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)

The withdrawal of heterocyclic antidepressants and antipsychotic agents can produce nausea, emesis, anorexia, diarrhoea, rhinorrhoea, diaphoresis, myalgias, paraesthesias, anxiety, agitation, restlessness and insomnia. The withdrawal of monoamine oxidase (MAO) inhibitors may result in severe anxiety, agitation, pressured speech, sleeplessness or drowsiness, hallucinations, cognitive impairment, delirium, suicidality and delusions of persecution. The withdrawal of antipsychotic agents may give rise to symptoms preceding the onset of psychosis. These potential harbingers of relapse include anxiety, agitation, restlessness and insomnia. The withdrawal phenomena reviewed are usually prevented by gradually reducing the total daily dosage of the pertinent drug. Antimuscarinic agents often alleviate the distress produced by the withdrawal of tricyclic antidepressants and antipsychotic agents. MAO inhibitor withdrawal syndromes may constitute medical emergencies. The prevention of the evolution of a MAO inhibitor withdrawal-precipitated syndrome is a high priority.
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PMID:Withdrawal phenomena associated with antidepressant and antipsychotic agents. 791 78

A 25-year-old woman suffered from hyperemesis gravidarum when she was seven weeks pregnant. Since her vomiting continued, she received intravenous dextrose and electrolytes without thiamine in a hospital. One month later, she developed gait disturbance, followed by confusion and dysarthria. On admission to our department, she was confusional and had ataxic dysarthria. Spontaneous and gaze evoked nystagmus was present. Limb coordination was bilaterally ataxic. Based on her clinical course and symptoms, she was diagnosed as having Wernicke's encephalopathy. From the admission day, intravenous infusion of vitamin B1 (600 mg/day) was started. A few days later, her consciousness and limb ataxia began to improve. However, truncal ataxia and polyneuropathy became evident. Eight weeks after onset, she developed Korsakoff's psychosis such as anterograde and retrograde amnesia, disorientation and confabulation. We administered large amounts of corticosteroid (methylprednisolone 500 mg/day) in order to reduce brain edema or stabilize the impaired blood-brain barrier. Soon after, her psychosis began to improve gradually. She recovered remarkably from the psychosis, but she was left with persistent nystagmus, mild ataxic gait and polyneuropathy. The present case suggests that corticosteroid may have the beneficial effect on Wernicke-Korsakoff syndrome.
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PMID:[Beneficial effect of steroid pulse therapy on Wernicke-Korsakoff syndrome due to hyperemesis gravidarum]. 795 22

Over a 3-year period, 15 patients with severe hyponatremia were referred to our emergency room from a nearby psychiatric institution. This article reports on 36 episodes of symptomatic hyponatremia in those 15 patients. All but two of the patients were receiving antipsychotic medications; one patient was taking a nonsteroidal anti-inflammatory drug, and one patient was taking an oral hypoglycemic agent. Thirteen patients were chronic schizophrenics, one had a bipolar depressive disorder with psychotic features, and one patient had no psychiatric disorder. Patients presented with seizures, change in mental status, and vegetative symptoms (nausea, vomiting, and diarrhea) associated with hyponatremia and water intoxication. Exacerbation of the patients' underlying illness, psychogenic polydipsia, compulsive smoking, alcoholic cirrhosis, drug abuse, and neuroleptic and other medications are thought to be the major causes of acute hyponatremia in these patients.
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PMID:Symptomatic hyponatremia associated with psychosis, medications, and smoking. 809 75

The present study was designed to examine withdrawal from a therapeutic, non abused drug, haloperidol. Rats were trained to discriminate the anxiogenic compound pentylenetetrazol (PTZ) from water in a two lever, food reinforced, drug discrimination procedure. Dose effect curves were then determined for PTZ and the antipsychotic drug, haloperidol (0.1-1 mg/kg). Haloperidol did not substitute for PTZ, even at a dose that decreased rates of responding to approximately 15% of control values. Rats were then treated chronically with either 1 or 2 mg/kg/day haloperidol while training was suspended. After 5 days of chronic haloperidol 4/6 animals in the 1 mg/kg/day group and 5/7 in the 2 mg/kg/day group chose the PTZ lever when tested 24-48 hours after the last haloperidol injection. Haloperidol, 1 or 2 mg/kg, did not reverse PTZ-lever responding. After an additional 5 days of chronic haloperidol, 3/6 rats in the 1 mg/kg/day group and 5/7 rats in the 2 mg/kg/day group responded on the PTZ lever 24 hours after the last injection, and this was reversed with the anxiolytic, chlordiazepoxide (3.2-5.6 mg/kg). The current findings indicate that there is an anxiogenic component to withdrawal from haloperidol. In psychotic patients, abrupt discontinuation of haloperidol results in nausea, vomiting and sweating, as well as a "relapse into psychosis" characterized by anxiety, depression and internal chaos (1). Interestingly, the authors caution that the so-called relapse into psychosis may simply be a sign of withdrawal. The current findings support their view and suggest that abrupt discontinuation of psychoactive therapeutic agents may result in anxiety.
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PMID:Withdrawal from chronic haloperidol substitutes for the pentylenetetrazol discriminative stimulus. 846 31

