Idiopathic Gastric Acid Hypersecretion Research Articles

Idiopathic Gastric Acid Hypersecretion in a Patient With MUTYH-Associated Polyposis

To the Editor: MUTYH (mutY homolog)–associated polyposis (MAP) is a recently discovered autosomal recessive precancerous colorectal condition caused by germline mutations in the BER (base excision repair) gene, MUTYH (MYH) (1). Its mutation spectrum and phenotype have yet to be fully elucidated. We report a case of comorbid MAP and idiopathic gastric acid hypersecretion.

Esomeprazole controls acid output in patients with Zollinger-Ellison syndrome or idiopathic gastric acid hypersecretion,

Esomeprazole controls acid output in patients with Zollinger-Ellison syndrome or idiopathic gastric acid hypersecretion,

Effects of Esomeprazole on Acid Output in Patients With Zollinger-Ellison Syndrome or Idiopathic Gastric Acid Hypersecretion

To evaluate the efficacy and safety of oral esomeprazole in the control of gastric acid hypersecretion in patients with hypersecretory states. In this 12-month, open-label, multicenter study, acid output (AO) was evaluated at baseline, day 10, and months 3, 6, and 12. The starting dose of esomeprazole was 40 mg or 80 mg twice daily. On day 10, patients with controlled AO were maintained on the same dose, while those with uncontrolled AO had their doses increased (maximum dose 240 mg/day) until control was attained. Esophagogastroduodenoscopy (EGD) was performed at baseline and at 6 and 12 months. Safety and tolerability were assessed throughout the study by EGD, gastric analysis, and adverse events. Twenty-one patients (19 with Zollinger-Ellison syndrome [ZES], 2 with idiopathic gastric acid hypersecretion [IGH]) completed the study. Of the 20 patients with controlled AO at day 10, 18 (90%) had sustained AO control for the rest of the study. At 12 months, AO was controlled in 14 of 16 patients receiving esomeprazole 40 mg twice daily, in all 4 patients receiving esomeprazole 80 mg twice daily, and in the 1 patient receiving esomeprazole 80 mg 3 times daily. At 6 and 12 months, no patient had endoscopic evidence of mucosal disease. Esomeprazole was well tolerated; 1 patient had a serious adverse event (hypomagnesemia) attributed to treatment that resolved with magnesium supplementation during continued treatment. Esomeprazole in appropriately titrated doses controls AO over 12 months in patients with hypersecretory states and is well tolerated.

Rabeprazole is an effective treatment for Zollinger-Ellison syndrome (ZES) or idiopathic gastric acid hypersecretion (IGAH),

Rabeprazole is an effective treatment for Zollinger-Ellison syndrome (ZES) or idiopathic gastric acid hypersecretion (IGAH),

An open‐label study of rabeprazole in patients with Zollinger–Ellison syndrome or idiopathic gastric acid hypersecretion

Omeprazole and lansoprazole are both of proven efficacy in the treatment of Zollinger-Ellison syndrome and idiopathic gastric acid hypersecretion. Rabeprazole, which has a similar mechanism of action, has not previously been studied in these diseases. To determine the dose of rabeprazole that decreased basal acid output to safe levels in patients with Zollinger-Ellison syndrome or idiopathic gastric acid hypersecretion. Patients with Zollinger-Ellison syndrome or idiopathic gastric acid hypersecretion were given rabeprazole 60 mg once daily for uncomplicated disease or 40 mg twice daily for complicated disease. Doses were titrated according to response and continued for 2 years. Efficacy was assessed primarily by measuring basal acid output. All patients had basal acid output before the next dose controlled to <10 mmol/h either at the starting dose or after minor dose titration. Control of acid output was maintained for 2 years. Consistent with this, most patients reported few gastrointestinal symptoms. Gastric biopsy showed no enterochromaffin-like cell dysplasia or neoplasia. Rabeprazole was an effective and well-tolerated treatment for Zollinger-Ellison syndrome or idiopathic gastric acid hypersecretion, which reliably reduced gastric acid output to safe levels. Although a dose of 60 mg once daily was appropriate for most patients in this study, doses may need adjustment according to individual response.

