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)

A double-blind random study compared lorazepam with diazepam as i.m. premedicants in 84 healthy women undergoing uterine curettage. Anxiety, assessed by a self-rating test by the patient and by a trained observer, was reduced 90 min after both lorazepam (P less than 0.001) and diazepam (P less than 0.01). There was more sedation and a longer recovery time after lorazepam than after diazepam. Amnesia at 24 h after operation (lack of recall rather than lack of recognition) was greater after lorazepam. There was transient local discomfort at the site of the injection in most patients in both groups, but no serious effects. Local erythema was present in 12 patients who received lorazepam and 10 who received diazepam 90 min after the injection, disappearing after 24 h in the former group but remaining in the latter. The incidence of nausea, vomiting and headache in both groups was small and similar, but there was more restlessness and dizziness after diazepam in the early recovery period.
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PMID:Comparison of lorazepam and diazepam as premedicants. 2 39

In the dose range of 4.0--32.0 mg/kg s.c., caffeine produced most of the signs which are commonly seen after the administration of naloxone (0.05 mg/kg s.c.) to morphine-dependent monkeys. The signs designated as lying on side or abdomen, avoiding contact, vocalizing, crawling or rolling, restlessness or pacing, tremors, retching, vomiting, coughing, vocalizing when abdomen palpated, rigid abdomen and salivation were noted. A randomized and blind experimental design, which included vehicle and positive (naloxone) controls was used. The significance of the differences between total scores for the whole syndrome was tested by the Mann-Whitney U-test. In preliminary studies in naive monkeys, caffeine was found to elicit some withdrawal signs but the results were equivocal. Na benzoate also elicited some withdrawal signs in morphine-dependent monkeys at 32.0 mg/kg s.c., but few signs were seen in naive monkeys. Caffeine was found to be approximately 10X more active than Na benzoate in inhibiting cAMP phosphodiesterase activity in a neuroblastoma cell whole homogenate assay. These results are consistent with the observations of Collier and Francis that morphine abstinence in rodents is associated with increased brain levels of cAMP.
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PMID:Caffeine elicited withdrawal signs in morphine-dependent rhesus monkeys. 21 Oct 41

Ten patients with severe dementia due to Alzheimer's disease (AD) or multi-infarct dementia (MID) or both, were treated with the precursor amino acids of the neurotransmitters serotonin and dopamine. The precursor amino acids (PAA) were given orally in a preparation that included tyrosine (4 gm daily) and 5-hydroxy-tryptophan (5-HTP) (800 mg daily), plus carbidopa (100 mg daily) as an aromatic amino-acid decarboxylase inhibitor. Diagnosis was established by an electroencephalogram, brain scan, computerized axial tomographic scan, and in one case by necropsy findings. Serial clinical evaluations and measurements of neuropsychologic function were performed. Levels of homovanillic acid (HVA) and 5-hydroxyindole-acetic acid (5-HIAA) were determined before and after administration of probenecid. Side effects of the PAA therapy were diarrhea, drowsiness, nausea, vomiting and agitation, all of which were controlled by reducing the dosage. One patient with MID and one with AD+MID showed clinical and psychologic improvement, but the others did not improve. Analysis of the cerebrospinal fluid for HVA and 5-HIAA before and after the probenecid test indicated some improvement in the metabolic turnover of these acid metabolites of serotonin and dopamine after administration of their precursor amino acids.
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PMID:Neurotransmitter precursor amino acids in the treatment of multi-infarct dementia and Alzheimer's disease. 30 Nov 48

The effect of guancydine (1-cyano-3-tert-amylguanidine) on systemic and renal hemodynamics was studied in nine patients with arterial hypertension. Antihypertensive drugs were withheld for 15 days before beginning the investigation. Average sodium intake was 105 meq/24 hours in some patients and 25 meq/24 hours in others. Patients received placebo during a control period that averaged 14 days. Guancydine was given for 7 to 18 days at an average dose of 21 mg/kg of body weight. Although mean arterial blood pressure decreased significantly in all patients, it reached normal levels in only two. There was no change in cardiac output. Glomerular filtration rate and renal plasma flow remained unchanged, whereas urinary sodium excretion diminished, suggesting an activation of the renin-angiotensin-aldosterone system. A substantial gain in body weight was noted. Nausea, vomiting, constipation, somnolence, restlessness, mental confusion, asthenia, and urine retention were observed. The anti-angiotensin effect of guancydine that has been described in animals was not observed.
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PMID:Effect of guancydine on systemic and renal hemodynamics in arterial hypertension. 32 1

