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)

When treating patients with psychoses, clinicians must often consider changing their treatment from one antipsychotic agent to another. The transition may be necessary because the patient experiences serious side effects or because the existing therapy no longer controls the patient's symptoms. A principal problem in changing antipsychotic agents is the potential for withdrawal symptoms resulting from discontinuation of the existing therapy. These syndromes can manifest as reemergence or worsening of psychosis, rebound or unmasked dyskinesia, and cholinergic-rebound symptoms. Withdrawal signs and symptoms may include insomnia, nausea, vomiting, anxiety, and agitation. When switching a patient to the new antipsychotic agent risperidone, the clinician can keep withdrawal symptoms to a minimum by considering the patient's clinical history and current status. For some patients, abrupt withdrawal of the current antipsychotic may be possible. For others, the dose of the previous medication must be gradually reduced before risperidone is initiated. In many cases, the transition is best made by overlapping the existing therapy and risperidone.
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PMID:Changing antipsychotic medication: guidelines on the transition to treatment with risperidone. The Consensus Study Group on Risperidone Dosing. 887 89

Esophageal involvement is a common situation found in 50 to 80% of patients with scleroderma, but Boerhaave's syndrome is rare in this context. The authors report the first case of spontaneous esophageal rupture occurring in a chronic renal failure patient treated by continuous ambulatory peritoneal dialysis. In this observation, sclerodermal esophageal dyskinesia, chronic renal failure which is a classical cause of vomiting and the peritoneal dialysis which play an increasing role in the intraabdominal pressure are potential contributing factors to Boerhave's syndrome. In such patients presenting risk factors, even if they are asymptomatic, it seems reasonable to propose esophageal explorations with manometry or/and endoscopy looking for dyskinesia or other complications of gastro-esophageal reflux.
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PMID:[Spontaneous rupture of the esophagus (Boerhaave syndrome) in a patient with scleroderma treated by continuous ambulatory peritoneal dialysis]. 925 75

Ropinirole is a novel, nonergoline, selective D2-type dopamine agonist developed to treat Parkinson's disease. Safety data from therapeutic studies involving 1364 patients receiving ropinirole are reported (mean daily dose 8.7 mg, early therapy; 8.2 mg adjunct therapy). In early therapy, the emergent adverse experiences more common with the ropinirole group compared with placebo were nausea, somnolence, leg edema, abdominal pain, vomiting, dyspepsia, and hallucinations. In adjunct therapy, they were dyskinesia, nausea, hallucinations, and confusion. Most adverse experiences were mild and associated with a similar withdrawal rate compared with the placebo group. Except for hallucinations, the incidence of emergent adverse experiences decreased with time, despite increasing doses. Long-term adverse experiences particularly associated with ergoline-type dopamine agonists have so far not been observed with ropinirole. Only 1.2% of patients receiving ropinirole developed dyskinesia compared with 11.2% receiving L-dopa in early therapy over a mean period of 17 months. There were no clinically significant changes in cardiovascular parameters or laboratory data. The incidence of adverse experiences in the bromocriptine group was low, possibly because of a slow titration scheme and low average dose. Overall, the safety profile of ropinirole appears similar to that of other dopamine agonists. Clinical studies are continuing to assess the long-term safety and efficacy of ropinirole.
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PMID:The safety of ropinirole, a selective nonergoline dopamine agonist, in patients with Parkinson's disease. 961 8

