10 citations found

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Am J Emerg Med 2002 May;20(3):212-7

ED utilization of computed tomography in a poisoned population.

Patel MM, Tsutaoka BT, Banerji S, Blanc PD, Olson KR

Department of Emergency Medicine, Emory University School of Medicine, Atlanta, GA.

[Medline record in process]

The objective of this prospective, analytic study was to identify predictors and describe the demographic and clinical correlates of head computed tomography (CT) evaluation in patients with poisoning or drug overdose and altered mental status. Forty-three patients that were evaluated by head CT and 109 that were not evaluated by head CT were entered into the study at a poison control center. None of the 43 scanned patients had any acute findings on head CT. A logistic regression model yielded 4 predictors that were statistically associated with the ordering of a head CT scan: Glasgow Coma Scale (GCS) </=8 (odds ratio [OR]: 2.3; 95% confidence interval [CI] 1.03-5.7); age >/=41 years (OR 5.3; 95% CI 2.2-13); use of drugs or abuse by history (OR 2.8; 95% CI 1.04-7.6); and witnessed seizure activity (OR 4.8; 95% CI 1.3-17.9). We also tested 2 additional models to identify predictors of hospital admission, 1 with and 1 without CT scan included as a covariate. In the first model, only GCS </=8 was a significant predictor of admission (OR 10.7; 95% CI 2.4-47.2). When the use of head CT was added to the second model, it also emerged as an independent explanatory predictor of admission (OR 4.8; CI 95% 1.2-20.4) in addition to GCS (OR 10.1; 95% CI 2.2-45.4). In this pilot study, patients presenting to the emergency department (ED) with suspected poisoning or drug overdose were found to have a low likelihood of abnormal findings on head CT scan. Those among whom CT scans were obtained were more likely to be admitted to the hospital from the ED, despite negative findings. (Am J Emerg Med 2002;20:212-217. Copyright 2002, Elsevier Science (USA). All rights reserved.)

PMID: 11992342, UI: 21987619


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Ann Intern Med 2002 Apr 16;136(8):I42

Summary for patients. Liver failure associated with the dietary supplement LipoKinetix.

Publication Types:

PMID: 11955047, UI: 21952299


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Ann Intern Med 2002 Apr 16;136(8):616-8

Balancing safety of dietary supplements with the free market.

Lewis JD, Strom BL

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PMID: 11955030, UI: 21952282


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Ann Intern Med 2002 Apr 16;136(8):590-5

Severe hepatotoxicity associated with the dietary supplement LipoKinetix.

Favreau JT, Ryu ML, Braunstein G, Orshansky G, Park SS, Coody GL, Love LA, Fong TL

Cedars-Sinai Medical Center, Burns and Allen Research Institute, University of California, Los Angeles, School of Medicine, Los Angeles, California 90048, USA. joya.favreau@cshs.org

BACKGROUND: LipoKinetix (Syntrax, Cape Girardeau, Missouri) is a dietary supplement marketed for weight loss. OBJECTIVE: To describe a possible causal association between LipoKinetix and hepatotoxicity. DESIGN: Case series. SETTING: Outpatient clinic, tertiary care hospital, and U.S. Food and Drug Administration databases. INTERVENTION: Routine medical and supportive care. MEASUREMENTS: Clinical and laboratory evaluation. RESULTS: All patients developed acute hepatotoxicity within 3 months of starting LipoKinetix. At presentation, symptoms and results of laboratory tests were characteristic of acute hepatitis. All patients recovered spontaneously after LipoKinetix use was discontinued. Three of the seven patients, including one who developed fulminant hepatic failure complicated by cerebral edema, were taking LipoKinetix alone at the time of presentation. Of the four patients who were taking multiple supplements, two resumed taking supplements other than LipoKinetix without incident. CONCLUSIONS: The use of LipoKinetix may be associated with hepatotoxicity. Despite extensive evaluations, no other cause for hepatotoxicity could be identified in the seven patients studied.

PMID: 11955027, UI: 21952279


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Br J Dermatol 2002 Mar;146(3):528-9

Fixed drug eruption due to loratadine.

Ruiz-Genao DP, Hernandez-Nunez A, Sanchez-Perez J, Garcia-Diez A

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PMID: 11952560, UI: 21949846


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Brain 2002 Apr;125(Pt 4):871-9

Force overflow and levodopa-induced dyskinesias in Parkinson's disease.

Wenzelburger R, Zhang BR, Pohle S, Klebe S, Lorenz D, Herzog J, Wilms H, Deuschl G, Krack P

Department of Neurology of the Christian-Albrechts Universitat Kiel, Germany.

We assessed force coordination of the hand in Parkinson's disease and its relationship to motor complications of levodopa therapy, particularly to levodopa-induced dyskinesias (LID). We studied two groups of Parkinson's disease patients with (Parkinson's disease + LID, n = 23) and without levodopa-induced dyskinesias (Parkinson's disease - LID, n = 10), and age-matched healthy controls. The motor score of the Unified Parkinson's Disease Rating Scale, a dyskinesia score and force in a grip-lift paradigm were assessed ON and OFF levodopa. A pathological increase of forces was seen in ON-state in Parkinson's disease + LID only. In Parkinson's disease + LID, the force involved in pressing down the object before lifting was significantly increased by levodopa (by 61%, P < 0.05). An overshooting of peak grip force by 51% (P < 0.05) and of static grip force by 45% (P < 0.01) was observed in the ON- compared with the OFF-drug condition. In contrast, no excessive force was found in Parkinson's disease - LID. Peak grip force in ON-state was 140% (P < 0.05) higher in Parkinson's disease + LID than in Parkinson's disease - LID, while static grip force was increased by 138% (P < 0.01) between groups. Severity of peak-dose dyskinesias was strongly correlated with grip force in ON-state (r = 0.79 with peak force, P < 0.01). No correlation was observed between forces and the motor score as well as with the daily dose of dopaminergic medication. Force excess was only observed in patients with LID and motor fluctuations. A close relationship was seen between the overshooting of forces and dyskinesias in the ON-drug condition. We postulate that both LID and grip force excess share common pathophysiological mechanisms related to motor fluctuations.

