Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using a 12-hour infusion of salmon synthetic calcitonin (S-CT), distinct and sustained inhibition of gastric acid and pepsin secretion has been demonstrated in 4 normal subjects, 3 patients with peptic ulcer disease and 3 high risk patients. In 3 patients with Zollinger-Ellison syndrome, treated in the same way, elevated serum gastrin was reduced by about 50% and acid secretion by more than 90%. In healthy volunteers oral administration of human synthetic CT (H-CT) led to reduction in basal and pentagastrin-stimulated acid and pepsin secretion by about 50%, lasting for more than 2 hours after the instillation of CT. In 4 subjects receiving CT intravenously, slight nausea and headache were registered, while there were no side effects after the oral route. Serum calcium did not change after i.v. or oral administration of CT. Wheras therapeutical applications of CT, given by i.v. route, seem to be restricted to selected cases, i.e. acute gastric ulcerations with imminent or existent bleeding, the eventual benefit or orally administered CT in peptic ulcer disease should be evaluated in controlled long-term trials.
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PMID:Long-term effects of calcitonin on gastric secretion in normals, peptic ulcer and high risk patients. 6 56

Although calcitonin and somatostatin are polypeptid hormones of entirely different structure, in pharmacological doses they possess a similar effect to secretions of stomach and pancreas. Given intravenously, they generally inhibit the basal secretion of organs, stimulated by pentagastrin or pancreozymin, as well as the contraction of the gallbladder. Orally, calcitonin also suppresses by direct contact the secretion of the stomach. While calcitonin in higher doses shows only very slight and tolerable side effects (nausea, headache), somatostatin acts suppressively on many other hormone-regulated systems. Apart from this, disturbances of blood coagulation in monkeys and man were observed, findings which necessitate very careful application. Therapeutical trials appear reasonable with calcitonin in treating acute pancreatitis, in prophylaxis and treatment of stress ulcers with the danger of bleeding, in intensive care medicine, in preoperative procedure of Zollinger-Ellison syndrome as well as in duodenal ulcers (oral calcitonin). Double blind studies are carried out at present to answer most of these questions (acute pancreatitis, stress ulcers, duodenal ulcers), results of which should definitely be awaited.
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PMID:[Summary of work session 4: Effects of calcitonin and somatostatin on the stomach and pancreas--a possible therapeutic principle]. 82 14

The Roux-en-Y syndrome was defined as chronic nausea, intermittent vomiting, and chronic abdominal pain worsened by eating in patients who have undergone a gastrojejunostomy Roux-en-Y reconstruction for peptic ulcer. When these patients fasted, the Roux limb showed striking abnormalities in motor function; when postprandial, they failed to convert to normal fed-state motor activity. In contrast, patients with Zollinger-Ellison syndrome do well after similar surgery; they can eat most foods and maintain their body weight. We studied the motility of the Roux limb and jejunum in six patients with Zollinger-Ellison after an esophagojejunostomy Roux-en-Y anastomosis. Roux-limb motor activity in these patients, as characterized by the migrating motor complex, was more frequent, well organized, and in synchrony with the remaining jejunum; most subjects also converted to the fed state after a liquid meal. We suggest that the enteric nervous system is intact and functions normally in patients who have had a Roux-en-Y reconstruction for ulcer disease secondary to Zollinger-Ellison, but not in patients with idiopathic peptic ulcer disease.
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PMID:Roux-limb motility after total gastrectomy and Roux-en-Y anastomosis in patients with Zollinger-Ellison syndrome. 155 44

This review comprises data from more than 19,000 individuals who have taken part in clinical studies of omeprazole. Isolated, non-specific adverse events which might be attributable to omeprazole have included nausea, dizziness, headache and diarrhoea. These events have been generally mild and transient and have not usually required either a reduction of dose or cessation of therapy. The frequency and spectrum of adverse events have been the same in those over 65 years of age as in younger patients. No drug-related adverse events have been found in patients with renal insufficiency or severe liver failure. More than 1.2 million patient treatments of omeprazole have now been given. The overall incidence of adverse events with omeprazole is low, and in comparative studies has been in the same range as that found with H2-receptor antagonists. Importantly, no dose-related adverse events have been observed with omeprazole in the dose range 10-60 mg/day. Furthermore, none of the serious adverse events that have been reported have been attributable to omeprazole. No histological changes in oxyntic endocrine cells have been found after short-term periods of treatment with either omeprazole or H2-receptor antagonists in patients with peptic ulcer disease. Long-term continuous high-dose omeprazole treatment of patients with Zollinger-Ellison syndrome has not induced any significant increase in the oxyntic endocrine cell hyperplasia. Investigations of the gastric mucosa from patients in a compassionate use programme who have received omeprazole, usually 20 mg daily, for periods of up to 37 months, have been performed. Two hundred and forty-eight patients had their last biopsy taken after at least 11 months of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The clinical safety of omeprazole. 209 17