Studies in animal models show a selective D1 receptor agonist with full functional efficacy compared with dopamine to have antiparkinsonian efficacy of similar magnitude to levodopa, without the same propensity for inducing dyskinesia. To date, no such agent has been tested in humans. ABT-431 is the prodrug of A-86929, a full, selective D1 receptor agonist. Subjects (n = 14) with levodopa-responsive Parkinson's disease received five doses of ABT-431 (5, 10, 20, 30, and 40 mg) and one of placebo after a 12-hour levodopa holiday. Response was assessed by using the Unified Parkinson's Disease Rating Scale motor subsection. Dyskinesia was separately graded. ABT-431 showed efficacy significantly superior to placebo at doses of 10 mg and more, and of similar magnitude to that seen with levodopa. Dyskinesia was reduced in several patients after receiving ABT-431. There were no serious adverse events, the most common minor events being nausea and emesis, dizziness, and hypotension. Assuming that ABT-431 is not transformed in humans into an unknown active D2 metabolite, and remains selective for D1 receptors, it is the first dopamine D1 receptor agonist to demonstrate a full antiparkinsonian effect in patients with Parkinson's disease. These preliminary findings also suggest that it may exhibit a reduced tendency to provoke dyskinesia. The emergence of a well-tolerated D1 agonist should allow for the development of a better understanding of the relation between motor efficacy and dyskinesia in Parkinson's disease.
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PMID:ABT-431, a D1 receptor agonist prodrug, has efficacy in Parkinson's disease. 1036 Jul 65

The most effective method to maintain clinical improvement in the course of schizophrenia is the continuation of neuroleptic therapy. Sometimes we face the dilemma whether neuroleptic administration could be discontinued. There are some unconditional indications for treatment cessation (signs of intolerance, complications, general medical conditions); all other situations can be considered as relative indications. The risk and benefit of treatment discontinuation should be carefully evaluated. Neuroleptic withdrawal seems to be safer among older patients, with single episode of the psychosis of mild severity, with no family history of schizophrenia. It is necessary to achieve a stable clinical improvement before neuroleptic withdrawal. Worsening of the clinical status creates the most important risk of treatment discontinuation. Other risk factors include unacceptable threatening behavior, increase of family burden. The appearance of withdrawal symptoms such as nausea, vomiting, dyskinesia, insomnia, anxiety, etc. are to be considered. These symptoms are rare, and the risk of relapse is smaller when patients were treated with depot neuroleptics before treatment discontinuation than in the case of treatment with oral neuroleptics. Neuroleptic discontinuation and introduction of placebo cause more risk of relapse than continuation of active treatment.
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PMID:[The risk of neuroleptic discontinuation in schizophrenia]. 1078 16

When peripheral decarboxylation is blocked by carbidopa or benserazide, the main metabolic pathway of levodopa is O-methylation by catechol-O-methyltransferase (COMT). Entacapone and tolcapone are new potent, selective and reversible nitrocatechol-type COMT inhibitors. Animal studies have demonstrated that entacapone mainly has a peripheral effect whereas tolcapone also inhibits O-methylation in the brain. In human volunteers, both entacapone and tolcapone dose-dependently inhibit the COMT activity in erythrocytes, improve the bioavailability and decrease the elimination of levodopa, and inhibit the formation of 3-O-methyldopa (3-OMD). Entacapone is administered with every scheduled dose of levodopa whereas tolcapone is administered 3 times daily. The different administration regimens for these agents are based on their different pharmacokinetic and pharmacodynamic profiles. Both entacapone and tolcapone enhance and extend the therapeutic effect of levodopa in patients with advanced and fluctuating Parkinson's disease. They prolong the duration of levodopa effect. Clinical studies show that they increase the daily ON time by an average 1 to 3 hours, improve the activities of daily living and allow daily levodopa dosage to be decreased. Correspondingly, they significantly reduce the daily OFF time. No comparative studies between entacapone and tolcapone have been performed. Tolcapone also appears to have a beneficial effect in patients with nonfluctuating Parkinson's disease. The main adverse effects of the COMT inhibitors are related to their dopaminergic and gastrointestinal effects. Enhancement of dopaminergic activity may cause an initial worsening of levodopa-induced adverse effects, such as dyskinesia, nausea, vomiting, orthostatic hypotension, sleep disorders and hallucinations. Levodopa dose adjustment is recommended to avoid these events. Tolcapone is associated with diarrhoea in about 16 to 18% of patients and entacapone in less than 10% of patients. Diarrhoea has led to discontinuation in 5 to 6% of patients treated with tolcapone and in 2.5% of those treated with entacapone. Urine discoloration to dark yellow or orange is related to the colour of COMT inhibitors and their metabolites. Elevated liver transaminase levels are reported in 1 to 3% of patients treated with tolcapone but very rarely, if at all, in patients treated with entacapone. The descriptions of acute, fatal fulminant hepatitis and potentially fatal neurological reactions, such as neuroleptic malignant syndrome and rhabdomyolysis, in association with tolcapone led to the suspension of its marketing authorisation in the European Community and Canada. In many other countries, the use of tolcapone is restricted to patients who are not responding satisfactorily to other therapies. Regular monitoring of liver enzymes is required if tolcapone is used. No such adverse reactions have so far been described for entacapone and no laboratory monitoring has been proposed. COMT inhibitors added to levodopa therapy are beneficial, particularly in patients with fluctuating disease. They may be combined with other antiparkinsonian drugs, such as dopamine agonists, selegiline and anticholinergics without adverse interactions. They provide a new treatment possibility in patients with Parkinson's disease who have problems with their present levodopa therapy.
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PMID:Clinical pharmacology, therapeutic use and potential of COMT inhibitors in Parkinson's disease. 1088 60