Severe hyponatraemia may be cause unconsciousness, vomiting, seizures or exogenous psychosis and is associated with a high mortality. We report on a 44-year-old woman who presented with somnolence and psychomotor unrest. After rousing stimuli she showed no verbal response and did not follow any instructions. For three days she suffered from nausea and vomiting. Laboratory values included a natrium serum level of 97 mmol/l. CT scan demonstrated no abnormal findings. Because of severe arterial hypertonia she received for 12 days intensive diuretic therapy with 50 mg hydrochlorothiazide and 100 mg triamterene. Retrospectively, we proved that as a result of saluretic therapy, chronic hyponatremia had already existed before admission. Serum sodium was corrected slowly (< 12 mmol/l) with fluid restriction and normal saline solution. This is considered to be the first case report of a complete restitution after hyponatremia less than 100 mmol/l. We suggest that the preexisting chronic hyponatremia and the slow correction of serum sodium level are responsible for the favorable outcome of this case of severe hyponatremia.
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PMID:[Reversible exogenous psychosis in thiazide-induced hyponatremia of 97 mmol/l]. 868 11

Cam-2445 is a selective, high-affinity NK1 receptor antagonist that is a potentially useful treatment for arthritis, asthma, migraine, anxiety, psychosis, and emesis. Cam-2445 exhibits low aqueous solubility and high lipophilicity and has a molecular weight of 470. Cam-2445 has poor oral bioavailability and the purpose of this research was to examine the potential barriers to the oral bioavailability of Cam-2445. Cam-2445 was relatively stable at 37 degrees C in 0.1 N HCl, 5 microM alpha-chymotrypsin, rat intestinal perfusate, and in rat jejunal brush border membrane suspension. High permeability was observed from CACO-2 cells and from rat single-pass intestinal perfusions. Cam-2445 was administered as a solution to rats by intravenous (i.v.), oral (p.o.), intraduodenal (i.d.), and intraportal (i.p.v.) routes. The total oral bioavailability was poor at 1.4%. Absorption appeared to be rapid after i.d. dosing; bioavailability was 26%, and 54% of the dose was absorbed intact into the portal system. After i.p.v. dosing, 48% of the dose was available to the systemic circulation. The elimination t1/2 after i.d. dosing (2.91 h) was comparable to that i.v. dosing (2.93 h), whereas it was significantly longer after p.o. dosing (12.4 h). The p.o. dose apparently precipitated in the gastrointestinal (GI) tract, resulting in low oral bioavailability. These results indicated that neither stability in the GI tract nor membrane transport were major obstacles to the absorption of Cam-2445. While hepatic extraction of 52% was significant, the low aqueous solubility of Cam-2445, as well as the differences noted between p.o. and i.d. studies, strongly support GI dissolution and/or precipitation as the limiting factor for the oral bioavailability of the compound.
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PMID:Absorption of Cam-2445, and NK1 neurokinin receptor antagonist: in vivo, in situ, and in vitro evaluations. 869 23

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

Following the conduct of a 28-day inpatient bioequivalence study of clozapine in schizophrenia patients, withdrawal effects after abrupt discontinuation from clozapine were assessed. Thirty patients who met DSM-III-R criteria for schizophrenia, residual type, or schizophrenia in remission were enrolled in the study. Patients were evaluated for symptoms of withdrawal effects for 7 days after clozapine 200 mg/day was abruptly withdrawn. Of 28 patients who completed the study, 11 had no withdrawal symptoms; 12 had mild withdrawal adverse events of agitation, headache, or nausea; four patients experienced moderate withdrawal adverse events of nausea, vomiting, or diarrhea; and one patient experienced a rapid-onset psychotic episode requiring hospitalization. Cholinergic rebound is a likely explanation for the mild to moderate withdrawal symptoms and is easily treated with an anticholinergic agent. Mesolimbic supersensitivity, as well as specific properties of clozapine, are discussed as likely causes for rapidonset psychosis. Our findings are consistent with previous reports of withdrawal reactions associated with clozapine, further reminding clinicians to monitor patients closely following abrupt discontinuation of clozapine.
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PMID:Cholinergic rebound and rapid onset psychosis following abrupt clozapine withdrawal. 893 13

Disulfiram is used in alcohol rehabilitation because it inhibits aldehyde dehydrogenase and consequently causes the disulfiram-ethanol reaction (vomiting, vertigo, anxiety, cardiovascular effects) after ingestion of alcoholic beverages. However, adverse effects on the central nervous system (for the most part psychotic reactions, acute organic brain syndrome, catatonia) may appear as a direct result of the drug itself. Disulfiram and its metabolite carbon disulfide inhibit dopamine beta-hydroxylase, increasing the levels of dopamine and reducing those of norepinephrine in the central nervous system. We observed direct disulfiram-induced toxicity on the central nervous system in 8 abstinent patients in whom a disulfiram-ethanol reaction had been excluded. Risk is increased when 1) excessive amounts of the drug are ingested; 2) the patient is already suffering from a major psychiatric illness; 3) the patient has anatomical brain lesions. In all cases observed, the toxic effects appeared in the first weeks and were reversed after suspension of the drug (except in one patient who died from severe bronchopulmonary infection). We thus suggest the following protocol: 1) physical examination and interview 3-4 weeks after initiation of treatment; 2) as a general rule, in abstinent patients, the lowest possible maintenance dosage should be administered. This strategy, despite the risk of underdosage, meets the goals inherent in an integrated medical and psychosocial approach to the treatment of alcoholism with which these patients seem better able to comply.
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PMID:[Collateral effects of disulfiram on the central nervous system in alcoholics that have become totally abstemious. Description of 8 cases]. 907 70

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


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