• The patient must be fasting overnight, 12 to 14 hours
  • Fasting for a blood test
• This test may exhibit interference when sample is collected from a person who is consuming a supplement with a high dose of biotin (also termed as vitamin B7 or B8, vitamin H, or coenzyme R).
  • It is recommended to ask all patients who may be indicated for this test about biotin supplementation. Patients should be cautioned to stop biotin consumption at least 72 hours prior to the collection of a sample.

Gold serum separator (SST) tube

Immediately following collection, thoroughly mix sample by gently inverting 5 times

1. Allow sample to clot for a minimum of 30 minutes
2. Spin within two (2) hours of sample collection
3. Transfer serum to a Screw-cap polypropylene frozen transport vial/tube - 4mL (LabCorp), labelled as serum
4. Freeze immediatley

Screw-cap polypropylene frozen transport vial/tube - 4mL (LabCorp)

Red serum vial/tube, 5 mL

1. Allow sample to clot
2. Spin within two (2) hours of sample collection
3. Transfer serum to a Screw-cap polypropylene frozen transport vial/tube - 4mL (LabCorp), labelled as serum
4. Freeze immediatley

Frozen (strict) - 14 days

Freeze/thaw cycles - stable x 3

Ambient - NO

Refrigerated - NO

• Gross hemolysis
• Patient not fasting
• Specimen not received frozen
• Gross lipemia
• Plasma specimen

Immunochemiluminometric assay (ICMA)

0 - 1 month:    69−190 pg/mL

2 - 22 months: 55−186 pg/mL

22 months to 16 years:

− Fasting 3 - 4 hours: 2−168 pg/mL

− Fasting 5 - 6 hours: 3−117 pg/mL

− Fasting >8 hours:    1−125 pg/mL

> 16 years: 0−115 pg/mL

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. Antral G-cell hyperplasia may relate to high gastrin levels and duodenal ulcer.

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. I.V. secretin normally diminishes gastrin, but serum gastrin increases in gastrinoma patients. Wolfe provides an explanation for this paradoxical effect. 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.

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. 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