The ability of transdermal administration of the dopamine D2/D3 agonist piribedil (1-[3,4-methylenedioxybenzyl)]-4-[(2-pyrimidinyl)]piperazine) to reverse hypokinesia and other motor deficits observed in MPTP-treated common marmosets was investigated. Piribedil (2.5-10.0 mg/animal), applied directly to the skin of the abdomen as a paste, produced a long-lasting and concentration-dependent reversal of motor deficits. The antiparkinsonian actions of piribedil occurred within 10 minutes of drug administration and lasted as long as 10 hours. Transdermally applied piribedil produced a pattern of locomotor activity characteristic of normal motor behavior in this species. Symptoms of nausea (marked excessive salivation, retching, and/or vomiting) were not observed after transdermal application of piribedil. Additionally, pretreatment with the peripheral dopamine antagonist domperidone enhanced the antiparkinsonian effects of piribedil. Application to the skin of monolayer or bilayer patches impregnated with piribedil also produced a marked increase in locomotor activity and reversal of motor deficits. After application of various patch fractions (whole, one-half, or one-fourth), the increase in locomotor activity and reversal of disability correlated well with the surface area of skin covered. Measurement of serum levels of piribedil after single application of bilayer patches showed a positive relationship between drug levels and antiparkinsonian activity. Repeated daily application of piribedil bilayer patches for 5 days to MPTP-treated common marmosets primed to show dyskinesia by previous exposure to L-Dopa produced antiparkinsonian activity accompanied by dyskinetic movements. Transdermal administration of dopamine agonists such as piribedil may provide a useful means of producing a long-lasting reversal of motor deficits in Parkinson's disease while avoiding acute adverse effects such as nausea.
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PMID:Transdermal administration of piribedil reverses MPTP-induced motor deficits in the common marmoset. 1089 96

Adrogolide (ABT-431; DAS-431) is a chemically stable prodrug that is converted rapidly (<1 min) in plasma to A-86929, a full agonist at dopamine D1 receptors. In in vitro functional assays, A-86929 is over 400 times more selective for dopamine D1 than D2 receptors. In rats with a unilateral loss of striatal dopamine, A-86929 produces contralateral rotations that are inhibited by dopamine D1 but not by dopamine D2 receptor antagonists. Adrogolide improves behavioral disability and locomotor activity scores in MPTP-lesioned marmosets, a model of Parkinson's disease (PD), and shows no tolerance upon repeated dosing for 28 days. In PD patients, intravenous (i.v.) adrogolide has antiparkinson efficacy equivalent to that of L-DOPA with a tendency towards a reduced liability to induce dyskinesia. The adverse events associated with its use were of mild-to-moderate severity and included injection site reaction, asthenia, headache, nausea, vomiting, postural hypotension, vasodilitation, and dizziness. Adrogolide can also attenuate the ability of cocaine to induce cocaine-seeking behavior and does not itself induce cocaine-seeking behavior in a rodent model of cocaine craving and relapse. In human cocaine abusers, i.v. adrogolide reduces cocaine craving and other cocaine-induced subjective effects. The results of animal abuse liability studies indicate that adrogolide is unlikely to have abuse potential in man. Adrogolide has also been reported to reverse haloperidol-induced cognitive deficits in monkeys, suggesting that it may be an effective treatment for the cognitive dysfunction associated with aging and disease. Adrogolide undergoes a high hepatic "first-pass" metabolism in man after oral dosing and, as a result, has a low oral bioavailability (approximately 4%). This limitation may potentially be circumvented by oral inhalation formulations for intrapulmonary delivery that greatly increase the bioavailability of adrogolide. As the first full dopamine D1 receptor agonist to show efficacy in PD patients and to reduce the craving and subjective effects of cocaine in cocaine abusers, adrogolide represents an important tool in understanding the pharmacotherapeutic potential of dopamine D1 receptor agonists.
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PMID:Adrogolide HCl (ABT-431; DAS-431), a prodrug of the dopamine D1 receptor agonist, A-86929: preclinical pharmacology and clinical data. 1160 45

