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Gastric Polyps and Metaplasia, and Hypersecretory Disorders

Gastric Polyps and Metaplasia, and Hypersecretory Disorders

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 Gastric Metaplasia, Hypertrophic and Hypersecretory Disorders1.0 Hypertrophic & Hypersecretory GastropathiesDisorders of gastric mucosal growth and acid secretion, while individually rare, present unique diagnostic and management challenges in clinical gastroenterology. A strategic approach is crucial for differentiating between these conditions, as their underlying pathophysiology, clinical trajectories, and therapeutic needs are starkly different. This section provides a framework for understanding and managing two classic, yet frequently contrasted, gastropathies: Ménétrier disease and Zollinger-Ellison syndrome.1.1 Ménétrier DiseaseOverview and PathophysiologyMénétrier disease is a rare, acquired hypertrophic gastropathy characterized by giant gastric folds. The core pathophysiological mechanism involves the overexpression of Transforming Growth Factor-α (TGF-α), which leads to excessive activation of the Epidermal Growth Factor Receptor (EGFR) on the gastric mucosa. This signaling cascade drives massive hyperplasia of foveolar (mucous) cells, which crowd out and lead to the atrophy of acid-producing parietal cells and enzyme-producing chief cells.Classic Diagnostic TriadThe hallmark clinical features of Ménétrier disease can be summarized in a classic triad:Giant Rugal Folds: Massive, convoluted folds are typically found on endoscopy, predominantly located in the gastric body and fundus.Protein-Losing Gastropathy: The hyperplastic, permeable mucosa leads to a significant leakage of plasma proteins, especially albumin, into the gastric lumen. This results in hypoalbuminemia, which manifests clinically as peripheral edema, ascites, and pleural effusions.Hypochlorhydria or Achlorhydria: Due to the progressive loss of parietal cells, gastric acid secretion is markedly reduced or absent. This stands in sharp contrast to hypersecretory states like Zollinger-Ellison syndrome.Diagnostic WorkupA definitive diagnosis is established through a combination of endoscopic, histologic, and laboratory findings.Endoscopy (EGD): Upper endoscopy is the initial diagnostic modality, revealing the characteristic enlarged, cerebriform gastric folds. It is essential to obtain biopsies to rule out mimics such as lymphoma or infiltrative carcinoma.Histology: A full-thickness mucosal biopsy is required for diagnosis. Histologic examination reveals marked foveolar hyperplasia, glandular atrophy with loss of parietal and chief cells, and cystic dilation of the gastric glands.Laboratory Confirmation: Key laboratory findings include low serum albumin and total protein. An elevated stool α-1 antitrypsin clearance confirms the presence of a protein-losing enteropathy.Management AlgorithmManagement is tailored to symptom severity, nutritional status, and the risk of malignant transformation.Supportive Care: A high-protein diet is fundamental to counteract ongoing protein loss and support nutritional status. Albumin infusions may be required in cases of severe hypoalbuminemia.Targeted Medical Therapy: For refractory cases with severe protein loss, Cetuximab—a monoclonal antibody that blocks EGFR—has shown significant benefit in improving symptoms and biochemical parameters.Symptomatic Control: Proton Pump Inhibitors (PPIs) are often used for symptomatic relief of epigastric pain or nausea, though they do not address the underlying pathophysiology.Surgical Intervention: A partial or total gastrectomy is reserved for patients with severe, debilitating symptoms refractory to medical therapy, unmanageable protein loss, or the development of gastric adenocarcinoma.Cancer Surveillance: Patients with Ménétrier disease have an increased risk of developing gastric adenocarcinoma. Therefore, periodic endoscopic surveillance with biopsies is advised.This profile of protein loss and low acid secretion provides a critical contrast to Zollinger-Ellison Syndrome, a key differential diagnosis.1.2 Zollinger-Ellison Syndrome (ZES)Overview and PathophysiologyZollinger-Ellison Syndrome (ZES) is caused by a gastrin-secreting neuroendocrine tumor (NET), known as a gastrinoma. Ectopic and unregulated gastrin secretion leads to massive parietal cell hyperplasia and profound gastric acid hypersecretion. Over 80% of gastrinomas are located within the "gastrinoma triangle," an anatomical region defined by the duodenum, pancreas, and peripancreatic lymph nodes. The duodenum is the most common primary site, followed by the pancreas and peripancreatic lymph nodes.When to Suspect ZESA high index of suspicion is required to diagnose ZES. The following clinical scenarios should trigger a diagnostic workup:Refractory or recurrent peptic ulcers that fail to heal with standard PPI therapy, especially when H. pylori is negative and NSAID use is excluded.Ulcers in atypical locations, such as the distal duodenum or the jejunum, or the presence of multiple simultaneous ulcers.The combination of peptic ulcer disease with chronic, unexplained diarrhea or ...
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