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

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.
 ...
PMID:Therapeutic evaluation of omeprazole. 306 85

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.
 ...
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.
 ...
PMID:Lansoprazole. An update of its pharmacological properties and clinical efficacy in the management of acid-related disorders. 927 7

There is a growing body of pathophysiological evidence that gastroesophageal reflux disease (GERD) is caused by disordered motility and not acid hypersecretion. The key factor in the pathogenesis of GERD is disordered function of the lower esophageal sphincter. Other factors include delayed gastric emptying and decreased peristalsis in the body of the esophagus. The principal symptoms of GERD are heartburn and regurgitation. Studies have demonstrated that up to 50% of patients may have other symptoms of dysmotility including epigastric discomfort or fullness, nausea and early satiety. The use of a prokinetic agent in such patients seems logical. Given its proven superior efficacy over domperidone and metaclopramide in treating GERD, cisapride has become the prokinetic drug of choice for the acute management and maintenance therapy of GERD. In the acute management of GERD, cisapride is superior to placebo and has the same efficacy as H2 receptor antagonists (H2RAs) in several clinical trials. It is also effective in maintenance therapy for GERD. These studies are reviewed. Cisapride (10 mg qid or 20 mg bid) is effective in the acute treatment of mild to moderate GERD, particularly in patients with heartburn associated with other symptoms of dysmotility, and particularly in patients with heartburn associated with gastroparesis. Combination therapy with an H2RA may be considered if symptoms (particularly dysmotility symptoms) persist with H2RA alone. In severe GERD that is not responsive to conventional doses of a proton pump inhibitor, cotherapy with cisapride or increasing the dose of the proton pump inhibitor are the two therapeutic options to consider. Cisapride 20 mg at bedtime is effective maintenance therapy for patients with mild to moderate GERD.
 ...
PMID:Prokinetic therapy in gastroesophageal reflux disease. 934 80

Rabeprazole is a proton pump inhibitor with antisecretory properties. In vitro animal experiments have indicated that the inhibition of the proton pump by rabeprazole is partially reversible. Rabeprazole has 2- to 10-fold greater antisecretory activity than omeprazole in vitro. However, it dissociates more readily from H+,K(+)-ATPase than omeprazole, resulting in a shorter duration of action. In comparative clinical trials rabeprazole was significantly more effective than placebo, famotidine or ranitidine and as effective as omeprazole in the treatment of patients with erosive or ulcerative gastro-oesophageal reflux disease or gastric or duodenal ulcers. Healing rates with rabeprazole were independent of Helicobacter pylori status. Rabeprazole in combination with either clarithromycin and metronidazole or clarithromycin and amoxicillin or amoxicillin and metronidazole or clarithromycin for 7 days produced eradication of H. pylori in 100, 95, 90 and 63% of patients. The tolerability profile of rabeprazole 20mg once daily was similar to that of famotidine 20mg twice daily, ranitidine 150mg 4 times daily or omeprazole 20mg once daily in comparative trials. The adverse events reported with once daily administration of rabeprazole 20mg include malaise, nausea, diarrhoea, headache, dizziness and skin eruptions in 0.7 to 2.2% of patients.
 ...
PMID:Rabeprazole. 950 45

Mallory-Weiss syndrome is one of the cause of upper gastrointestinal hemorrhage, which an abrupt rise in abdominal pressure due to nausea or vomiting induces a tear near the esophagogastric mucosal junction. Mallory-Weiss syndrome represents about 3-15% of all cases of upper gastrointestinal hemorrhage. Mallory-Weiss tear is mainly located on the cardia part of the stomach side and spanning across the esophagogastric mucosal junction, only in esophageal side is rarely seen. Hemorrhage frequently ceases spontaneously. When endoscopic findings reveal persistent hemorrhage, endoscopic hemostatic technique using heater probe thermocoagulation or hemoclipping is necessary. After endoscopic hemostasis, fasting and inhibitors of acid secretion (H2-receptor antagonists or proton pump inhibitors) are recommended.
 ...
PMID:[Mallory-Weiss syndrome]. 978 Jul 15

Rumination is an unusual gastrointestinal symptom that is characterized by the repetitive regurgitation of gastric contents into the oropharynx. The regurgitation occurs very soon after a meal and tends to persist for 1 to 2 hours. Rumination is defined by the setting in which it occurs. It is seen in three distinct populations: infants; individuals with psychiatric and neurologic disorders, particularly developmental disabilities; and adults who do not have overt psychiatric or neurologic disorders. The hallmark of rumination, which separates it from other disorders of the upper gastrointestinal tract (such as gastroesophageal reflux disease or cyclic vomiting syndrome), is the fact that in patients with rumination, the gastric contents appear in the oropharynx without retching or nausea. Rather, the patient makes a conscious decision on how to handle the regurgitated material after it presents into the oropharynx. The regurgitated meal usually consists of undigested or partially digested food. The regurgitation is effortless or at most is preceded by a sensation of belching immediately prior to the regurgitation itself. The management of patients with rumination needs to be accomplished in a highly individualized manner. Children with infant rumination syndrome often have symptoms related to significant defects in bonding with their mother. Thus, problems of mother-child bonding in pediatric patients with rumination syndrome should be identified and appropriately addressed. The management of adult patients with developmental disabilities or neurologic impairments who ruminate focuses mainly on behavioral modalities, including adversive conditioning and contingency management. The healthy adult who ruminates and has no evidence of neurologic or developmental disability is best seen as someone with a habit. Management in these patients is directed towards adjunctive therapies (ie, the use of proton pump inhibitors or H(2 )receptor antagonists to decrease acid injury to the esophagus) as well as identifying situations and emotions that trigger the patient's symptoms. Randomized controlled trials of various treatment modalities need to be undertaken; likewise, the evaluation strategy needed to best diagnose rumination is yet to be well defined. At this time, the challenge for gastroenterologists is to understand the nature of rumination, to identify individuals at high risk, and to use the management strategies most associated with good outcomes in patients with rumination in various clinical settings.
 ...
PMID:Rumination. 1146 94