In the course of treatment of psychiatric patients, it is often necessary to switch antipsychotic medications. In recent years, atypical antipsychotic agents have become the first-line therapeutic interventions for treating psychotic symptoms. Reasons for switching patients from the typical antipsychotics to the atypical agents can include enhanced efficacy against negative symptoms, improvement in cognitive capacity, and reduction of risk of extrapyramidal side effects. The presumed long-term benefits of switching to the new antipsychotic drug should be assessed. Pharmacokinetic and pharmacodynamic properties of antipsychotic agents and drug-drug interactions should be considered during the switch process. Two methods are employed for the switch process: crossover ("crosstitration") and an abrupt switch. With the crossover method, the patient's current medication is tapered over a period of several days to several months to prevent potential withdrawal symptoms, such as nausea, vomiting, insomnia, muscle aches, and diaphoresis. Due to withdrawal symptoms, clozapine is the only atypical agent recommended to proceed with a slow dose taper when switching to another atypical drug. Sudden cessation could also precipitate the emergence of motor symptoms, which can include pseudoparkinsonism, dystonia, akathisia, and dyskinesia. The initiation of the new antipychotic occurs concurrently with the tapering of the previous drug. In an abrupt switch, the previous antipsychotic is discontinued suddenly, independent of its dose, and the new antipsychotic is started on the next day. Both methods have been used in clinical practice and double-blind studies. To date, only two medications have been studied in large multicenter clinical trials. These are olanzapine and ziprasidone. The olanzapine study revealed optimal benefits when the previous agents were gradually withdrawn and olanzapine was initiated at 10 mg/day. The ziprasidone switch study demonstrated both reduced adverse side effects from the previous agents and improvements in clinical efficacy. Additional studies are needed to examine the optimal methods for switching patients from one atypical agent to another atypical antipsychotic.
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PMID:Clinical significance of drug binding, protein binding, and binding displacement drug interactions. 1247 62

Patients with biliary dyskinesia have biliary colic, a normal gallbladder ultrasound, and a gallbladder ejection fraction typically less than 35%. We report a retrospective review of 70 patients with biliary dyskinesia who underwent cholecystectomy. Seventy-seven percent of the patients were women. Average age was 40. The most common symptoms were right upper quadrant pain, nausea, vomiting, and fatty food intolerance. All patients underwent a cholecystokinin-hepatobiliary scan or cholecystokinin-oral cholecystogram. Average ejection fractions were 20.2% and 28.4% respectively. Average post-operation follow-up was 10.9 months. Eighty-four percent of patients (59 of 70) reported improvement at follow-up. Eight patients had ejection fractions greater than 35%; seven of them reported improvement after cholecystectomy. Eleven patients did not improve after cholecystectomy; their average ejection fraction was 25%. These patients also had atypical symptoms (mid-epigastric pain and reflux symptoms). We believe cholecystectomy is effective therapy for biliary dyskinesia. Surgical outcomes could be improved by careful histories distinguishing biliary colic from other complaints. Less reliance should be placed on the ejection fraction when the patient has biliary colic without another etiology of abdominal pain.
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PMID:Outcomes of surgical therapy for biliary dyskinesia. 1450 24


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