Diagnosis of Zollinger-Ellison syndrome and pernicious anemia, both of which bear relationship to high gastrin levels, evaluation of patients with severe duodenal ulcer, or recurrent symptoms after gastric surgery, evaluation of achlorhydria.
Fasting: 25-111 pg/ml
Antral G cell hyperplasia, gastric ulcer, renal disease, pyloric obstruction, carcinoma of stomach, vagotomy without gastric resection and short bowel syndrome may cause elevations of gastrin levels. H2-receptor blockers (cimetidine) may result in elevated results. Almost half of gastrin is metabolized through the kidney, gastrin levels may rise in renal failure. The patient should stop taking proton pump inhibitors (PPIs) (omeprazole-Prilosec; lansoprazole-Prevacid; rabeprazole-Aciphex; pantoprazole-Protonix; esomeprazole-Nexium, and Zegarid, a rapid release form of omeprazole) ONE WEEK prior to the blood draw. H2-receptor Blockers (i.e. cimetidine) should be stopped THREE DAYS prior to the blood draw.
The patient should stop taking proton pump inhibitors (PPIs) (omeprazole-Prilosec; lansoprazole-Prevacid; rabeprazole-Aciphex; pantoprazole-Protonix; esomeprazole-Nexium, and Zegarid, a rapid release form of omeprazole) ONE WEEK prior to the blood draw. H2-receptor Blockers (i.e. cimetidine) should be stopped THREE DAYS prior to the blood draw. The patient should fast overnight, preferably 12 hrs or more; postprandial specimen should be indicated on the requisition. Collect specimen in SST tube; place on ice immediately after collection. Keep cold until ready to aliquot. Centrifuge, aliquot serum into a plastic vial and freeze within 1 hour of collection.
Fasting specimen or indicate postprandial. Place on ice immediately and deliver to lab or aliquot within 1 hour.
Fasting venous serum gastrin concentrations are inversely related to rates of both unstimulated and maximum stimulated gastric HCl secretion. Elevated gastrin levels should be interpreted in light of gastric acid secretion. Tumors associated with the Zollinger-Ellison syndrome are characterized by extremely elevated rates of gastric HCl secretion, severe upper gastrointestinal ulcer disease, and non-beta islet cell tumors of the pancreas. Patients with gastric or less frequently with severe duodenal ulcer disease have been found to have significantly greater fasting serum gastrin concentrations than control subjects. Patients with pernicious anemia have elevated fasting serum gastrin levels. Gastrin levels more than 500 in a patient with basal acid hypersecretion usually indicates gastrinoma. Concurrent measurement of pepsinogen 1 (RIA) may be helpful. High levels have been observed after gastroscopy and in diabetic patients with autonomic neuropathy.