The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage and administration of omeprazole are reviewed. Omeprazole, a substituted benzimidazole, has a unique site and mechanism of action because it inhibits the proton pump--i.e., hydrogen, potassium adenosine triphosphatase (H+,K+-ATPase)--and consequently blocks the final common step in the gastric acid secretory pathway. Omeprazole inhibits basal and histamine-, gastrin- and pentagastrin-stimulated gastric hydrochloric acid secretion. It produces a dose-dependent reduction in gastric acidity, gastric acid output, and gastric juice volume and has variable effects on pepsin secretion. Omeprazole has no documented effect on esophageal motility or lower esophageal sphincter pressure. Omeprazole is variably absorbed from the gastrointestinal tract, and food appears to decrease the rate, but not the extent, of drug absorption. The drug is approximately 95% bound to plasma proteins and is metabolized to inactive components that are enterohepatically or renally eliminated. Omeprazole is more effective (in most studies) than H2-receptor antagonists in treating duodenal ulcer, at least as effective in treating benign gastric ulcer, and more effective in treating reflux esophagitis. Omeprazole has been used successfully in patients with Zollinger-Ellison syndrome refractory to treatment with H2-receptor antagonists. Gastrointestinal complaints (nausea and diarrhea) are the most commonly reported adverse effects associated with omeprazole therapy. The most frequently reported laboratory abnormality occurring with omeprazole use is elevation of serum aspartate aminotransferase and alanine aminotransferase concentrations. Omeprazole will serve a valuable role in the management of gastrointestinal tract ulcers and hypersecretory conditions.
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PMID:Therapeutic evaluation of omeprazole. 306 85

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)
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PMID:Idiopathic gastric acid hypersecretion. Comparison with Zollinger-Ellison syndrome. 802 53

Omeprazole has been marketed in France since 1989, for the healing of peptic ulcers, erosive reflux esophagitis and the Zollinger Ellison syndrome. It is a proton pump inhibitor which inhibits the acid secretion in the stomach. In the majority of the clinical trials, omeprazole has been found to be well tolerated: headache, dizziness, skin rash, constipation have just been noted. Since September 1989, 143 adverse reactions have been reported to pharmacovigilance centres and Astra France: 37 neurological and psychiatric side effects, especially confusion in patients with hepatic diseases and/or advanced age; 35 cutaneous reactions, generally rash and urticaria; 22 hematological effects: leucopenia and agranulocytosis have been reported but the relation with omeprazole is very uncertain; 10 gastrointestinal effects, generally diarrhoea, nausea, vomiting and abdominal pain; 8 hepatic disorders, especially moderate elevation of aminotransferases. This study confirms the safety of this drug, during short treatment; the frequency of notified adverse effects is about 1/12 200 treatments of 4 weeks. The ministry of health, has decided, in november 1991, to inform the prescribers of this potential toxicity of omeprazole, particularly, of the risk of confusion, hepatotoxicity and leucopenia.
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PMID:[Evaluation of unexpected and toxic effects of omeprazole (Mopral) reported to the regional centers of pharmacovigilance during the first 22 postmarketing months]. 814 27

