Basal Gastric Acid Hypersecretion Research Articles

Postprandial serum gastrin levels in patients with combined hypergastrinaemia and hyperchlorhydria.

We have determined the serum gastrin response to a standard test meal in 13 unoperated patients with combined fasting hypergastrinaemia (more than 150 ng/l) and basal hypersecretion of gastric acid (BAO more than 10 mmol/h). In 10 of 11 patients with proved of presumptive Zollinger-Ellison syndrome the peak postprandial rise in serum gastrin concentration was less than 50 per cent of basal value. The integrated gastrin response to feeding ranged from 71-9 to 211-8 mug/lX 150 min. In 2 patients with proved hypergastrinaemia of antral origin, however, serum gastrin rose to 223 per cent and 255 per cent respectively of basal value after ingestion of the meal. The integrated postprandial serum gastrin responses in these patients were 66-8 and 22-0 mug/lX 150 min. Two patiets with Zollinger-Ellison syndrome and total gastrectomy showed peak serum gastrin levels after feeding of 174 and 255 per cent of basal concentration. The integrated postprandial gastrin secretions were 365 and 366 mug/l X 150 min respectively. It is concluded that the serum gastrin response to feeding, when expressed as percentage change, may be helpful in the differential diagnosis of unoperated patients with fasting hypergastrinaemia and basal gastric acid hypersecretion.

Management of patients with Zollinger-Ellison syndrome.

Zollinger-Ellison syndrome (ZES) is caused by gastrin-secreting tumors called gastrinomas. Patients commonly present with peptic ulcer disease and may have recurrent, multiple, and atypically located ulcers, e.g. in the jejunum. Alternatively, severe diarrhea may be the only presenting symptom. Patients with multiple endocrine neoplasia Type I (MEN-I) and ZES become symptomatic at an earlier age than patients with sporadic ZES. Patients with ZES have elevated fasting serum gastrin concentrations (> 100 pg/ml) and basal gastric acid hypersecretion (> 15 mEq/h). The secretin stimulation test is the best test to distinguish ZES from other conditions resulting in elevated gastrin levels. Gastric acid hypersecretion can be controlled in virtually all patients with H2-receptor antagonists or omeprazole, thus rendering total gastrectomy unnecessary. Computed tomography (CT), magnetic resonance imaging (MRI), radionuclide octreotide scanning, endoscopic ultrasound, and the selective arterial secretin injection test are the recommended imaging studies for localization of gastrinoma; nevertheless, 50% of gastrinomas are not evident on preoperative imaging studies. All patients with sporadic gastrinoma who do not have unresectable metastatic disease should undergo exploratory laparotomy for potential curative resection. With increased awareness of duodenal tumors, gastrinoma can be found in 80-90% of patients. Surgery may be the most effective treatment for metastatic gastrinoma if most or all of the tumor can be resected. The management of patients with MEN-I and ZES remains controversial. Some clinicians advocate an aggressive surgical approach, whereas others have had little success in rendering patients eugastrinemic.

Marked Basal Gastric Acid Hypersecretion and Peptic Ulcer Disease

Marked Basal Gastric Acid Hypersecretion and Peptic Ulcer Disease

Marked Basal Gastric Acid Hypersecretion and Peptic Ulcer Disease

SummaryThree children with peptic ulcer disease had recurrent symptoms unresponsive to cimetidine or ranitidine therapy alone. Acid secretory studies showed a marked basal acid hypersecretion, which was atropinesensitive in two of three patients and was best suppressed by ranitidine in combination with an anticholinergic drug. Marked reduction in acid output following intravenous atropine suggested that the hypersecretion was under vagal, muscarinic control. However, in one patient, large doses of the selective m1‐muscarinic antagonist pirenzepine were ineffective in suppressing basal acid hypersecretion. Given the efficacy and safety of drug therapy used in these children over a 3‐year period, we conclude that medical management is an effective alternative to surgery for pediatric patients with refractory or recurrent peptic ulcer disease.

