Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic intestinal pseudo-obstruction is the term applied to a heterogeneous group of functional motility disorders sharing a common clinical expression: signs and symptoms of bowel obstruction in absence of mechanical occlusion. It is caused by ineffective intestinal propulsion. The chronic form of intestinal pseudo-obstruction may be primary or secondary. Primary pseudo-obstruction or chronic idiopathic pseudo-obstruction (CIIP) defines a group of propulsive disorders having no recognized underlying diseases. This study presents four female patients, aged between 4 months to 7 years, and makes a review of the literature. The symptoms, very similar in three of them, were bilious vomiting, abdominal distention and constipation, alternating with diarrhea and malnutrition. The fourth patient, different from the others in the age of onset and evolution, only had severe constipation and abdominal bloating. The diagnostic was made by full thickness biopsies during laparotomy, getting specimens by mapping, at different heights of intestine and stomach. Samples were studied by optic and electronic microscopy and visceral myopathies were found. None of them had urinary disorders. Medical treatment consisted of total parental nutrition and/or enteral nutrition. Cisapride was not effective in the two patients who received it.
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PMID:[Chronic idiopathic intestinal pseudo-obstruction: visceral myopathy. Report of 4 cases]. 820 87

Cisapride is a substituted benzamide with gastrointestinal prokinetic effects presumed to be due to the enhancement of the physiological release of acetylcholine at the myenteric plexus. In a multicentre study, 189 patients with nonulcer dyspepsia (NUD) received single-blind placebo treatment for two weeks. A total of 123 patients with no or minimal response to placebo and epigastric pain of at least moderate severity and frequency were randomly assigned to one of the three parallel double-blind treatments for six weeks: cisapride 10 mg tid, cisapride 20 mg tid or placebo. The severity and frequency of individual symptoms (epigastric pain, heartburn, nausea, vomiting anorexia, postprandial discomfort, regurgitation, lower abdominal pain, bloating and constipation) were assessed on a four- and five-point categorical scale, respectively, by the investigator at three on treatment visits and by patients in a daily diary. Analysis of investigator and patient assessments for differences in symptom severity x frequency composite scores among the three treatment groups showed no statistically significant differences for individual symptoms or symptom clusters. As assessed by the investigator, and compared with baseline, cisapride 20 mg tid significantly (P < 0.05) improved epigastric pain, bloating and early satiety as well as improved the total symptom cluster. Investigator evaluation of the five most severe and frequent symptoms for each patient showed statistically significant improvement in each treatment group. For patient diary assessments, statistically significant within-treatment improvement of the total symptom cluster, the five most severe symptoms cluster, bloating and early satiety was observed for both cisapride 20 mg and placebo, whereas epigastric pain significantly (P < 0.05) improved in all three treatment groups. Investigator evaluation of global response (good+excellent) rate at the end of the six week treatment period was 38% for cisapride 20 mg, 47% for cisapride 10 mg and 33% for placebo. No statistically significant difference in this parameter among treatments was noted. Cisapride was well tolerated at both doses with a side effect profile comparable with that of placebo. It is concluded that in this double-blind multicentre study with a single-blind two-week placebo run in phase, cisapride 10 mg tid and 20 mg tid were not effective compared with placebo in improving symptoms in NUD patients. This study re-emphasizes the good prognosis of patients with NUD, with 14% of patients improving in the two-week placebo run-in phase and a further 33% improving in the next six weeks while on placebo. Within-treatment analysis of investigator assessments showed improvement for cisapride 20 mg tid suggesting a trend of efficacy at this dose.
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PMID:A double-blind randomized study of cisapride in the treatment of nonulcer dyspepsia. The Canadian Cisapride Nud Study Group. 911 11

This article reviews the pathophysiology and pharmacology of emesis in relation to migraine pathogenesis. Also, the place of antiemetic and gastrointestinal prokinetic agents in current and future acute migraine treatment strategies is reviewed. The mechanisms of action of current and novel acute migraine therapies are considered with respect to the neurogenic and vascular hypothesis. Control of migraine-associated nausea and vomiting is often achieved with the benzamide dopamine D2 receptor antagonist metoclopramide. This drug also has 5HT3 receptor antagonist activity and reproducibly stimulates gastric motility to increase the availability of orally administered drugs. Other antiemetic and gastroprokinetic agents with potential value for the treatment of migraine-associated nausea and vomiting could speed absorption of oral antimigraine therapies without central nervous system side effects. Domperidone, a dopamine D2 receptor antagonist that does not cross the blood brain barrier is relatively free of the central side-effect liability of metoclopramide. Cisapride, a benzamide 5HT4 receptor agonist gastrointestinal prokinetic drug, lacks dopamine antagonist activity. A controlled comparison of these agents as migraine co-therapies could provide information on the importance of peripheral and central mechanisms in migraine-associated nausea and vomiting and improve antimigraine treatment options.
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PMID:Pathophysiology and pharmacology of migraine. Is there a place for antiemetics in future treatment strategies? 987 82

