Gastrin

Serum, frozen

0.5 mL

0.3 mL (Note: This volume does not allow for repeat testing.)

Red-top tube or gel-barrier tube

The patient must be fasting overnight, 12 to 14 hours.

Diagnose Zollinger-Ellison (Z-E) syndrome; diagnose gastrinoma. Gastrin >1000 pg/mL with gastric acid hypersecretion (basal acid secretion >15 mmol/hour in a patient with peptic ulcer who has not had surgery) establishes unequivocally the diagnosis of the Zollinger-Ellison syndrome.⁴ Antral G-cell hyperplasia may relate to high gastrin levels and duodenal ulcer.

Gastric hyperacidity must be documented. Gastric ulcer, chronic renal failure, hyperparathyroidism, pyloric obstruction, carcinoma of stomach,⁵ vagotomy without gastric resection, retained gastric antrum and short bowel syndrome have been reported with moderate elevations of gastrin levels. Gastrin levels are increased with pernicious anemia. H₂-receptor blockers (cimetidine) may result in elevated levels. Overlap of serum gastrin values between gastrinoma and other states occurs. Up to 40% of Z-E patients have fasting gastrin values between 100 and 500 pg/mL, while a few patients with gastric or duodenal ulcer without gastrinoma, have results in this range. At least half of patients with the Z-E syndrome lack diagnostic serum gastrin levels, although in nearly all, fasting serum gastrin levels are increased.⁴ One report describes a patient with Z-E syndrome with a normal initial gastrin level.⁶

Immunochemiluminometric assay (ICMA)

Pediatric^1-3 and adults:

• 0 to 1 month: 69−190 pg/mL

• 2 to 22 months: 55−186 pg/mL

• 22 months to 16 years:

− Fasting 3 to 4 hours: 2−168 pg/mL

− Fasting 5 to 6 hours: 3−117 pg/mL

− Fasting >8 hours: 1−125 pg/mL

• Older than 16 years: 0−115 pg/mL

Gastrin is secreted by antral G cells and stimulates gastric acid production, antral motility, and secretion of pepsin and intrinsic factor. The principle forms of gastrin in blood are G-34 (big gastrin, half-life is five minutes) and G-14 (minigastrin, half-life is five minutes). Each of these polypeptides circulates in nonsulfated (I) or sulfated (II) forms. Instilling acid into the stomach normally inhibits gastrin secretion. Elevated gastrin levels should be interpreted in light of gastric acid secretion and other parameters. The neuroendocrine tumors associated with the Zollinger-Ellison syndrome are characterized by elevated rates of gastric HCl secretion and upper gastrointestinal ulcer disease. Gastrin levels >500-600 pg/mL in a patient with basal acid hypersecretion often indicate gastrinoma, but antral G-cell hyperplasia cases can have gastrin levels >500 pg/mL and hyperchlorhydria. If gastrinoma is likely but fasting gastrin level is not diagnostic, the secretin test is the provocative test of choice. Absolute increase in serum gastrin level above the basal figure is preferred to percent change.⁴ I.V. secretin normally diminishes gastrin, but serum gastrin increases in gastrinoma patients. Wolfe provides an explanation for this paradoxical effect.⁴ Calcium infusion also stimulates gastrin release but does not distinguish other causes of ulcer as well as the secretin test. Protocols for stimulation tests are published.⁷

Fifteen percent to 26% of Z-E patients have evidence of Werner syndrome (multiple endocrine neoplasia type 1). It may include hyperparathyroidism, islet cell tumors of the pancreas, pituitary tumors, Cushing syndrome (adrenal glands), and hyperparathyroidism.⁸ Gastrinoma are malignant in 62% of cases, and 44% of patients have metastases.

No consistent relationship has been established between Helicobacter pylori (Campylobacter pylori) and gastric acid secretion or serum gastrin levels.

Features of gastrinoma additional to those of peptic ulcer may include diarrhea and steatorrhea.

Gastrinomas are usually found in the pancreas but they may be primary in the duodenum. A few cases in which a gastrinoma was primary in the stomach have been reported. The morphology is that of foregut carcinoids.⁹