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)

Gastroparesis is a chronic gastric motility disorder in which there is delayed gastric emptying of solids plus or minus liquids. Symptoms of gastroparesis may range from early satiety and nausea in mild cases to chronic vomiting, dehydration, and nutritional compromise in severe cases. Diagnosis of gastroparesis is based on demonstration of delayed gastric emptying of a radiolabeled solid meal in the absence of mechanical obstruction. A number of gastrointestinal and systemic disorders may impair gastric motility with resultant gastroparesis. Approximately one third of patients with gastroparesis have no identifiable underlying cause (so called idiopathic gastroparesis). Management of gastroparesis involves four areas: (1) nutritional support, (2) antiemetic drugs, (3) prokinetic drugs, and (4) surgical therapy (in a very small subset of patients). Gastroparesis is often a chronic, relapsing condition; 80% of patients require maintenance antiemetic and prokinetic therapy and 20% require long-term nutritional supplementation. In the near future, the most promising advances in the treatment of patients with gastroparesis will most likely come from the area of combination pharmacological therapy. In the long term, developments in the area of intestinal pacing and intestinal transplantation may offer further treatment options in this difficult disorder.
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PMID:Gastroparesis and the current use of prokinetic drugs. 804 84

A 53-years-old woman with bilateral untreated breast cancer is admitted for intractable vomiting. No obstructive gastric disease is found but a marked delayed gastric emptying, suggesting the diagnosis of gastroparesis. No classical cause being demonstrated, the diagnosis of paraneoplastic gastroparesis is proposed. Treatment with cisapride and chemotherapy lead to regression of digestive symptoms and of breast tumor. This uncommon entity, usually described in association with small cell lung cancer, may involve the whole gastrointestinal tract, sometimes in association with abnormalities of the autonomous nervous system. Destruction of the myenteric plexuses by auto-antibodies could be responsible for this pathology.
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PMID:[Paraneoplastic gastroparesis]. 831 Jan 96

Gastroparesis is a disabling complication in diabetic patients. It has been reported as the second most frequent cause of hospitalization in diabetic patients on continuous ambulatory peritoneal dialysis (CAPD). We analyzed infectious and noninfectious complications in our CAPD patients. We included 31 patients (12 diabetics and 19 nondiabetics) with an average time on CAPD of 14 +/- 7 months. The incidence of peritonitis was 1.68 episodes/patient/year in diabetics and 0.84 in nondiabetics. Nine (75%) diabetic patients had peritonitis, 5 (42%) had vomiting, and 4 (33%) had ischemic heart disease. The hospitalization index (days/year) was greater in diabetics: 11.83 +/- 11.36 versus 4.16 +/- 8.84 in nondiabetics (p < 0.05). Vomiting was the first cause of admission in diabetics. We were unable to control severe gastroparesis with cisapride and metoclopramide in 4 patients. Erythromycin, 100 mg/2-L bag of dialysate, improved symptoms in all of them. We concluded that gastroparesis is an important cause of morbidity in CAPD patients. Intraperitoneal erythromycin can improve symptoms if other prokinetic drugs fail.
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PMID:Gastroparesis: an important cause of hospitalization in continuous ambulatory peritoneal dialysis patients and the role of erythromycin. 839 60

The objective of this study was to investigate the effects of intravenous erythromycin and chronic oral dosing of erythromycin on gastric emptying in patients with idiopathic or diabetic gastroparesis. Symptoms were assessed on oral dosing and during long-term follow-up in an ambulatory setting at a University referral center. Fourteen patients (10 idiopathic and four diabetic gastroparesis) were studied. Four patients left during the 4-wk study; two due to rash, one with cramps and vomiting on erythromycin, and one due to other medical problems. Ten patients completed the 4-wk study and commenced long-term therapy. Five of these patients experienced enough symptomatic relief to continue oral erythromycin long-term, being followed for an average period of 8.4 months. After initial documentation of delayed gastric emptying, patients received 6 mg/kg intravenous erythromycin lactobionate before a second gastric emptying study. Erythromycin base was then given orally at a dose of 500 mg tid-ac and qhs, with a final gastric emptying study performed after 4 wk. During long-term follow-up, erythromycin dosage was adjusted to minimize symptoms. Radionuclide-labeled gastric emptying of a solid meal was studied at baseline, following intravenous erythromycin, and after 4 wk of oral treatment with erythromycin. Symptom scores were assessed at baseline, at 4 wk, and then at 8-wk intervals. The percentage of the solid meal retained in the stomach at 2 h decreased from 85% +/- 11% (SD) at baseline to 20% +/- 29% following intravenous erythromycin (p < 0.001), and to 48% +/- 21% after 4 wk of oral therapy (p < 0.01 vs. baseline). There was a reduction in total symptom scores and a significant reduction in global assessment scores (p = 0.03). We conclude that erythromycin has a strong gastric prokinetic effect in both idiopathic and diabetic gastroparesis, and may represent a useful new therapeutic approach to this problem.
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PMID:The treatment of idiopathic and diabetic gastroparesis with acute intravenous and chronic oral erythromycin. 842 15