Although combination antiemetics prevent vomiting during the initial 24 h after high-dose (> or =100 mg/m2) cisplatin, many patients experience delayed emesis 24-120 h afterwards despite receiving prophylactic dexamethasone and metoclopramide during this time. Cisapride is a prokinetic agent, which stimulates propulsive motility throughout the gastrointestinal tract without causing extrapyramidal effects. In this phase II trial, we tested the ability of cisapride to prevent delayed emesis following cisplatin. Twenty patients receiving initial cisplatin >100 mg/m2 were entered. All patients received intravenous dexamethasone with either metoclopramide or ondansetron to prevent acute emesis 0-24 h after receiving cisplatin. Patients who had experienced two or fewer acute vomiting episodes then received cisapride 20 mg orally four times daily for 4 days (24-120 h after cisplatin). Cisapride prevented delayed emesis in 2 patients (10%) during the entire 4-day period (95% confidence interval, 1-32%). Abdominal cramping and pain occurred in 35%. At the dose and schedule tested, oral cisapride prevented delayed emesis in only 10% of patients receiving cisplatin >100 mg/m2 and caused abdominal cramping in 35%. Since in prior trials among similar patients, placebo prevented delayed emesis in 11%, further study of cisapride and dose escalation for this indication are not recommended.
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PMID:Oral cisapride for the control of delayed vomiting following high-dose cisplatin. 992 74

A disorder of gastric motility should be suspected in patients with chronic vomiting. Imaging studies are used to confirm delayed gastric emptying, the most common form of a gastric motility disorder. Other causes of chronic vomiting, for example, metabolic or endocrine disorders, other abdominal disorders, mechanical causes of gastric obstruction, and lower gastrointestinal tract disease, are then ruled out. If no underlying cause is determined, a functional disorder of gastric emptying is presumptively diagnosed. Treatment consists of dietary management and gastric prokinetic agents. Cisapride is the drug of choice for treating delayed gastric emptying followed by erythromycin and ranitidine or nizatidine.
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PMID:Diagnosis and treatment of gastric motility disorders. 1020 95

Nutritional support is essential in treating patients with gastroparesis. Initially, dietary changes should be instituted to reduce extra fat and bulk, and patients should be encouraged to eat frequent small meals with liquid supplementation. Enteral feeding should be introduced in the event of weight loss or persistent vomiting. Medical therapy is usually necessary early in treatment. Cisapride is the initial agent of choice and may be combined with an antiemetic agent, such as promethazine or chlorpromazine or, if side effects occur, ondansetron and granesitron. If cisapride is ineffective or contraindicated, metoclopramide is a reasonable option, though limited by side effects. Erythromycin is useful in the acute treatment of postoperative ileus and hospitalized gastroparetic patients, but its role is limited based on concerns about poor long-term effectiveness and antimicrobial resistance. Once domperidone becomes available in the United States, it will be useful for its promotility and antiemetic qualities. Combination therapy should be considered if monotherapy with cisapride or metoclopramide alone is ineffective. While not yet well studied, combination therapy has the potential to offer dramatic benefit for patients with refractory gastroparesis. Metoclopramide may be added to cisapride for patients with breakthrough symptoms or refractory chronic symptoms. Other combinations include metoclopramide with erythromycin, domperidone with cisapride, and domperidone with erythromycin. In the future, gastric pacing may become an effective option for patients not responding to medical therapy. Total gastrectomy should be performed only for end-stage gastroparesis when all other therapy has failed. Both procedures should be reserved for centers that specialize in severe gastric motility disorders.
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PMID:Diabetic and Nondiabetic Gastroparesis. 1109 57

Management of delayed emesis (DE) remains unsatisfactory, and only 50% of the patients achieve complete protection. Cisapride is a strong prokinetic gastrointestinal drug that could have a role in the prevention of DE. We enrolled 31 adult naive outpatients who were scheduled to receive cisplatin chemotherapy at doses of > or = 75 mg/m2. All patients received the same prophylactic treatment for acute emesis (20 mg dexamethasone and 8 mg ondansetron i.v.) and, as preventive therapy for DE, oral cisapride, 10 mg every 8 h on days 2-4, combined with dexamethasone i.m., 8 mg twice daily on days 2 and 3, and 4 mg twice daily on day 4. All patients were evaluable for activity. Complete protection from acute vomiting was 80.7%, from nausea 71% and from nausea/vomiting 64.5%. The overall protection from DE (days 2-4) was 74.1% for vomiting, 64.5% for nausea and 58% for nausea/vomiting. In our study the combination of cisapride and dexamethasone was effective, giving 58% of complete protection from DE, and it is therefore worthy of further studies.
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PMID:Cisapride and dexamethasone in the prevention of delayed emesis after cisplatin administration. 1114 45