Controversies in the Management of ZollingerEllison Syndrome

Editorials1 December 1986Controversies in the Management of ZollingerEllison SyndromeAARON I. VINIK, M.B., B.Ch., M.D., NORMAN THOMPSON, M.D.AARON I. VINIK, M.B., B.Ch., M.D.Search for more papers by this author, NORMAN THOMPSON, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-105-6-956 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe Zollinger-Ellison syndrome is characterized by persistent basal gastric acid hypersecretion due to hypergastrinemia. Death from fulminant ulcer disease is now rarely seen, and death from progression of the tumor has become the major issue. Management of nearly all patients with this disease was previously by total gastrectomy, and no attempt was made to identify or remove the source of gastrin hypersecretion. Over the 3 decades since the syndrome's description, there has been much debate as to the optimal form of management (1-3). Controversial areas include definition of subvarieties of the syndrome, each of which requires a different approach to...

Gastric Acid Hypersecretion in Short Bowel Syndrome in Infants

Summary:To determine the frequency of gastric acid hypersecretion in infants with chronic malabsorption due to short bowel syndrome, acid secretory function was determined in 23 infants with malabsorption 2‐22 months following small bowel resection and in a control group of 14 chronically ill, age‐ and weight‐matched infants who did not undergo bowel resection. The prevalence of basal acid hypersecretion (defined as acid output 2 SD above the mean for the control group) was 17% (4 of 23). Basal gastric acid hypersecretion was associated with two factors: massive small bowel resection and initiation of enteral feeding. Basal acid hypersecretion was present on the initial study in 3 of 7 infants with less than one‐third of the small bowel remaining, but in only 1 of 16 with more than one‐third intact (p < 0.05). Hypergastrinemia was present in 3 of 6 infants following massive bowel resection, but in only 1 of 15 with more than one‐third intact (p < 0.05), but hypergastrinemia was not consistently associated with hypersecretion. In each of six previously unfed infants, a trial of enteral feeding resulted in increased basal and maximal acid output. Three infants developed basal acid hypersecretion during initiation of enteral feeding. There was no evidence of pentagastrin‐stimulated maximal acid hypersecretion in any of the infants.

Gastric Acid Hypersecretion in Short Bowel Syndrome in Infants

Summary: To determine the frequency of gastric acid hypersecretion in infants with chronic malabsorption due to short bowel syndrome, acid secretory function was determined in 23 infants with malabsorption 2-22 months following small bowel resection and in a control group of 14 chronically ill, age- and weight-matched infants who did not undergo bowel resection. The prevalence of basal acid hypersecretion (defined as acid output 2 SD above the mean for the control group) was 17% (4 of 23). Basal gastric acid hypersecretion was associated with two factors: massive small bowel resection and initiation of enteral feeding. Basal acid hypersecretion was present on the initial study in 3 of 7 infants with less than one-third of the small bowel remaining, but in only 1 of 16 with more than one-third intact (p < 0.05). Hypergastrinemia was present in 3 of 6 infants following massive bowel resection, but in only 1 of 15 with more than one-third intact (p < 0.05), but hypergastrinemia was not consistently associated with hypersecretion. In each of six previously unfed infants, a trial of enteral feeding resulted in increased basal and maximal acid output. Three infants developed basal acid hypersecretion during initiation of enteral feeding. There was no evidence of pentagastrin-stimulated maximal acid hypersecretion in any of the infants.

Gastric Acid Hypersecretion in Short Bowel Syndrome in Infants

To determine the frequency of gastric acid hypersecretion in infants with chronic malabsorption due to short bowel syndrome, acid secretory function was determined in 23 infants with malabsorption 2-22 months following small bowel resection and in a control group of 14 chronically ill, age- and weight-matched infants who did not undergo bowel resection. The prevalence of basal acid hypersecretion (defined as acid output 2 SD above the mean for the control group) was 17% (4 of 23). Basal gastric acid hypersecretion was associated with two factors: massive small bowel resection and initiation of enteral feeding. Basal acid hypersecretion was present on the initial study in 3 of 7 infants with less than one-third of the small bowel remaining, but in only 1 of 16 with more than one-third intact (p less than 0.05). Hypergastrinemia was present in 3 of 6 infants following massive bowel resection, but in only 1 of 15 with more than one-third intact (p less than 0.05), but hypergastrinemia was not consistently associated with hypersecretion. In each of six previously unfed infants, a trial of enteral feeding resulted in increased basal and maximal acid output. Three infants developed basal acid hypersecretion during initiation of enteral feeding. There was no evidence of pentagastrin-stimulated maximal acid hypersecretion in any of the infants.

