Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evidence from controlled clinical trials of oximes indicates that high doses given im or iv may cause transient disturbances of vision. Blurring of vision and diplopia present for up to an hour can occur. These are often accompanied by other side effects such as nausea, epigastric discomfort, drowsiness and dizziness. Visual effects have not been reported following high doses of oximes given po. Experimental studies provide evidence that some oximes given at high dosages may penetrate the blood-brain and blood-aqueous humor barriers. These suggest that the visual effects may be mediated through the CNS and/or by direct effects on the accommodation mechanisms of the eye. Although transient, the visual effects should be taken into account in clinical trials designed to assess the dosage necessary to achieve prophylaxis against OP antiChE poisoning in occupational situations.
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PMID:Ophthalmic effects of oximes: a review. 203 43

We compared the efficacy and tolerability of controlled-release carbamazepine (CBZ-CR) with conventional carbamazepine (CBZ) in 131 epileptic patients (both men and women, ages 6-65 years) in an open, multicentre, cross-over trial. Patients entered into the trial were previously on CBZ monotherapy or polytherapy. During the first 4 weeks, patients were treated with equivalent daily doses of CBZ and then switched to CBZ-CR for the subsequent 4 weeks. The majority of patients were switched to the more convenient b.i.d. dosing schedule of the controlled-release (CR) preparation without a detrimental effect on seizure frequency or adverse effects. In 44/131 (34%) of patients, the switch to CBZ-CR was accompanied by an improvement in tolerability, primarily due to a reduction in peak-dependent CNS side-effects such as tiredness, double or blurred vision, dizziness and ataxia. At the end of the study, investigators preferred CBZ-CR for 76% of their patients and 70% of the patients preferred CBZ-CR.
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PMID:A comparison of the efficacy and tolerability of controlled-release carbamazepine with conventional carbamazepine. 203 18

Anticholinergic syndrome (AS) due to accidental poisoning is exceptional. Mandragora contains a high concentration of atropine, hiosciamine and scopolamine. We have evaluated 15 patients with AS due to poisoning by Mandragora autumnalis, distributed in two family groups. The latency period since the ingestion was 1-4 hours (Means = 2.7 +/- 0.9). The clinical features corresponded to an AS of variable severity. All patients had blurred vision and dryness of mouth, nine (60%) had difficult micturition, nine dizziness, nine headache, eight (53%) vomit, two difficult swallowing and two abdominal pain. There was no correlation between the latency period and the clinical severity. Blushing, areactive mydriasis and tachycardia were found in all, dry skin and mucosae in 14 (93%), hyperactivity/hallucination in 14 and agitation/delirium in nine (60%). One patient developed a florid psychotic episode. Prostigmine (2-6 mg) was administered to 11 patients and physostigmine (0.5-2 mg) to six. The time until a definite response was observed was variable (3-36 hours). The patients treated with physostigmine had a better reversal of the psychoneurological symptoms. Mandragora was identified intermingled with chard [correction of stalwort] (Beta vulgaris) and spinach (Spinacia oleracea) leaves, and atropine and hiosciamine were identified.
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PMID:[Atropine poisoning by Mandragora autumnalis. A report of 15 cases]. 208 9