Gastropathy on the basis of mesenteric arterial ischemia can be masked in presentation as the typically more benign entities of gastritis, gastric ulceration, or gastric atony. Gastritis and ulceration are commonly associated with stress, hyperacidity, Helicobacter pylori infection, or medication injury. Gastric atony is less commonly seen and usually attributable to diabetes mellitus, vagotomy, or mechanical gastric outlet obstruction. Gastric ischemia as a cause of gastropathy is an underappreciated phenomenon with a particularly poor prognosis in which early diagnosis is essential to potentially successful intervention. Seven patients with ischemic gastropathy are described; all are women, aged 41 to 71 years, smokers, with hypertension. Nausea, vomiting, weight loss, and gastrointestinal bleeding were the common presenting symptoms. All patients had endoscopic or autopsy-proven gastric ulcerations or necrosis, and two patients had proven gastroparesis. Four of five patients with ischemic gastritis died within 3 months of diagnosis despite vascular reconstruction. The two patients with gastroparesis underwent aorto-celiac bypass and are well 9 and 20 months, respectively, after operation. Treatment results were distressingly unsatisfactory, especially in those patients in whom gastritis rather than gastroparesis was the presenting problem. Although the high mortality of mesenteric ischemia is well described, little documentation of gastric ischemia exists in the literature. This entity is generally not considered in the differential diagnosis of gastritis, ulceration, or gastroparesis. Empirically, an early diagnosis and treatment may improve the survival in this select patient group.
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PMID:Lethal nature of ischemic gastropathy. 848 53

Cutaneous electrogastrography was performed in nine healthy volunteers and in 43 patients presenting with various clinical conditions known to be associated with gastric motor disorders, including: 24 with functional dyspepsia, nine with longstanding diabetes mellitus, five with recent nausea/vomiting, three with pyloric stenosis, one with post-vagotomy gastroparesis, and one with idiopathic gastric distension and atony. The electrogastrography signal was recorded during 1h pre-prandial period and 1h after eating. The electrogastrography dominant frequency and power were determined using running spectral frequency analysis and the time-course of electrogastrography was evaluated in a pseudo three dimensional graphic. The electrogastrography dominant frequency was divided into four bands: 1. Bradygastria (0-2.4 cpm); 2. Normal (2.4-3.9 cpm); 3. Tachygastria (4.0-9.9 cpm); 4. Duod-resp (10.0-15.0 cpm). The percentage of the dominant electrogastrography power into those four frequency bands was determined. Electrogastrography was considered normal if functional dyspepsia was normal in more than 65% of the time. The electrogastrography was normal (dominant frequency into 3 cpm range in > 65%) in: 9/9 healthy volunteers, 3/3 pyloric stenosis, 4/5 nausea/vomiting, 3/9 diabetes mellitus, 13/24 functional dyspepsia. Gastric dysrhythmias were present in > 35% of the electrogastrography recording in: 1/5 nausea/vomiting, 11/24 functional dyspepsia, 6/9 diabetes mellitus, 1/1 post-vagotomy gastroparesis, 1/1 gastric distension and atony. Persistent tachygastria (> 10%) was found in: 1/1 gastric distension and atony (90% electrogastrography), 1/1 post-vagotomy gastroparesis, 1/5 nausea/vomiting, 6/9 diabetes mellitus, 6/24 functional dyspepsia. It was concluded that electrogastrography is a non-invasive, well-tolerated, reliable means of recording gastric myoelectric activity and gastric dysrhythmias. Patients presenting with gastric motor disorders, with chronic dyspeptic symptoms, or acute nausea may present transitory or persistent gastric dysrhythmias.
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PMID:[Myoelectric gastric activity using cutaneous electrogastrography--electrogastrogram]. 854 Aug