Omeprazole is a proton pump inhibitor that is used commonly in the treatment of acid-peptic disorders. Although omeprazole is generally well tolerated, serious adverse effects such as renal failure have been reported. Thus far, 17 cases of acute interstitial nephritis (AIN) secondary to omeprazole have been described. Another case of AIN is described in a 36-yr-old woman presenting with nausea, vomiting, weight loss, and a rising serum creatinine concentration. Omeprazole therapy had ceased 2 wk before admission. AIN was diagnosed by renal biopsy and corticosteroid therapy was initiated. After 4 wk of therapy the serum creatinine concentration had normalized. Among the reported cases in the literature, AIN was diagnosed after an average of 2.7 months of therapy with 20-40 mg of omeprazole daily. Recurrence was universal on rechallenge. Common symptoms included fatigue, fever, anorexia, and nausea. The classic triad of fever, rash, and eosinophilia was uncommon. Typical laboratory features included hematuria, proteinuria, pyuria, eosinophilia, and anemia. Management consisted of withdrawal of omeprazole and corticosteroid therapy in some patients. All but one patient recovered normal renal function. Corticosteroid therapy was well tolerated and may have been beneficial.
 ...
PMID:Acute interstitial nephritis due to omeprazole. 1177 62

Functional (nonulcer) dyspepsia refers to upper abdominal pain or discomfort with or without symptoms of early satiety, nausea, or vomiting with no definable organic cause. The current Rome II criteria help to diagnose functional dyspepsia and avoid misdiagnosis of gastroesophageal reflux disease and irritable bowel syndrome as functional dyspepsia. Assessment of gastric emptying with scintigraphy or breath testing may be useful in identifying delayed gastric emptying in patients with dyspeptic symptoms and may be helpful in patient management. Electrogastrography is a noninvasive test that evaluates for gastric dysrhythmias. Satiety testing is being evaluated as an indirect test for impaired fundic relaxation and visceral hypersensitivity. The symptom response to Helicobacter pylori therapy in patients with functional dyspepsia and a negative endoscopy examination but a positive H. pylori test is marginal. Lifestyle modifications often are suggested for initial treatment of functional dyspepsia. Dietary changes such as frequent small meals, low-fat diet, and avoidance of certain aggravating foods may improve symptoms. Additional measures include cessation of smoking, avoiding excess alcohol intake, and minimizing coffee intake. Antacids and over-the-counter histamine type 2 receptor antagonists may be helpful as an "on-demand" therapy for intermittent symptoms. They are safe and relatively inexpensive. Different subgroups of functional dyspepsia are based on the predominant symptom and may help in choosing an appropriate drug to initiate therapy. If the predominant symptom is epigastric pain (ulcer-like functional dyspepsia), histamine-2 receptor antagonists or proton pump inhibitors are the initial treatment of choice. If fullness, bloating, early satiety or nausea is the predominant complaint (dysmotility-like functional dyspepsia), a prokinetic agent may help. Metoclopramide is the only available effective prokinetic agent at present. If metoclopramide is used, short-term treatment and discussion of possible side effects with the patient are advised. If there is no response to these initial treatments, switching therapy from proton pump inhibitor to prokinetic or vice versa can be tried. If these treatment options fail, patient re-evaluation for other disorders (including other functional bowel disorders) is advised. A low-dose tricyclic antidepressant at bedtime may be helpful for treatment of visceral hypersensitivity.
 ...
PMID:Functional (Nonulcer) Dyspepsia. 1187 96

Dyspepsia describes a symptom complex thought to arise in the upper gastrointestinal tract and includes, in addition to epigastric pain or discomfort, symptoms such as heartburn, acid regurgitation, excessive burping or belching, a feeling of slow digestion, early satiety, nausea and bloating. Based on the evidence that heartburn cannot be reliably distinguished from other dyspeptic symptoms, the Rome definition appears to be too narrow and restrictive. It is particularly ill suited to the management of uninvestigated dyspepsia at the level of primary care. In patients presenting with uninvestigated dyspepsia, a symptom benefit is associated with a 'test and treat' approach for Helicobacter pylori infection. A substantial proportion of those who do not benefit prove to have esophagitis on endoscopy. In those with functional dyspepsia, the benefits of H pylori eradication, if any, appear to be modest. Hence, a 'symptom and treat' acid-suppression trial with proton pump inhibitors, and a 'test and treat' strategy for H pylori are two acceptable empirical therapies for patients with univestigated dyspepsia.
 ...
PMID:Etiology of dyspepsia: implications for empirical therapy. 1236 18


1 2 3 4 5 6 7 Next >>