Duodenal ulcer with unexplained marked basal gastric acid hypersecretion

Out of 1012 gastric analyses performed in 6 yr, 40 persons had basal acid output ≥ 15 mmol/hr. Of these, 8 had known causes for hypersecretion (6 had Zollinger-Ellison syndrome and 2 systemic mastocytosis); 1 died before further study, leaving 31 with unexplained basal acid hypersecretion (19.5 ± 0.60 mmol/hr) and peptic ulcer (30 duodenal ulcer and 1 gastric ulcer). All were male compared with the 72:28 M : F ratio in the duodenal ulcer population from which these were drawn. From among the same 1012 patients 29 male controls with duodenal ulcer and basal acid output < 6 mmol/hr (2.7 ± 0.31 mmol/hr) were matched for age, sex, and length of follow-up (3–81 mo). The hypersecretion group had higher fasting residual volume (154 ± 14 vs. 76 ± 8 ml, P < 0.01) and peak acid output (53 ± 3 vs. 33 ± 3 mmol/hr, P < 0.01). In 17 of the 31 subjects repeat testing of basal secretion (r = 0.64) was not significantly different (P > 0.1). In controls basal acid output was related to body weight (r = 0.65) but in the hypersecretors it was not (r = 0.11). In the hypersecretors, however, basal acid output was related to length of ulcer history (r = 0.71), but in the controls it was not (r = 0.06). A significant cholinergic contribution to the hypersecretion was inferred from >90% reduction by either atropine (15 μg/kg) or vagotomy in all 12 of the 31 hypersecretion subjects who were so studied. The clinical course of the two groups was not different as regards number of hospitalizations, episodes of bleeding, number of operations, number of perforations or obstruction, and the same proportion (9/31 vs. 8/29) remained free of complications during the average 12.5-yr period of total ulcer history. The finding of massive basal acid hypersecretion does not necessarily imply a Zollinger-Ellison syndrome nor call for unusually extensive surgery for peptic ulcer, vagotomy being sufficient to correct the hypersecretion.

Cause and effect of massive basal gastric acid hypersecretion (MBH) not due to zollinger-ellison syndrome (ZES)

Cause and effect of massive basal gastric acid hypersecretion (MBH) not due to zollinger-ellison syndrome (ZES)

Detection of a Circulating Gastric Secretagogue in Plasma Extracts from Normogastrinemic Patients With Acid Hypersecretion

Extracts were prepared from plasma of 12 subjects with normal serum gastrin concentration (less than 125 pg/ml), 5 normal subjects and 7 patients with duodenal ulcer and basal gastric acid hypersecretion (greater than 15 mEg/hr). Bioassays of plasma extracts were performed in anesthetized rats with perfused stomachs and acid out-puts were compared with those produced by normal saline and by 50 ng pentagastrin given in random order. Compared with saline, plasma extracts from 5 of 7 hypersecretor patients produced significant stimulation of acid secretion while none of the extracts from normal subjects produced acid stimulation. The stimulant identified in plasma from hypersecretor patients appears to be distinct from gastrin.

Hypergastrinemia in familial multiple endocrine adenomatosis.

Fasting serum gastrin levels of 46 members of 5 families with familial multiple endocrine adenomatosis were measured; 14 patients had hypergastrinemia (a serum gastrin level greater than 200 pg/ml), including all 6 patients with intractable peptic ulcer disease. Eight patients had asymptomatic hypergastrinemia, and 12 of the patients with hypergastrinemia had a history or findings of hyperparathyroidism. Fasting gastrin levels were not significantly correlated with calcium levels. Normal gastrin levels were found in six patients with hyperparathyroidism. Hypergastrinemia was found in six patients with normal or low serum calcium values who were studied after parathyroid surgery. Basal gastric acid hypersecretion and a marked rise in serum gastrin levels on intravenous calcium infusion were associated with fasting hypergastrinemia but were not found with hyperparathyroidism alone in the few patients tested.