The pH in the small intestine is the lower pH of the small intestinal fluid because primary bile acids cannot be dissolved and the formation of lipid microclusters is reduced. What we call small intestinal fluid is secreted by the small intestinal glands in the small intestinal mucosa and is weakly alkaline if the ulcer can be properly controlled, there is usually no major problem. So how can low pH in the small intestine be prevented and treated? Until effective acid suppression therapy is available, the main cause of death in gastrinoma is peptic ulcer and its complications. The introduction of H2 receptor blockers and proton pump inhibitors has greatly reduced the incidence and mortality of this condition in combination with peptic ulcers, thus effectively circumventing total gastrectomy. Nowadays, the greatest threat to life from gastrinoma is not the complication of ulcers but the invasion of malignant tumors, and data show that more than 50% of patients with gastrinoma without surgical resection die from direct tumor invasion. The goals of treatment for patients with gastrinoma are ulcer control, prevention of complications and control of tumor progression. The main goals of medical therapy for patients with gastrinoma are to reduce clinical symptoms, suppress gastric acid secretion and prevent peptic ulcers, and the basis of treatment is the use of drugs that suppress gastric acid secretion. All patients with gastrinoma should be titrated periodically to determine the dosage of acid-suppressing drugs, which should reduce acid secretion to a level below 10 mmol/h before the next dose. Surgical removal of gastrinoma is the best treatment for patients with gastrinoma. The goal of treatment is to completely remove the tumor, eliminate high gastrin secretion, high acid secretion and peptic ulcers, and protect the patient from malignant tumors. Careful localization and evaluation of gastrinoma should be made before surgery, except for patients with contraindications to surgery, those who refuse surgery and those with multiple liver metastases that are no longer possible to be surgically removed. If no metastases are found on surgical exploration or if metastases are limited to lymph nodes, it is unlikely that the patient will die from tumor metastasis. Liver metastasis is a sign of poor prognosis. Nearly 20% to 30% of patients have liver metastasis at the time of diagnosis, and 15% of patients with liver metastasis are limited to one lobe. It is thought that aggressive resection of intrahepatic metastases has a better clinical response, and if metastatic gastrinoma is limited to one lobe of the liver, complete resection is considered safe and feasible. Liver transplantation is also feasible in patients with metastases limited to the liver, but whether this improves survival remains uncertain. Cure of a single gastrinoma with primary origin in the liver has also been reported by complete resection of the hepatic tumor focus. The surgical treatment of patients with combined MEN-Ⅰ gastrinomas has been controversial. It is believed that patients with combined MEN-Ⅰ are not suitable for surgical treatment because of the pleomorphic and multicentric nature of these tumors. Removal of gastrinomas is neither curative nor does it restore serum gastrin levels to normal. It is generally accepted that patients with MEN-Ⅰ in combination with hyperparathyroidism should first undergo parathyroidectomy. Patients with gastrinoma are not considered for partial gastrectomy, and patients with gastrinoma who have undergone total gastrectomy should receive monthly intramuscular vitamin B12 and early oral calcium and vitamin D to prevent osteoporosis and osteochondrosis. This approach is particularly valuable in patients who have complete resection of the tumor but still cannot resolve high acid secretion. Most authors believe that proximal gastric vagotomy should be performed in all patients during exploratory surgery. In a study of 124 patients with no tumor metastases on imaging and treated surgically, a reduced mortality rate was observed, with only 3% of 98 patients with liver metastases at 6.3 years of follow-up after tumor resection, compared with 23% of 26 patients treated medically at 8.7 years of follow-up, with 2 deaths from metastatic gastrinoma in the medically treated group and no deaths directly attributable to the tumor in the surgical group. In the surgical group, no patient died directly from the tumor. Gastric acid secretion does not always return to normal after resection of gastrinoma, probably because of the trophic effect on the cells of the gastric lining of the preoperative chronically elevated gastrin and the residual excess gastrin after surgery. Nearly 40% of patients still require extended acid medication to control high gastric acid secretion after surgery, and these patients also require monitoring of gastric acid secretion. Patients with gastrinoma who have complete removal of the tumor usually have an immediate decrease in serum gastrin levels to normal, a decrease in acid secretion, healing of the ulcer, disappearance of diarrhea, and survival close to that of a normal person. Nearly 40% of patients with gastrinoma can have their tumors completely removed, and long-term omeprazole treatment in patients who cannot have their tumors removed can also reduce gastric acid secretion, reduce ulcer and diarrhea symptoms, and allow the ulcers to heal. When long-term omeprazole therapy has been started, it should not be discontinued or reduced because of the potential for tumor infiltration and tumor recurrence after discontinuation of the drug. Patients who have undergone proximal gastric vagotomy without surgical removal of gastrinoma may be able to reduce the omeprazole dose. Patients with total gastrectomy for gastrinoma may have symptomatic improvement and disappearance of ulcers, but serum gastrin concentrations are unchanged in most patients, with only a moderate decrease in serum gastrin levels in nearly one third of cases, which may be due to the removal of gastrinoma in the first duodenal segment during total gastrectomy. Treatment of patients with gastrinoma is a lifelong process, and although the course and monitoring of each patient varies individually, some procedural monitoring methods are described below: After definitive gastrinoma resection, a routine annual evaluation should be performed, including history and physical examination, fasting serum gastrin and gastric acid secretion measurements, and pancreatin stimulation tests. If there is a progressive increase in fasting gastrin levels, tumor recurrence should be alerted. If fasting serum gastrin levels are normal in the first year after surgical resection of the tumor, fasting serum gastrin levels are also normal in 95% of patients at 3 years. In cases of recurrence in patients with seemingly successfully resected gastrinomas, pancreatic stimulation tests are considered to be the best method of detection, and periodic associated imaging is not necessary unless fasting serum gastrin levels are elevated or pancreatic stimulation tests are positive. In patients with unlocated or resected or only partially resected gastrinomas, the monitoring method is the same as before, except that a pancreatic stimulation test is not required, and in these patients the rate of gastric acid secretion before the next dose should be measured to determine the dose of the drug. In addition, patients with gastrinoma that cannot be localized should be evaluated periodically, including imaging every 2 to 3 years to find the tumor and surgical resection.