Esomeprazole maintains normal gastric levels in patients with Zollinger-Ellison syndrome (ZES) or idiopathic gastric acid hypersecretion

Esomeprazole maintains normal gastric levels in patients with Zollinger-Ellison syndrome (ZES) or idiopathic gastric acid hypersecretion

Idiopathic gastric acid hypersecretion

Norwegian University of Science and Technology, Trondheim, Norway Correspondence to Helge L. Waldum, MD, PhD, Norwegian University of Science and Technology, Department of Cancer Research and Molecular Medicine, Trondheim University Hospital, N-7006, Trondheim, Norway. Tel: +47 73 96 85 41; fax: +47 73 86 75 46; e-mail: [email protected]

Effects of Esomeprazole on Acid Output in Patients with Zollinger-Ellison Syndrome (ZES) and Idiopathic Gastric Acid Hypersecretion (IGH)

Effects of Esomeprazole on Acid Output in Patients with Zollinger-Ellison Syndrome (ZES) and Idiopathic Gastric Acid Hypersecretion (IGH)

Response to Dr Waldum??s letter regarding ???Idiopathic gastric acid hypersecretion presenting as a diarrheal disorder and mimicking both Zollinger???Ellison syndrome and Crohn??s disease???

Blonski, Wojciech C.a b; Katzka, David A.a; Lichtenstein, Gary R.a; Metz, David C.a Author Information

Idiopathic gastric acid hypersecretion presenting as a diarrheal disorder and mimicking both Zollinger???Ellison syndrome and Crohn??s disease

Many gastric acid hypersecretory states (basal acid output of greater than 15.0 mEq/h) exist for which the etiology is known, such as Zollinger-Ellison syndrome, systemic mastocytosis, antral exclusion, antral predominant Helicobacter pylori gastritis (antral G cell hyperplasia), chronic gastric outlet obstruction, short gut syndrome and basophilic leukemias. However, many hypersecretory patients have no identified etiology for their acid hypersecretion and are designated as idiopathic gastric acid hypersecretors with a basal acid output of greater than 10 mEq/h and a normal serum gastrin level. Because of the gastric acid hypersecretion these patients also commonly have an increased frequency of stools. Idiopathic gastric acid hypersecretion represents a known cause of gastric acid hypersecretion that is far more common than Zollinger-Ellison syndrome and it has a markedly different treatment regimen and natural history. We report a case of a patient with idiopathic gastric acid hypersecretion previously misdiagnosed as having Crohn's disease because of a presenting complaint of diarrhea and mimicking Zollinger-Ellison syndrome because her fasting serum gastrin level was elevated when incorrectly measured in the presence of antisecretory treatment.

Intravenous pantoprazole rapidly controls gastric acid hypersecretion in patients with Zollinger–Ellison syndrome

Background & Aims: Parenteral control of gastric acid hypersecretion in conditions such as Zollinger–Ellison syndrome (ZES) or idiopathic gastric acid hypersecretion is necessary perioperatively or when oral medications cannot be taken for other reasons (e.g., during chemotherapy, acute upper gastrointestinal bleeding, or in intensive care unit settings). Methods: We evaluated the efficacy and safety of 15-minute infusions of the proton pump inhibitor pantoprazole (80–120 mg every 8–12 hours) in controlling acid output for up to 7 days. Effective control was defined as acid output >10 milliequivalents per hour (mEq/h) (<5 mEq/h in patients with prior acid-reducing surgery) for 24 hours. Results: The 21 patients enrolled had a mean age of 51.9 years (range, 29–75) and a mean disease duration of 8.1 years (range, <0.5–21); 13 were male, 7 had multiple endocrine neoplasia syndrome type I, 4 had undergone acid-reducing surgery, 2 had received chemotherapy, and 13 had undergone gastrinoma resections without cure. Basal acid output (mean ± SD) was 40.2 ± 27.9 mEq/h (range, 11.2–117.9). In all patients, acid output was controlled within the first hour (mean onset of effective control, 41 minutes) after an initial 80-mg intravenous pantoprazole dose. Pantoprazole, 80 mg every 12 hours, was effective in 17 of 21 patients (81%) for up to 7 days. Four patients required upward dose titration, 2 required 120 mg pantoprazole every 12 hours, and 2 required 80 mg every 8 hours. At study end, acid output remained controlled for 6 hours beyond the next expected dose in 71% of patients (n = 15); mean acid output increased to 4.0 mEq/h (range, 0–9.7). No serious or unexpected adverse events were observed. Conclusions: Intravenous pantoprazole, 160–240 mg/day administered in divided doses by 15-minute infusion, rapidly and effectively controlled acid output within 1 hour and maintained control for up to 7 days in all ZES patients. GASTROENTEROLOGY 2000;118:696-704

