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)

Vomiting is a physiological reflex to protect the body from harmful influences, whereas "pathological vomiting" occurs irrespective of its primary purpose or causes secondary disturbances. Artificially induced vomiting and enemas were prophylactic and therapeutic procedures to purge the body that were employed in ancient times and reached their zenith by the end of the 18th century. The act of vomiting is regulated by the vomiting centre, where neural afferents from the chemoreceptor trigger zone, vagal and sympathetic nerve system, and from other trigger areas, are coordinated. Differential diagnosis of vomiting, emphasizing metabolic/endocrine and psychogenic vomiting--including anorexia nervosa and bulimia--are briefly discussed. Symptomatic treatment of vomiting primarily consists of the use of receptor antagonists, e.g. dopamine, histamine and 5-hydroxytryptamine-3 antagonists. Acupuncture/-pressure are also discussed as an alternative treatment method.
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PMID:[Persistent vomiting]. 848 71

Chemotherapy-induced emesis is one of the most common and severe side effects of systemic cancer therapy. During the 1980s, the development of metoclopramide-based combination antiemetic regimens resulted in complete or near-complete control of emesis in 60-70% of patients receiving cisplatin-based chemotherapy. However, 30-40% of patients remained poorly controlled with these regimens, and bothersome side effects such as extrapyramidal symptoms and sedation hindered therapy in some patients. The selective 5-hydroxytryptamine (serotonin) inhibitors are a new class of antiemetics that have further improved the control of chemotherapy-related nausea and vomiting. Ondansetron, the first of these compounds available commercially, has proven superior to high-dose metoclopramide in controlling cisplatin-induced emesis. In addition, no extrapyramidal side effects have been observed with ondansetron. Although the currently approved dosing schedule for ondansetron is 0.15 mg/kg intravenously (IV) every 4 hours for three doses, recent data indicate that a single 32 mg dose prior to chemotherapy may be superior. The addition of dexamethasone (10-20 mg IV prior to chemotherapy) improves the efficiency of ondansetron; this combination should be considered in all patients receiving cisplatin-based chemotherapy. The role of ondansetron in non-cisplatin chemotherapy is not completely defined, but patients unresponsive to other antiemetic therapy often have improved control with the addition of ondansetron.
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PMID:Development of serotonin antagonists for the control of chemotherapy-induced emesis. 851 17

In species which vomit, elevated intestinal serotonin (5-hydroxytryptamine, 5-HT) may stimulate abdominal vagal afferent fibers, which in turn evoke the vomiting reflex. The release of 5-HT from intestinal enterochromaffin (EC) cells is regulated by polymodal mechanisms. The object of this study was to evaluate the involvement of 5-HT autoreceptors in the regulation of 5-HT release from the small intestine. Functional studies were carried out using 5-HT3 receptor agonist and antagonists, and 5-HT4 receptor agonist. Ferret and rat ileal tissue were isolated and 5-HT released into the bathing solution was determined using HPLC with an electrochemical detector (ECD). We previously reported that cisplatin produced a significant increase in cumulative 5-HT release and that ondansetron, a selective 5-HT3 receptor antagonist, did not alter the 5-HT release from the ferret ileum. In this study, a selective 5-HT3 agonist, 2-methyl-5-HT, induced a dose-dependent increase of 5-HT from the rat ileum. This release of 5-HT was significantly reduced by granisetron, a selective 5-HT3 receptor antagonist. Furthermore, a selective 5-HT4 receptor agonist, 5-methoxytryptamine induced a concentration-dependent increase of 5-HT in the rat ileum. These results suggest that both 5-HT3 and 5-HT4 receptors may be involved in intestinal 5-HT release.
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PMID:Chemical modulation of 5-HT3 and 5-HT4 receptors affects the release of 5-hydroxytryptamine from the ferret and rat intestine. 855 68

Fluoxetine (Prozac) is an effective and increasingly widely used antidepressant. It is a 5-hydroxytryptamine (5-HT) re-uptake inhibitor. It produces its pharmacological effects by preventing the elimination of the 5-HT produced at nerve synapses, thus increasing its concentration at that location. Ondansetron (Zofran), is a 5-HT3 antagonist, which produces its pharmacological effect by competing with 5-HT receptors at the synapse. When both fluoxetine and ondansetron are used together, there is the possibility that the accumulation of 5-HT resulting from the use of fluoxetine may compete with ondansetron at the receptors, potentially reducing the antiemetic effects of ondansetron. Clinically, this has been observed in three patients treated with both compounds at the same time, while they were receiving carboplatin combination chemotherapy. The possibility that concurrent administration of the 5-HT re-uptake inhibitors, fluoxetine, may reduce the antemetic effectiveness of ondansetron is relevant to the established role of antidepressants in the management of patients with malignant disease, in whom the prevention of emesis is also important. Further investigation of this possible interaction is recommended.
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PMID:Fluoxetine treatment comprises the antiemetic efficacy of ondansetron in cancer patients. 859 Jun 98