Case histories of four elderly patients with central nervous system signs of digitalis toxicity were reviewed. Evidence of toxicity included lethargy, depression which was not present previously, confusion, restlessness, emotional instability, hyperventilation, and vertigo. Vomiting developed four days after the onset of the mental changes. No cardiac arrhythmias were observed. Digoxin serum levels ranged between 4.2 and 7.0 ng/ml. Serum potassium values were within normal limits. Three of the four patients recovered with a return of their mental status to the pretoxic state. The fourth case was fatal. At autopsy long-standing myocardial ischemia was the only significant finding.
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PMID:Digitalis delirium in elderly patients. 53 71

As a causative factor in spontaneous subarachnoid hemorrhage, vascular anomalies, especially aneurysm or arteriovenous malformation, have been generally recognized. On the other hand, subarachnoid hemorrhage from brain tumor and cryptic vascular malformation are rare. We experienced two cases showing subarachnoid hemorrhage from angioblastic meningioma and vascular hamartoma as an initial symptom. Case 1: A 48-year-old woman, who complained of severe headache and vomiting on Feb. 10th, 1972, gradually became lethargic. Lumbar puncture revealed moderately hemorrhagic C.S.F.. On the fifth day after the onset, she was admitted to our hospital. On admission she showed disorientation and disturbance of resent memory. Aphasia and agnosia were slightly observed. On ophthalmologic examination right homonymous lower quadrant hemianopsia was observed. The carotid angiogram showed slight square shift of the anterior cerebral artery to the right side, elevation of the middle serebral artery and a homogeneous tumor stain in the occipital region in capillary phase. A walnut sized tumor invading the middle portion of the left lateral sinus and showing firm adhesion to the tentrium was found. There was an intracerebral hematoma behined the tumor. The tumor, the tentrium and the lateral sinus were extirpated en bloc and the intracerebral hematoma was aspirated. Histologically, the tumor was angioblastic meningioma. Case 2: A 7-year-old boy, who complained of severe abrupt headache, nuchal pain and vomiting on Sept. 17th, 1972, became gradually lethargic. Lumbar puncture revealed hemorrhagic C.S.F., On the tenth day after the onset, he was admitted to our hospital. He showed confusion and agitation. The carotid angiogram showed an unrolling of the pericallosal artery, but no findings of space taking lesions. An air study indicated a globular filling defect protruding into the anterior horn of the right lateral ventricle. The tumor located in the laterobasal wall of the anterior horn was removed picemiel by transventricular approach. Histologically, the tumor was vascular hamartoma. Furthermore, we discussed various brain tumors showing subarachnoid hemorrhage as an initial symptom, its frequency and bleeding mechanism on the literature.
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PMID:[Two cases showing subarachnoid hemorrhage from angioblastic meningioma and vascular hamartoma (author's transl)]. 98 94

The case is reported of a non-diabetic young woman who attempted suicide by ingesting 2,500 mg of phenformin. The most marked clinical and laboratory findings during the first 24 hrs included nausea, vomiting, anxiety, agitation, polydipsia, polyuria, increased appetite, tachycardia, tachypnea, persistent lactic acidosis, hypoglycemia and hypokalemia. Treatment at the ICU 10 hrs after ingestion of the overdose was essentially symptomatic and included measures to correct acidosis and hypoglycemia. The patient recovered completely.
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PMID:Acute self-poisoning with phenformin. 102 Jun 9

In 70 patients (maxillo-facial-, neurosurgical-, abdominal- and gynaecological operations) the technique of "analgetic anaesthesia" using high doses of fentanyl (0.025 mg/kg body weight) and naloxone as its antagonist (0.02 mg/kg body weight) has been employed. All patients were artificially ventilated with N2O/O2 in a 3:1 ratio. Muscle relaxation was achieved with pancuronium-bromide (0.08 mg/kg). The patients had no apparent heart or lung disease. The youngest patient was 4 years of age, the oldest 82 years of age (average age 48.9). The necessity for a reinjection of fentanyl (half the initial dose) was determined by continously monitoring heart rate. This variable appeared to be the most subtle index indicating a reduction in analgesia. Sufficient analgesia was maintained once the heart rate stayed 20% below preanaesthetic levels. At the end of the operation naloxone reversed the respiratory depression. There was no evidence indicating postoperative pain, which may have required administration of additional analgesics. If deep analgesia was maintained up to the last surgical procedures no emesis appeared in the post operative period. The incidence of emesis was higher 10% compared to the classical neuroleptanalgesia with droperidol this was often noted in cases where blood accumulated in the stomach (maxillo-facial operations) (70%). In 3% of all cases psychomotor agitation with delirium appeared right after the injection of naloxone. This lasted for about 15 minutes. We suspect that due to the sudden and powerful effect of naxolone, in replacing fentanyl from its receptor site, acute withdrawal symptoms may be precipitated.
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PMID:[High doses of fentanyl as the sole anaesthetic agent and naloxone as its antagonist (author's transl)]. 113 60