Lansoprazole is a proton pump inhibitor that reduces gastric acid secretion. It has proved effective in combination regimens for the eradication of Helicobacter pylori and as monotherapy to heal and relieve symptoms of gastric or duodenal ulcers and gastro-oesophageal reflux. After initial healing, it may be used to prevent recurrence of oesophageal erosions or peptic ulcers in patients in whom H. pylori is not the major cause of ulceration and to reduce basal acid output in patients with Zollinger-Ellison syndrome. Usual dosages are 15 to 60 mg/day, although dosages of < or = 180 mg/day have been used in patients with hypersecretory states. In patients with duodenal or gastric ulcer, short term lansoprazole monotherapy was similar to omeprazole and superior to histamine H2 receptor antagonists in achieving healing rates > 90%. Lansoprazole was as effective a component of H. pylori eradication regimens as omeprazole, tripotassium dicitrato bismuthate (colloidal bismuth subcitrate) or ranitidine. Lansoprazole was superior to ranitidine in symptom relief and healing of gastro-oesophageal reflux disease and tended to relieve symptoms more rapidly than omeprazole, although initial healing was similar. As maintenance treatment, lansoprazole was similar to omeprazole and superior to ranitidine in relieving symptoms and preventing relapse. Lansoprazole was also superior to ranitidine in healing and relieving symptoms of oesophageal erosions associated with Barrett's oesophagus; healing was maintained for a mean of 2.9 years in > or = 70% of patients. Lansoprazole was also superior to ranitidine in prophylaxis of redilatation of oesophageal strictures. After > or = 4 years of use in patients with Zollinger-Ellison syndrome, lansoprazole 60 to 180 mg/day effectively controlled basal acid output. Dosages may be reduced in some patients once healing and symptom relief has been achieved. Preliminary studies of lansoprazole in patients at risk of aspiration pneumonia or stress ulcers show promise. Although studies show lansoprazole is potentially effective in treating gastrointestinal bleeding, future studies should assess patients' H. pylori status. Lansoprazole has been well tolerated in clinical trials, with headache, diarrhoea, dizziness and nausea appearing to be the most common adverse effects. Tolerability of lansoprazole does not deteriorate with age and the drug is well tolerated in long term use (< or = 4 years) in patients with Zollinger-Ellison syndrome or reflux disease. Thus, lansoprazole is an important alternative to omeprazole and H2 receptor antagonists in acid-related disorders. In addition to its efficacy in healing or maintenance treatment, it may provide more effective symptom relief than other comparator agents.
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PMID:Lansoprazole. An update of its pharmacological properties and clinical efficacy in the management of acid-related disorders. 927 7

Four patients with gastroduodenal ulcers in the absence of Helicobacter pylori illustrate the decreasing prevalence of this microorganism. One was a 19-year-old boy with nausea, diarrhoea and weight loss caused by multiple gastroduodenal ulcers due to the Zollinger-Ellison syndrome. Another was a 36-year-old man with abdominal discomfort caused by an ulcer due to Crohn's disease. The other two cases concerned a 29-year-old man and a 68-year-old woman with relapsing ulcer disease and active bleeding, in whom no causal factors could be determined. Recent studies suggest a decreasing prevalence of H. pylori leading to both a relative and an absolute decrease of gastroduodenal ulcers attributed to H. pylori. Future treatment strategies will have to take these altered prevalence rates into consideration.
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PMID:[Decreasing prevalence of Helicobacter pylori: a consequence of treatment of gastroduodenal ulcers]. 1092 45

The authors describe the case of a 51-year-old male with Zollinger-Ellison syndrome manifested by epigastralgia, nausea, vomiting, hypergastrinemia and multiple endocrine neoplasia type 1. History included a Billroth II procedure for a perforated duodenal ulcer. Multiple metastatic liver lesions were found that were gastrin-negative and chromogranin-positive. Endoscopy revealed a large ulcerated gastro-jejuno-colonic fistula which was surgically repaired. Pre- and postoperative imaging studies, including the highly sensitive somatostatin-receptor scintigraphic scan using In-pentetreotide, have consistently failed to disclose other tumors. Recent reports indicate that most Zollinger-Ellison syndrome-associated gastrinomas are small, easily overlooked lesions located in the proximal duodenum rather than in the pancreas as formerly believed. In the present patient therapy with omeprazole and alpha-interferon has produced complete remission of the Zollinger-Ellison syndrome and a stabilization of tumor growth has occurred during the last 7 years, allowing the patient to live a normal life. This peculiar response to therapy is discussed.
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PMID:Liver metastases of endocrine tumour associated with multiple endocrine neoplasia type 1: a sustained response to interferon therapy or a peculiar benign course? 1110 Mar 30


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