We conducted a prospective randomized study to compare granisetron, a 5-hydroxytryptamine-3 receptor antagonist with standard anti-emetics (control group) consisting mainly of metoclopramide, in the prophylaxis of emesis induced by conditioning prior to stem cell transplantation. Fifty-eight patients were evaluable for analysis. The number of emetic episodes expressed in terms of patient-days was significantly lower in the granisetron group than in the control group (P < 0.001). During the first 24 h of conditioning, 27 of the 31 patients (87.1%) in the granisetron group achieved control of emesis with less than three emetic episodes (major < or = ) a day compared with 37.0% in the control group (P < 0.001). The same degree of emesis control was maintained throughout the conditioning period in 51.% of patients in the granisetron group compared with 0% in the control group (P < 0.001). Adverse reactions were observed in 11.4% of patients in the granisetron group and in 25.9% in the control group. None of the events were serious. Based on these data, we conclude that granisetron is superior to standard antiemetics in protecting against the vomiting induced by conditioning for stem cell transplantation.
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PMID:Granisetron in the prevention of vomiting induced by conditioning for stem cell transplantation: a prospective randomized study. 873 81

Central serotoninergic (5-hydroxytryptamine, 5HT) pathways are believed to be involved in the mechanisms of anorexia and/or emesis evoked by the trichothecene mycotoxin deoxynivalenol (DON). Using an in vitro membrane receptor binding assay, the competitive potency of DON was investigated against several radioactive ligands that have a high affinity for selective 5HT receptor subgroups. Receptor site densities and displacement profiles in twelve selected regions of pig brain were investigated. Overall, DON possessed only minimal efficacy to competently block any of the 5HT-ligands tested. IC50 values (50% inhibitory concentration) of at least 5 mM DON were required to inhibit binding, and in certain regions concentrations of 100 mM were ineffective. In comparison, several standard 5HT-antagonists showed 10(3)-10(5) times greater capability than DON to displace binding of these ligands. Because these results indicated DON possesses only weak affinity for the 5HT-receptor subtypes investigated here, this suggested that in vivo, unless relatively high concentrations of the toxin are present, its pharmacological effects may be mediated by mechanisms other than a functional interaction with serotoninergic receptors at the central level.
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PMID:A study on the effect of deoxynivalenol on serotonin receptor binding in pig brain membranes. 875 51

Most anticancer drugs are cytotoxic and produce various side-effects, among which nausea and vomiting are almost ubiquitous and usually extremely distressing to the patient. Cancer chemotherapy elicits two main phases of vomiting: an intense, acute phase of vomiting that occurs almost immediately following anti-cancer therapy and a milder, delayed phase of nausea and vomiting of longer duration. The mechanisms underlying the induction of nausea and vomiting after cancer chemotherapy are poorly understood but may be mediated by serotonin (5-hydroxytryptamine or 5-HT), particularly in the acute phase. Serotonin activates 5-HT3 receptors, which function as ligand-gated ion channels located either in the periphery and/or in the central nervous system to produce emesis, among other effects. The peripheral 5-HT3 receptors may be pharmacologically distinct from the central 5-HT3 receptors and may exhibit some association with GTP-binding proteins. In addition, different populations may exist as distinct subtypes of the same receptor. The 5-HT3 receptor antagonist ondansetron (GR 38032F) is effective in preventing the emesis induced by cytotoxic agents currently used in the treatment of many forms of cancer. Ondansetron has, comparatively, a much higher efficacy in the treatment of acute emesis following cancer chemotherapy than it does in the delayed phase, suggesting that the late phase of emesis may be mediated by other distinct mechanisms.
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PMID:Role of 5-hydroxytryptamine3 (5-HT3) antagonists in the prevention of emesis caused by anticancer therapy. 876 66

We report a case of bullous mastocytosis in a 30-month-old girl, who developed disseminated pruritic urticarial and bullous lesions on the trunk accompanied by episodes of vomiting and generalized flushing. Her problems began at the age of 6 months. Her stool was repeatedly positive for occult blood. Histamine and 5-hydroxytryptamine were measured in the urine and serum; urine 5-hydroxytryptamine levels were elevated. In addition, trypsin and chymotrypsin levels were raised in the blister fluid. Metachromatic staining of the mast cells in a skin biopsy specimen confirmed the diagnosis. A combination of oral disodium cromoglycate and ketotifen produced a dramatic improvement of the cutaneous and gastrointestinal features.
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PMID:[Bullous mastocytosis in a child]. 917 60