Diabetic gastroparesis is a common and debilitating condition affecting millions of patients with diabetes mellitus worldwide. Although gastroparesis in diabetes has been known clinically for more than 50 years, treatment options remain very limited. Until recently, the scientific literature has offered few clues regarding the precise aetiology of gastric dysfunction in diabetes.Up to 50% of patients with diabetes may experience postprandial abdominal pain, nausea, vomiting and bloating secondary to gastric dysfunction. There is no clear association between length of disease and the onset of delayed gastric emptying. Gastroparesis affects both type 1 (insulin dependent) and type 2 (non- insulin dependent) forms of diabetes. Diagnosis requires identifying the proper symptom complex, while excluding other entities (peptic ulcer disease, rheumatological diseases, medication effects). The diagnosis of gastroparesis may be confirmed by demonstrating gastric emptying delay during a 4-hour scintigraphic study. Treatment options are limited and rely on dietary modifications, judicious use of available pharmacological agents, and occasionally surgical or endoscopic placement of gastrostomies or jejunostomies. Gastric pacing offers promise for patients with medically refractory gastroparesis but awaits further investigation. Current pharmacological agents for treating gastroparesis include metoclopramide, erythromycin, cisapride (only available via a company-sponsored programme) and domperidone (not US FDA approved). All of these drugs act as promotility agents that increase the number or the intensity of gastric contractions. These medications are not uniformly effective and all have adverse effects that limit their use. Cisapride has been removed from the open market as a result of over 200 reported cases of cardiac toxicity attributed to its use. Unfortunately, there is a paucity of clinical studies that clearly define the efficacy of these agents in diabetic gastroparesis and there are no studies that compare these drugs to each other. The molecular pathophysiology of diabetic gastroparesis is unknown, limiting the development of rational therapies. New studies, primarily in animals, point to a defect in the enteric nervous system as a major molecular cause of abnormal gastric motility in diabetes. This defect is characterised by a loss of nitric oxide signals from nerves to muscles in the gut resulting in delayed gastric emptying. Novel therapies designed to augment nitric oxide signalling are being studied.
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PMID:Current concepts in diabetic gastroparesis. 1282 60

The aim of this study was to investigate the presence of gastroesophageal reflux with 24-hour pH monitoring in children with cerebral palsy. In the second part of the study, we started cisapride with the children with documented gastroesophageal reflux and evaluated the efficacy of cisapride with the second 24-hour pH monitoring. This study was performed before discontinuation of cisapride with US Food and Drug Administration reports in Turkish markets. Twenty-eight children who had been followed up in the Department of Pediatric Neurology between 1999 and 2000 were enrolled in the study. Twenty-four-hour pH monitoring was performed on all patients. Two parameters were evaluated as pathologic: a reflux index (percentage of time the pH value was <4) over 4.5% and reflux longer than 15 minutes even when the reflux index was below 4.5%. Cisapride treatment was assigned to the patients with pathologic monitoring results at a dose of 0.2 mg/kg/day for 3 months. Electrocardiograms (ECGs) were analyzed before and after cisapride treatment. Symptoms suggestive of gastroesophageal dysfunction were dysphagia in 18 cases (64.3%), constipation in 8 cases (28.6%), vomiting in 6 (14.2%) cases, and recurrent pneumonia in 2 cases (8.5%). The reflux index was > or =4.5% in 13 (46.4%) of the 28 cases. Reflux was longer than 15 minutes in 2 (7.1%) cases. Cisapride was started in 15 cases with pathologic monitoring results. Appetite improved in 6 cases and dysphagia disappeared in 8 cases after cisapride therapy (P < .05). pH monitoring was repeated in 12 cases after 3 months and was normal in 8 of them. Improvement in the reflux index and total reflux episodes was statistically significant after therapy (P = .008). No adverse effects occurred. Even though the drug is no longer marketed, we concluded that it improved the symptoms and quality of life in spastic children with gastroesophageal reflux.
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PMID:Gastroesophageal reflux in children with cerebral palsy: efficacy of cisapride. 1570 73


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