Nonsalicylate, nonsteroidal anti-inflammatory drugs (NSAIDs) can be divided into 4 chemical classes: acetic acids, fenamic acids, oxicams and propionic acids. Most NSAID overdoses result in a benign outcome. Of 50,614 exposures reported to poison centres in the United States in a 2-year period, 131 (0.26%) had a major outcome, with 10 deaths. Despite the generally mild effects reported in large patient series, isolated case reports have documented serious toxicity, such as seizures, hypotension, apnoea, coma and renal failure. The majority of these consequences occur after ingestion of substantial quantities by adults attempting suicide. Rarely, with ibuprofen and piroxicam, children who ingest small amounts in accidental exposure develop serious toxicity. Typical signs and symptoms of NSAID overdose include nausea, vomiting, headache, drowsiness, blurred vision and dizziness. Seizures are rarely documented across all NSAID classes, with the exception of mefenamic acid (where seizures occur in over one-third of cases), or following massive ingestion of other agents. Drugs in the propionic acid group have produced metabolic acidosis, respiratory depression and coma in severe cases. Ibuprofen is the agent with the most published data on overdose, probably because it is available without a prescription in many countries. Symptoms are unlikely after ingestion of 100 mg/kg or less, and are usually not life-threatening unless more than 400 mg/kg is ingested. There is some relationship between plasma concentrations and the potential for development of symptoms, but plasma concentrations have no impact on treatment decisions. Treatment of NSAID overdose is entirely supportive. Recent trends in emergency department procedures regarding gastric decontamination are evolving towards the recommended administration of activated charcoal without gastric emptying in patients presenting more than 1 hour after ingestion, although gastric lavage, followed by administration of activated charcoal, may be advisable in patients who present earlier. Home administration of syrup of ipecac is still recommended if treatment is given shortly after ingestion, with a few exceptions: for example, ipecac is contraindicated after ingestion of mefenamic acid or ibuprofen in amounts greater than 400 mg/kg. Urine alkalinisation and diuresis have been recommended to enhance the elimination of NSAIDs, based on a pKa in the range of 3 to 5. However, because the drugs are universally highly protein bound, with little unchanged renal excretion, this technique is not likely to be beneficial. Haemodialysis is also unlikely to enhance elimination, but may be required if oliguric renal failure develops. Multiple dose activated charcoal may be useful in enhancing elimination of NSAIDs with long half-lives, such as piroxicam and sulindac.
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PMID:Toxic effects of nonsteroidal anti-inflammatory drugs in overdose. An overview of recent evidence on clinical effects and dose-response relationships. 219 51

In a placebo-controlled double-blind crossover pilot study of acute Coriolis-induced motion sickness treatment/prevention in humans employing an anticonvulsant dose of phenytoin, a mean increase in tolerance to motion stress from 4.87 min (S.D. = 5.55) to 46.87 min (S.D. = 32.6) was obtained. This represents a greater than fourfold improvement in efficacy over any currently available single agent and is more than twice as effective as the scopolamine/dexadrine combination. There were none of the usual side effects of blurred vision, dizziness, dry mouth, or sedation.
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PMID:Use of phenytoin in the prevention of motion sickness. 225 75

Encainide is a class IC antiarrhythmic agent having little or no effect on action-potential duration or maximum diastolic potential but decreasing the maximum rate of phase O depolarization as well as increasing atrial and ventricular effective refractory periods. In intact animals or humans, encainide increases the AH, PR, QRS, and H-V intervals while not affecting the sinus node cycle length or JT interval. QT interval increases only by the concomitant increase in the QRS interval. Encainide is metabolized to O-demethyl encainide (ODE) and 3-methoxy-ODE (MODE), both of which are also antiarrhythmics with similar pharmacology to encainide. Encainide and its metabolites have little negative inotropic activity and ancillary pharmacology. Consequently, encainide has little or no effect on hemodynamic variables in patients with either normal or compromised cardiac function. The drug is well tolerated, with side effects being mainly those associated with its local anesthetic activity such as blurred vision and dizziness. Encainide is particularly effective in patients with excessive premature ventricular complexes (PVCs) and less so in patients with sustained ventricular tachycardia (VT). Like all antiarrhythmics, encainide may aggravate or precipitate new arrhythmias (proarrhythmia). The overall incidence of proarrhythmia is about 10%, with less occurring in patients with PVCs and more in those with sustained VT; also, the incidence of proarrhythmia is higher in patients with underlying heart disease. Encainide is also effective for the treatment of supra-ventricular arrhythmias, including atrial fibrillation, PSVT (both PAF as well as reentry of the nodal or W-P-W type), and ectopic atrial tachycardia. Its dosage and role in antiarrhythmic therapy are discussed.
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PMID:Encainide. 251 80