Flumazenil, a specific benzodiazepine antagonist, was evaluated as adjunctive therapy in the management of benzodiazepine overdose. Thirteen emergency departments enrolled 326 patients in this double-blind, placebo-controlled trial; 162 patients were randomly allocated to receive flumazenil (maximum dose, 30 ml, providing 3 mg of flumazenil), and 164 were allocated to receive placebo (maximum dose, 30 ml). A successful response was the attainment of a score of 1 or 2 on the Clinical Global Impression Scale (CGIS), denoting a very much improved or much improved status, 10 minutes after the start of intravenous administration of the test drug. Among those patients whose drug screen revealed the presence of benzodiazepines, 75 (77%) of 97 patients given flumazenil and 13 (16%) of 83 given placebo attained such a response. The mean CGIS score at 10 minutes for benzodiazepine-positive patients treated with flumazenil was 1.95 versus 3.58 for those given placebo. As determined by the Neurobehavioral Assessment Scale, 61% of patients who initially responded became resedated; in these patients, the effect of flumazenil lasted a median of 90 minutes. At the investigator's discretion, patients who did not achieve a criterion response in the double-blind trial could receive open-label flumazenil, titrated as in the double-blind phase. Among the benzodiazepine-positive patients, 9 (53%) of 17 patients from the flumazenil group responded to the additional flumazenil, and 58 (81%) of patients previously given placebo responded. Safety was assessed in all 326 patients given the test drug. The most frequent adverse experiences after the administration of flumazenil were agitation (7%), vomiting (7%), abnormal crying (4%), and nausea (4%); these effects were observed with a lower frequency in the placebo group. Serious adverse experiences were reported in 4 patients; these included seizures and cardiac arrhythmias. Of the 3 patients with seizures, 2 had ingested large doses of cyclic antidepressants in addition to the benzodiazepine. The toxicology screen for 1 of the 2 showed 1900 ng/ml of amoxapine and 900 ng/ml of nortriptyline; the toxicology screen for the other, who also had ventricular tachycardia, showed 1928 ng/ml of loxapine and 301 ng/ml of amoxapine. The results of this study confirm published reports of the efficacy of flumazenil in reversing benzodiazepine-induced sedation in patients with benzodiazepine overdose. This was accomplished irrespective of the presence of coingested drugs. Flumazenil is not recommended for patients with serious cyclic antidepressant poisoning or those who use benzodiazepines therapeutically to control seizure disorders. When used as recommended, however, flumazenil has been shown to have an acceptable safety level.
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PMID:Treatment of benzodiazepine overdose with flumazenil. The Flumazenil in Benzodiazepine Intoxication Multicenter Study Group. 128 3

A review of the safety and tolerability of fluvoxamine in worldwide marketing studies involving 24,624 patients, predominantly receiving fluvoxamine treatment in uncontrolled studies in depression, has been conducted. There was a marked preponderance of female patients and patients aged between 30 and 50 years. The majority of patients were treated for 6 weeks, with the most frequent modal total daily dose being 100mg. The greatest proportion of adverse experiences occurring, by COSTART body system, affected the digestive system (24.1%), the nervous system (23.7%), and the body as a whole (15.3%). The only adverse experience with an incidence greater than 10% was nausea (15.7%), with somnolence (6.9%) and asthenia (6.2%) as the next most frequent experiences. Notably, the rates of agitation and anxiety were only 1.4 and 1.3%, respectively. The incidences of adverse experiences increased with age, and were slightly higher in females than males. 15.1% of patients discontinued treatment prematurely as a result of adverse experiences, principally nausea, dizziness, vomiting, somnolence, abdominal pain, and headache. The overall incidence of serious adverse events associated with fluvoxamine treatment was 2.5%, and the incidence of overall suicidality, including suicidal ideation, overdose, and intentional overdose as well as attempted and completed acts of suicide, was remarkably low at 0.8%.
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PMID:Review of fluvoxamine safety database. 137 74


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