The high volume of gastric acid that is produced decreases intestinal pH.Pancreatic lipases, which require an alkaline environment to function, are inactivated and can no longer emulsify fats. Moreover, gastrin acts directly on the intestine and prevents sodium and water reabsorption, resulting in secretory diarrhea.
Clinical features
Refractory peptic ulcer disease (PUD): Multiple, recurrent, large (>2 cm) ulcers, often located distal to the duodenal bulb (e.g., jejunum).
Chronic watery diarrhea: Excess gastric acid floods the duodenum, inactivating pancreatic lipase and causing malabsorption and steatorrhea.
GERD: Severe, refractory heartburn, esophagitis, or esophageal strictures.
Abdominal pain and weight loss.
Possible symptoms of other endocrine neoplasias. See MEN1
Diagnostics
Initial Screening:
Fasting serum gastrin (FSG) level: Hold PPIs for 1–2 weeks prior to checking. FSG > 1000 pg/mL is highly suggestive.
Gastric pH: Must be measured simultaneously. An FSG > 1000 pg/mL with a gastric pH ≤ 2 confirms the diagnosis.
Confirmatory/Provocative Testing:
Secretin stimulation test: Performed if FSG is borderline (110–1000 pg/mL) with a pH ≤ 2. A paradoxical ↑ in serum gastrin (>200 pg/mL) is diagnostic (normal G-cells are inhibited by secretin, whereas gastrinoma cells are stimulated). t
Tumor Localization (Imaging):
Somatostatin receptor scintigraphy (SRS) / Gallium-68 DOTATATE PET/CT: Best overall imaging modalities for localization and staging (gastrinomas express somatostatin receptors).
Endoscopic Ultrasound (EUS): Highly sensitive for detecting small tumors within the duodenal wall or pancreas.
Abdominal CT/MRI: Used to rule out hepatic metastases.