Hydroxyzine, a potent H1-receptor antagonist often used for relief of pruritus in patients with hepatic dysfunction, was studied in eight patients, mean age 53.4 +/- SD 11.2 years, with primary biliary cirrhosis. The patients ingested a single dose of hydroxyzine, 0.7 mg/kg (mean dose 43.9 +/- 6.6 mg). Before the dose, then hourly for 6 hours, every 2 hours from 6-12 hours, at 24 hours, and every 24 hours for 6 days, serum hydroxyzine and cetirizine were measured and an intradermal injection of 0.01 mL of a 0.1 mg/mL solution of histamine phosphate was performed. Wheals and flares were traced at 10 minutes and the areas were calculated. Mean peak hydroxyzine levels of 116.5 +/- 60.6 ng/mL occurred at 2.3 +/- 0.7 hours and mean peak cetirizine levels of 500.4 +/- 302.0 ng/mL occurred at 4.8 +/- 2.8 hours. The mean serum elimination half-life of hydroxyzine was 36.6 +/- 13.1 hours, and the mean serum elimination half-life of cetirizine was 25.0 +/- 8.2 hours. The mean hydroxyzine clearance rate was 8.65 +/- 7.46 mL/min/kg, and the mean volume of distribution was 22.7 +/- 13.3 L/kg. The mean wheal area was suppressed (P less than 0.01) from 1 to 120 hours, with maximal suppression from 2 to 48 hours. The mean flare area was suppressed from 1 to 144 hours, with maximal suppression from 3 to 24 hours (P less than 0.01). All patients became sleepy from 0.5 to 6 hours. Blurred vision, dizziness and dry mouth each occurred in two patients. Hydroxyzine elimination is impaired in patients with primary biliary cirrhosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The pharmacokinetics and pharmacodynamics of hydroxyzine in patients with primary biliary cirrhosis. 257 11

A 30 year old white woman presented at term with vaginal bleeding, dizziness and blurred vision due to bilateral serous retinal detachments. Extensive areas of choroidal occlusion with focal leakage of dye from the posterior retinal pigment epithelium and choroid were demonstrated by fluorescein angiography. With the diagnosis of abruptio placentae, a dead fetus and disseminated intravascular coagulation (DIC) the patient underwent removal of the uterine contents by cesarean section. DIC and retinal detachments resolved with improvement of vision, DIC, frequently observed in obstetric complications, has a tendency to occlude the posterior choroidal vessels, which often results in serous retinal detachments. In the setting of pregnancy, especially complicated late pregnancy, the occurrence of serous retinal detachments may be an early ocular sign of DIC.
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PMID:Ocular complications of disseminated intravascular coagulation (DIC) in abruptio placentae. 267 8

The three best-described genetic polymorphisms of drug metabolism--the debrisoquin/sparteine type of oxidative polymorphism (hereafter referred to as the debrisoquin polymorphism), the polymorphism of N-acetylation, and the mephenytoin type of oxidative polymorphism--are reviewed. For all three polymorphisms, the poor-metabolizer phenotype is inherited as an autosomal recessive trait. The debrisoquin and mephenytoin oxidative polymorphisms involve defects in two separate cytochrome P450 enzymes. The prevalence of the poor-metabolizer phenotype for debrisoquin ranges between 2% and 10% for groups of various ethnic origins. The poor-metabolizer phenotype for mephenytoin comprises about 5% of the Caucasian population and about 20% of the Japanese population. N-acetyltransferase is a cytosolic enzyme whose clinical polymorphism was discovered using isoniazid as the substrate probe. The prevalence of the slow-acetylator phenotype among American and European Caucasian and American black groups is about 50%; among the Japanese it is about 10%. More than 20 agents are substrates for debrisoquin hydroxylase, about 15 for N-acetyltransferase, and 3-5 for mephenytoin. In poor metabolizers, debrisoquin can cause hypotension, and sparteine can cause blurred vision, headache, and dizziness. Clinical consequences of the slow-acetylator phenotype include increased susceptibility to systemic lupus erythematosus induced by procainamide and hydralazine, peripheral neuropathy induced by isoniazid, hydralazine, and dapsone, and sulfasalazine-induced dose-related leukopenia, nausea, vomiting, headache, and vertigo. After administration of mephenytoin, poor metabolizers have increased somnolence and intellectual impairment. Awareness of genetic polymorphisms of drug metabolism should improve understanding of interindividual variability in drug disposition and response.
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PMID:Polymorphic drug metabolism. 268 60

Reflex sweating can be a problem for cervical spinal cord injured patients. Patient comfort and skin breakdown have been the major concerns. Five patients were studied prospectively, using a patch containing 1.5mg of scopolamine. Patches were changed every third day. Each patient was carefully monitored before and after application of the patch for signs and symptoms of anticholinergic side effects such as dizziness, blurred vision and dry mouth. Patients were also monitored for changes in patch signs before and after use, including residual urine volumes, blood pressure, heart rate, and mental status. Our study indicates that topical scopolamine successfully controlled reflex sweating in 5 patients without anticholinergic side effects.
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PMID:Management of reflex sweating in spinal cord injured patients. 274 72


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