One fourth of gastrinomas are related to multiple endocrine neoplasia type 1, Zollinger–Ellison syndrome, peptic ulcer disease.

[6] Gastrinoma in the early stages will have signs and symptoms of indigestion[3] or similar to irritable bowel disease (IBD) such as: Gastrin is secreted by the G cells.

[12] The primary function of gastrin is to induce the release of hydrochloric acid (HCl) from the parietal cells located in the fundus of the stomach.

Parietal cells are responsible for hydrochloric (HCl) secretion along with intrinsic factor that binds to vitamin B12 and helps with its uptake in the terminal ileum.

These mechanisms of the gastrointestinal tract (GIT) are up-regulated by the vagus nerve of the parasympathetic nervous system (PNS), which carries out the majority of its functions by the release of neurotransmitter Acetylcholine (Ach), and to a lesser extent gastrin releasing peptide (GRP) protein.

In gastrinoma, GRP protein causes larger than normal amounts of gastrin secretion, which leads to hyperplasia of the parietal cells.

[citation needed] In many cases, gastrinoma is diagnosed based on the patient's history which is typically characterized by recurrent episodes of peptic ulcer disease or by severe reflux esophagitis and/or diarrhea or by acid-related symptoms which fail to respond to standard treatment regimens.

If patients present with hepatic metastases they might have remaining life span of one year with a five-year survival rate of 20–30%.

[19] Gastrinoma is the second most common functional pancreatic neuroendocrine tumor (pNET), with a yearly incidence of approximately 0.5 to 21.5 cases per a million of people worldwide.

The study concluded that the wide use of proton pump inhibitors itself might further induce hypergastrinemia (increased gastrin levels in circulatory system) by feedback inhibition.