Ranitidine therapy in patients with idiopathic gastric acid hypersecretion

One hundred twenty-four patients with idiopathic gastric acid hypersecretion (basal acid output greater than 10.0 meq/hr) were prospectively evaluated and treated with ranitidine twice a day. Fifty-four patients (44%) required standard doses of ranitidine 300 mg/day for adequate treatment, and the other 70 patients (56%) required increased doses of ranitidine (mean 994 mg/day, range 600-3000 mg/day). Mean basal acid outputs for these two groups were 14.0 and 16.6 meq/hr, respectively, which were not significantly different. Nevertheless, there was a significant correlation between basal acid output and daily ranitidine dose required for therapy (r = 0.18, P = 0.05). The duration of ranitidine therapy consisted of: < 1 year (N = 46), 1 year (N = 16), 2 years (N = 19), 3 years (N = 22), 4 years (N = 15), 5 years (N = 6). Only five patients required progressive increases in ranitidine during the time of treatment, which consisted of an average of 0.5 dose adjustments per year. No side effects occurred with any of these high doses of ranitidine. These results indicate that, as in Zollinger-Ellison syndrome, ranitidine is effective therapy for patients with idiopathic gastric acid hypersecretion; however, markedly increased doses as large as 3000 mg/day may be required.

Idiopathic gastric acid hypersecretion

Many patients with acid-peptic disease have idiopathic gastric acid hypersecretion defined as a basal acid output > 10.0 meq/hr; however, a significant proportion have basal acid outputs > 15.0 meq/hr, which is within the range found in Zollinger-Ellison syndrome. Although idiopathic gastric acid hypersecretion is more common than Zollinger-Ellison syndrome, it is important that these two disorders be differentiated because of differences in treatment and natural history. In the present study, we compared 124 patients with idiopathic gastric acid hypersecretion and 137 patients with Zollinger-Ellison syndrome. There were no significant differences with regard to age at diagnosis, history of upper gastrointestinal hemorrhage, nausea, vomiting, and family history of duodenal ulcer and other acid-peptic disease. However, significant differences were observed between patients with idiopathic gastric acid hypersecretion and patients with Zollinger-Ellison syndrome with regard to percentage of males: 77% compared to 64% (P = 0.008), mean serum gastrin: 60 pg/ml compared to 3679 pg/ml (normal < 100 pg/ml) (P < 0.001), mean basal acid output: 15.4 meq/hr compared to 47.0 meq/hr (P < 0.001), mean age at onset of symptoms: 33 years compared to 41 years (P < 0.001), mean duration of symptoms before diagnosis: 11 years compared to five years (P < 0.001), percentage with abdominal pain: 67% compared to 82% (P = 0.00004), percentage with diarrhea: 12% compared to 75% (P < 0.000001), percentage with pyrosis: 58% compared to 40% (P = 0.003), percentage with duodenal ulcer: 53% compared to 74% (P < 0.000001), and percentage with esophagitis: 31% compared to 42% (P = 0.0004).(ABSTRACT TRUNCATED AT 250 WORDS)

Helicobacter pylori in duodenal ulcer patients with idiopathic gastric acid hypersecretion

Thirty-three consecutive patients with idiopathic gastric acid hypersecretion (defined as a basal acid output > 10.0 meq/hr with a normal fasting serum gastrin level and negative secretin stimulation test) who were being treated for duodenal ulcer disease and other acid-peptic disorders were evaluated for the presence of Helicobacter pylori by means of a rapid urease test. Fourteen patients had duodenal ulcer and 19 had other acid-peptic disorders (gastroesophageal reflux in 14, including six with Barrett's esophagus; four with nonulcer dyspepsia; and one with erosive gastritis). Helicobacter pylori was present in 12 of the 14 ulcer patients (86%) compared to only two of the 19 nonulcer patients (11%) (P < 0.0001). The distribution of basal acid output for patients with duodenal ulcer was similar to that for nonulcer patients, and no significant difference in the mean basal acid output was found among Helicobacter pylori-positive compared to Helicobacter pylori-negative patients. Seven of the duodenal ulcer patients with a basal acid output greater than 15.0 meq/hr were Helicobacter pylori-positive, suggesting that the organism can withstand even extreme levels of gastric acidity. In conclusion, this study demonstrates that the prevalence of Helicobacter pylori infection in patients with duodenal ulcer disease associated with idiopathic gastric acid hypersecretion is not different from a majority of ulcer patients with normal acid secretory profiles and offers additional evidence that extreme levels of gastric acid are not bactericidal for the organism.