Ondansetron was the first of several selective 5-hydroxytryptamine (5-HT3) antagonists to be available as an antiemetic. Its uses in the setting of highly and moderately emetogenic chemotherapy and radiotherapy are well established. Ondansetron has also been used to manage nausea and vomiting in other patients. We report a retrospective analysis of its use in all 16 patients who were commenced on ondansetron after admission to our institution for nausea and/or vomiting over a 4-year period. Nine patients had advanced human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS), and seven had malignancy. These patients were not undergoing disease-modifying treatment and had inadequate responses to therapeutic doses of standard antiemetics, used either singly or in combination. Responses were independently reviewed and graded by two investigators. Response was judged at 48 hr after commencing therapy. Potential causes of nausea were also reviewed. Overall, 13 of 16 [81%, 95% confidence interval (CI) 54%-96%] derived benefit. Twelve of 15 patients (80%) with nausea had a demonstrable improvement, and ten of 14 patients (71%) with vomiting also improved. Eight of ten patients (80%) admitted with nausea and/or vomiting as one of their presenting problems had the symptom controlled within 48 hr of ondansetron therapy. Treatment with ondansetron was well tolerated, onset of action was rapid, and response rates were high and sustained over time. Seven of the 16 patients continued ondansetron therapy for more than 10 days. With minimal reductions in inpatient bed stays, the total costs of ondansetron could be met while at the same time better supporting patients remaining in the community.
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PMID:Use of ondansetron in palliative medicine. 918 36

The emetic effect of clonidine injected into the cerebral ventricles through chronically implanted cannulae was investigated in unanaesthetized cats. Clonidine (0.1-300 micrograms) induced dose-dependent and shortlasting emesis. The emesis induced by the supramaximal dose of clonidine (100 micrograms) was not abolished after the ablation of area postrema. Both the alpha 2 adrenoceptor blocking agent idazoxan and the mixed alpha 1 and alpha 2 adrenoceptor antagonist phenoxybenzamine, injected intracerebroventricularly, attenuated or abolished the emesis induced by clonidine (100 micrograms). On the other hand, the alpha 2 adrenoceptor blocking agent yohimbine, the alpha 1 adrenoceptor blocking drug prazosin and the non-selective beta-adrenoceptor antagonist propranolol, injected into the cerebral ventricles, had no significant effect on clonidine-induced emesis. The antimuscarinic drug atropine injected into the cerebral ventricles prevented the clonidine-induced emesis in a dose-dependent manner. The dopamine antagonist chlorpromazine, the 5-hydroxytryptamine blocking agent methysergide and the histamine H1 and H2 receptor antagonists, antazoline and cimetidine, injected intracerebroventricularly reduced or abolished the emesis produced by clonidine. The ganglionic blocking substance mecamylamine and the opioid antagonist naloxone, all injected into the cerebral ventricles, had no significant effect on clonidine-induced emesis. In cats pretreated with the intracerebroventricular competitive inhibitor of the synthesis of catecholamines, alpha-methyl-p-tyrosine, as well as with the inhibitor of acetylcholine synthesis hemicholinium-3, the emesis caused by clonidine was depressed or abolished. The clonidine-induced emesis was also abolished when catecholamine stores were depleted by intracerebroventricular reserpine. However, the clonidine-induced emesis was not significantly changed when 5-hydroxylryptaminergic nerve terminals were damaged by 5,6-dihydroxytryptamine. It follows, therefore, that cholinergic and noradrenergic mechanisms are of basic importance for the emetic action of clonidine. With regard to receptors, the emesis induced by clonidine injected into the cerebral ventricles, is mediated at least in part through alpha-adrenoceptors, muscarinic cholinoceptors, 5-hydroxytryptamine receptors and H1 and H2 histamine receptors. These receptors appear to be located mostly presynaptically and they transmit emetic impulses to neurones integrating them into emesis. However, the direct effect of clonidine on postsynaptic receptors cannot be excluded, particularly when muscarinic and 5-hydroxytryptamine receptors are implicated. Taken together, these results point to the existence of a multitransmitter pathway/s outside the area postrema, subserving the central regulation of emesis.
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PMID:Clonidine-induced emesis: a multitransmitter pathway concept. 926 44


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