A 72-year-old woman with chronic fatigue, malaise, weight loss, nausea, and vomiting was treated unsuccessfully for gastroparesis for more than 2 years. Clinical and biochemical features of hypopituitary disease and symptoms of a nonsecreting pituitary tumor had been overlooked and became apparent only after the differential diagnosis of hyponatremia was considered. Transsphenoidal resection of the pituitary tumor and appropriate 1-thyroxine and hydrocortisone replacement returned her gastric emptying time to normal and relieved her symptoms. Primary and secondary deficits of l-thyroxine and cortisol should be considered when making a possible diagnosis of gastroparesis.
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PMID:Case report: reversible gastroparesis in patients with hypopituitary disease. 868 31

Gastroparesis is delayed gastric emptying of either solids or liquids, which occurs in the absence of mechanical obstruction. Although associated with many diseases, the most frequent cause of gastroparesis is diabetes mellitus. It is estimated that up to 50% of diabetic patients may have this problem. Symptoms of gastroparesis include postprandial nausea, epigastric pain/burning, bloating, early satiety, excessive eructation, anorexia and vomiting. The vomiting associated with gastroparesis often has the following two features: (1) emesis of undigested foods ingested more than four hours previous; and (2) emesis of undigested foods in the middle of the night or in the morning prior to eating breakfast. It is important to recognize and treat gastroparesis not only to decrease symptoms but also to prevent bezoar formation and nutritional deficiencies as well as to improve glycemic control in brittle diabetics. The purpose of this article is to review the physiology of gastric emptying and to use this information to understand the pharmacological therapies for this debilitating problem.
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PMID:Gastroparesis: current management. 878 40

Cyclic vomiting is a rare syndrome that over the years has variously been ascribed to psychogenic causes, sensory seizures, abdominal migraine, and more recently, to mechanical or electrical disturbances in gastric physiology. We describe the case of a 65-year-old white diabetic female with a 10-yr history of recurrent episodes of nausea and vomiting, occurring every 10-12 days and lasting approximately 1-3 days at a time. These episodes were accompanied by edema, mild temperature elevations, and remarkable elevations in blood pressure. In between these episodes, the patient remained asymptomatic. Initial screening tests were also negative except for moderate gastroparesis. However, antral motility was found to be normal, as was an electrogastrogram. Detailed neurological and psychiatric evaluations were negative. Trials of erythromycin, metoclopramide, naloxone, ondansetron, and amitryptiline were unsuccessful. Serial endocrinological testing revealed that an episode of vomiting was always preceded by an abnormal elevation in at least one of the following: serum adrenocorticotropic hormone, serum cortisol, or urinary cortisol. In the midst of an episode, all three values were exceedingly high (e.g., > 10-fold increases in 24-hr urinary cortisol levels). Fluctuations of a milder degree, though still abnormally high, were also noted in between cycles at times when the patient was completely asymptomatic. High-dose dexamethasone suppressed these hormonal surges completely but not the clinical symptoms, which continued undisturbed. The patient was finally given a trial of intramuscular ketorolac during one of her episodes, which produced prompt and sustained relief. During the next few weeks, she was given this drug each time her symptoms commenced, and each time it appeared that her cycle had been aborted. She has since been able to terminate her episodes promptly and completely by self-administration of ketorolac. We speculate that her syndrome is caused by a poorly characterized disorder of endogenous prostaglandin release, resulting not only in derangements in the hypothalamic pituitary system but also in nausea and vomiting.
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PMID:Cyclic vomiting: association with multiple homeostatic abnormalities and response to ketorolac. 885 55

Gastrointestinal prokinetics promote or increase the coordination of the gut wall contractions leading to enhancement of propulsive motility and, consequently, caudal displacement of luminal contents. Currently, they are considered drugs of choice for the treatment of upper gastrointestinal tract functional motor disorders such as those associated with gastrooesophageal reflux disease, chronic dyspepsia, gastroparesis (idiopathic or secondary to other diseases) and acute or chronic idiopathic intestinal pseudo-obstruction. The aim of the present review is to give an outline of the pharmacology of currently available prokinetics and of novel drugs endowed with gastrointestinal prokinetic action that require further pharmacological and/or clinical testing. The novel drugs include recent generations of benzamide and non-benzamide 5-HT4 receptor agonists, motilin receptor agonists, and inhibitors of nitric oxide synthase. Furthermore, based on our improved knowledge of the role of 5-HT in emesis and gastrointestinal motility, the therapeutic potential of potent mixed 5-HT4 agonists--5-HT3 antagonists in the control of cytotoxic-drug-induced emesis and associated gut motor disturbances will be discussed. Lastly, a section of this review deals with the colon as a possible target for the action of prokinetics.
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PMID:Recent advances in the pharmacology of gastrointestinal prokinetics. 893 12


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