PMID: 11912119, UI: 21909248


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J Emerg Med 2002 Apr;22(3):235-9

Bupropion seizure proportion among new-onset generalized seizures and drug related seizures presenting to an emergency department.

Pesola GR, Avasarala J

Department of Emergency Medicine, St. Vincent's Hospital, New York, New York, USA.

Bupropion is a relatively new and popular medication with seizures as its major side effect. This drug can produce seizures with an overdose. The purpose of this investigation was to determine the relative importance of this medication as the etiology of new-onset seizures relative to other drugs and new-onset seizures in general. The study design was a retrospective case series. All new onset generalized seizures were evaluated over a 4-year period in subjects 16 years of age and older. Etiologic diagnosis was determined from the neurology consultation and all patients with new-onset seizures were admitted to the hospital as per hospital policy and received a routine chemistry screening and a neuroimaging study as a minimum. The results indicate that 17 of 279 or 6.1% of the new-onset seizures were drug related. After cocaine intoxication (6/279 or 2.2%) and benzodiazepine withdrawal (5/279 or 1.8%) seizures, bupropion (4/279 or 1.4%) was the third leading cause of drug related seizures. In addition, all the bupropion related seizures occurred in patients taking what was considered to be a therapeutic dose or 450 mg/day or less. Sleep deprivation, previous history of attention deficit disorder and bulimia, and previous heavy alcohol use were associated in three of the patients taking bupropion who had seizures. We conclude that although drug related new-onset seizures are not a common cause of seizures overall, bupropion might be a more common cause of drug related new-onset generalized seizures presenting to the Emergency Department than previously thought, occurring in more than one-fifth of this subgroup of cases. Possibly, greater exclusion criteria are needed than currently recommended for the use of bupropion at therapeutic doses.

PMID: 11932084, UI: 21929951


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J R Soc Med 2002 Apr;95(4):178-81

Prions and dentistry.

Porter SR

Oral Medicine, Eastman Dental Institute for Oral Health Care Sciences, UCL, University of London, 256 Gray's Inn Road, London WC1X 8LD, UK. s.porter@eastman.ucl.ac.uk

Publication Types:

PMID: 11934906, UI: 21932721


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J Toxicol Clin Toxicol 2002;40(1):81-90

Status epilepticus after massive carbamazepine overdose.

Spiller HA, Carlisle RD

Kentucky Regional Poison Center of Kosair Children's Hospital, Louisville 40232-5070, USA. henry.spiller@nortonhealthcare.org

[Medline record in process]

We report two patients who experienced status epilepticus after carbamazepine overdose. The first patient was an 18-year-old female with a history of epilepsy. She experienced 4 hour of persistent and prolonged seizures resistant to sodium amytal therapy. The status epilepticus ended with her death. The second patient was an 18-year-old male with a history of bipolar disorder. He experienced 5 hour of persistent and prolonged seizures that appeared to be resistant to diazepam, phenytoin, and phenobarbital. The seizures abated with the infusion of midazolam. This is a report of status epilepticus associated with wide complex tachycardia after carbamazepine overdose, which may be resistant to conventional therapy.

PMID: 11990208, UI: 21985579


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J Toxicol Clin Toxicol 2002;40(1):77-80

Treatment of a 1,4-butanediol poisoning with fomepizole.

Megarbane B, Fompeydie D, Garnier R, Baud FJ

Reanimation Medicale et Toxicologique, Universite Paris VII, INSERM U26, Hjpital Laribosiere, France. bruno-megarbane@wanadoo.fr

[Medline record in process]

BACKGROUND: Toxicity of 1,4-butanediol, an industrial solvent and a substance of abuse, is still misunderstood and not well documented. To date, only supportive treatments are used in this poisoning. CASE REPORT: The case of a 43-year-old man who ingested 30 mL of a homemade 1,4-butanediol solution and who developed general seizures and coma has been reported here. An intravenous loading dose of fomepizole 10 mg/kg was started on admission and followed by two other doses of 10 mg/kg every 12 hour. He awoke shortly after fomepizole administration. Initial plasma 1,4-butanediol and gamma-hydroxybutyric acid concentrations, measured by gas chromatography-mass spectrometry, were 24 and 222 mg/L, respectively. Subsequent 1,4-butanediol and gamma-hydroxybutyric acid determination suggest that there was some further formate of gamma-hydroxbutyric acid after fomepizole was administered. CONCLUSION: Fomepizole administration appeared safe in this 1,4-butanediol-intoxicated patient. It is unknown whether fomepizole influenced his clinical course, but the rapid awakening observed suggests that it may have been usefuL Further experience is needed, however, to define the efficacy of this antidotal therapy in 1,4-butanediol intoxication.

PMID: 11990207, UI: 21985578


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