After

Hajime Teshima1, Hidehiko Takigawa1, Takahiro Kotachi1

  • 1Department of Gastroenterology, Graduate School of Biomedical and Health Sciences, Hiroshima University Hospital, Hiroshima 734-8551, Japan.

Journal of Clinical Medicine
|November 9, 2024

View abstract on PubMed

Summary
This summary is machine-generated.

Elevated serum gastrin, independent of proton pump inhibitor use, may predict metachronous gastric cancer (MG) after endoscopic submucosal dissection (ESD) in patients with gastric cancer after Helicobacter pylori eradication (GCAE). This finding aids in post-ESD cancer surveillance.

Keywords:
endoscopic submucosal dissectiongastric cancermetachronous multiple carcinomasserum gastrin

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Area of Science:

  • Gastroenterology
  • Oncology
  • Biomarker Research

Background:

  • Serum gastrin and pepsinogen are established gastric cancer risk markers.
  • Their role in predicting metachronous gastric cancer (MG) post-endoscopic submucosal dissection (ESD) in gastric cancer patients after Helicobacter pylori eradication (GCAE) remains unclear.

Purpose of the Study:

  • To identify predictive factors for metachronous gastric cancer (MG) after ESD in GCAE patients.
  • To specifically evaluate the utility of serum markers, particularly gastrin, in this prediction.

Main Methods:

  • Retrospective analysis of 197 GCAE patients (224 lesions) who underwent ESD.
  • Exclusion of PPI users, female patients, and undifferentiated-type cases for focused analysis.
  • ROC curve analysis and multiple logistic regression to assess serum marker predictive value and association with carcinogenesis.

Main Results:

  • Serum gastrin demonstrated the highest discriminative ability for MG (AUC 0.77).
  • Severe mucosal atrophy and elevated serum gastrin were independent predictors of MG (p < 0.01).
  • Elevated gastrin in PPI users did not correlate with increased MG risk.

Conclusions:

  • PPI-independent elevated serum gastrin, alongside severe mucosal atrophy, may indicate an increased risk of MG post-ESD.
  • Serum gastrin shows potential as a valuable marker for surveillance in GCAE patients after ESD.