Definition for idiopathic gastric acid hypersecretion

Zollinger-Ellison syndrome and other gastric acid hypersecretory states in which a specific etiology is identified are defined as a basal acid output of greater than 15.0 meq/hr. To determine the level of basal acid output that defines idiopathic gastric hypersecretion, basal acid outputs were investigated in normal subjects and patients with duodenal ulcers, and functional and statistical definitions for idiopathic gastric acid hypersecretion were developed. Sixty-five normal subjects were evaluated to define idiopathic gastric acid hypersecretion on a statistical basis, and 22 patients with refractory duodenal ulcers were evaluated to define idiopathic gastric acid hypersecretion on a functional basis. Mean basal acid output for the 65 normal subjects was 3.0 +/- 2.7 meq/hr. Even though the mean basal acid output for the group of 28 normal male subjects was slightly higher than for the group of 37 normal female subjects, the groups were not significantly different. The 95% confidence interval around the mean basal acid output for all normal subjects was 2.4-3.7 meq/hr, with little difference between the male and female groups. The mean basal acid output plus two standard deviations and the mean basal acid output plus three standard deviations for the 65 normal subjects were 8.4 meq/hr and 11.1 meq/hr, respectively. Of 109 patients with active duodenal ulcers treated for eight weeks with standard doses of antisecretory medication, 22 showed no healing as documented by endoscopy.(ABSTRACT TRUNCATED AT 250 WORDS)

Idiopathic gastric acid hypersecretion: treatment implications for refractory acid/peptic disorders

Although in most patients with duodenal ulcer disease the ulcer heals after 8 weeks of treatment with standard doses of H2 blockers or other agents, in about 10% the ulcer does not heal. These patients are considered 'refractory' to treatment. Reasons often cited for non-healing include poor patient compliance, cigarette smoking, and non-steroidal anti-inflammatory drug (NSAID) use. Gastric acid hypersecretion also appears to be an important factor in non-healing with standard doses of antisecretory agents. We have defined idiopathic gastric acid hypersecretion as a basal acid output of greater than 10 mmol/h in the absence of an elevated fasting serum gastrin level (or a negative secretin test if gastrin level greater than 100 pg/ml) to exclude persons with Zollinger-Ellison syndrome. Among the acid/peptic-related disorders in which idiopathic gastric acid hypersecretion should be considered are refractory duodenal ulcer, refractory gastro-oesophageal reflux disease (especially patients with oesophagitis), postbleeding duodenal ulcer, and certain rare disorders such as hereditary angioedema. Some children with atypical abdominal pain may also be hypersecretors of gastric acid. Once identified, patients with refractory duodenal ulcer or gastro-oesophageal reflux disease are treated with incremental doses of ranitidine titrated against the level of gastric acid secretion that remains during therapy. Ranitidine was selected to avoid the dose-related antiandrogenic effects and potential hepatic cytochrome P450 system-related drug interactions that may occur with cimetidine. In most cases of refractory duodenal ulcer, doubling the standard dose of ranitidine (to 300 mg b.d.) is sufficient to achieve symptomatic relief and mucosal healing. Higher doses appear to be necessary for refractory oesophagitis. To date, no side effects have been associated with high doses of ranitidine (up to 1800 mg/day) for periods of longer than 6 months. Idiopathic gastric acid hypersecretion is an important factor in explaining why not all patients respond to a 'standard' ulcer-healing dose of H2 blocker, and it provides a rationale for use of higher-dose therapy as a safe and effective alternative to omeprazole or to combination drug therapy in refractory acid/peptic disease.

Zollinger-Ellison Syndrome in the Intensive Care Setting

Management of patients with Zollinger-Ellison syn drome differs markedly from management of patients with idiopathic gastric acid hypersecretion or routine peptic ulcer disease. Because of the possible complica tions arising from gastric acid hypersecretion or from complications caused by the gastrinoma itself, patients with these disorders frequently present to critical care physicians. It is important that critical care physicians be familiar with the acute presentation of patients with Zollinger-Ellison syndrome as well as the appropriate treatment. We review the important points pertaining to the recognition and treatment of Zollinger-Ellison syn drome in the acute care setting.

Antiandrogen effects of ulcer drug averted with experimental agent

Impotence has been reported to occur in a few men taking cimetidine for duodenal or gastric ulcers. In fact, in a study reported at the recent Digestive Disease Week meetings in Chicago, impotence, breast tenderness, and gynecomastia occurred in almost half of a small group of men taking high doses of cimetidine. These adverse effects disappeared, however, in those of the men who were switched to the investigational agent ranitidine, also an H₂-receptor antagonist which has been used for some years in Europe. The study, described by gastroenterologist Robert T. Jensen, MD, senior investigator at the National Institute of Arthritis, Diabetes, and Digestive and Kidney Diseases, Bethesda, Md, was carried out by Jensen and colleagues at that institute and elsewhere at the National Institutes of Health (NIH). The 19 patients in the study had either Zollinger-Ellison syndrome or idiopathic gastric acid hypersecretion. Doses of cimetidine used to control