10 citations found

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Ann Intern Med 2002 Oct 15;137(8):I32

Summaries for patients. Short-course treatment for latent tuberculosis is associated with more frequent liver injury than long-course treatment is.

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PMID: 12379094, UI: 22266750


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Ann Intern Med 2002 Oct 15;137(8):640-7

Short-course rifampin and pyrazinamide compared with isoniazid for latent tuberculosis infection: a multicenter clinical trial.

Jasmer RM, Saukkonen JJ, Blumberg HM, Daley CL, Bernardo J, Vittinghoff E, King MD, Kawamura LM, Hopewell PC

San Francisco General Hospital Medical Center, University of California, San Francisco, California, USA. rjasmer@itsa.ucsf.edu

BACKGROUND: Rifampin and pyrazinamide are recommended for treatment of latent tuberculosis infection in adults without HIV infection, but reports of severe hepatotoxicity have raised concerns about its safety. Clinical trials have not compared this treatment with isoniazid in adults without HIV infection. OBJECTIVE: To compare the safety and tolerance of a 2-month regimen of rifampin and pyrazinamide with that of a 6-month regimen of isoniazid for treatment of latent tuberculosis infection. DESIGN: Multicenter, prospective, open-label trial. SETTING: Three urban public health tuberculosis clinics in the United States. PATIENTS: 589 adults with latent tuberculosis infection who met U.S. criteria for treatment. INTERVENTION: Patients were assigned in alternate weeks to receive rifampin and pyrazinamide daily for 2 months (n = 307) or isoniazid daily for 6 months (n = 282). MEASUREMENTS: Primary end points were hepatotoxicity, other adverse events, and percentage of patients who completed treatment. RESULTS: Sixteen of 207 (7.7%) patients assigned to rifampin and pyrazinamide developed grade 3 or 4 hepatotoxicity compared with 2 of 204 (1%) patients assigned to isoniazid (odds ratio, 8.46 [95% CI, 1.9 to 76.5]; P = 0.001). The rifampin plus pyrazinamide regimen was more likely than the isoniazid regimen to be discontinued because of hepatotoxicity (odds ratio, 5.19; P = 0.033). The overall percentage of nonhepatotoxic adverse events was 20% in the rifampin-pyrazinamide group and 16% in the isoniazid group. The proportion of patients who completed the study treatment was 61% and 57%, respectively. CONCLUSIONS: A 2-month regimen of rifampin and pyrazinamide was associated with an increased risk for grade 3 or 4 hepatotoxicity compared with a 6-month regimen of isoniazid. Liver enzymes should be measured routinely during treatment to screen for liver injury and prevent progression to severe toxicity.

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PMID: 12379063, UI: 22266719


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Ann Pharmacother 2002 Nov;36(11):1791-1795

Cardiotoxicity Following Bupropion Overdose.

Druteika D, Zed PJ

Deon Druteika BSc BSc(Pharm) PharmD, at time of writing, PharmD student, Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, British Columbia, Canada; now, Pharmacotherapeutic Specialist-Internal Medicine, University of Alberta Hospital, Edmonton, Alberta, Canada.

[Record supplied by publisher]

OBJECTIVE: To determine whether bupropion overdose has been associated with cardiovascular toxicity. DATA SOURCES: MEDLINE (1966-January 2002), EMBASE (1980-January 2002), Current Contents (January 2002), and PubMed (January 2002) databases for English-language human reports. Search terms included bupropion, overdose (drug), intoxication, poisoning, and acute ingestion. DATA SYNTHESIS: Articles describing toxicity following bupropion overdose were evaluated independently by both authors to identify cases of cardiotoxicity. RESULTS: Thirteen articles describing bupropion overdose in 116 patients were identified. Only 3 patients exhibited cardiotoxicity following acute ingestion; 2 of these patients also ingested other medications. All 3 patients experienced tachycardia and conduction delays (widened QRS complex and/or prolonged QTc interval), but none of these delays progressed to a life-threatening arrhythmia. All patients recovered, with resolution of cardiotoxicity within 2-4 days following ingestion. CONCLUSIONS: We recommend that all patients with an overdose of bupropion should have an electrocardiogram performed on admission and should be monitored for the development of conduction delays and/or life-threatening arrhythmias.

PMID: 12398578


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Ann Pharmacother 2002 Nov;36(11):1736-40

Nightmares and panic disorder associated with carvedilol overdose.

Maebara C, Ohtani H, Sugahara H, Mine K, Kubo C, Sawada Y

Chiharu Maebara, MS (Pharm) Student, Department of Medico-Pharmaceutical Sciences, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.

[Medline record in process]

OBJECTIVE: To report a case of nightmares and sleep disorder associated with improper use of carvedilol, an alpha/beta-blocker, and to model the time course of receptor occupancy in this patient. CASE SUMMARY: A 41-year-old man with panic disorder had been treated with alprazolam 1.2 mg/d (3 times daily), carvedilol 10 mg/d (once in the morning), and etizolam 0.5 mg (for anxiety attack). Although the physical and psychological symptoms gradually improved, he reported nightmares and panic attacks. An interview revealed that he had been taking carvedilol 5 mg twice a day after lunch and dinner on his own initiative, in addition to the prescribed dosage. The patient was asked to take carvedilol 10 mg only after breakfast, as had been advised. Consequently, the sleep disorder and nightmares disappeared. METHODS: We calculated the time courses of beta(2)-adrenoceptor binding occupancy in the central nervous system after oral administration of carvedilol with the ordinary and improper regimens by using pharmacokinetic/pharmacodynamic parameters obtained from the literature. RESULTS: Compared with the ordinary dose of carvedilol 10 mg once a day, the improper regimen (10 mg after breakfast followed by 5 mg after lunch and dinner) increases the beta(2)-adrenoceptor binding occupancy at night (2300) to as high as the mean beta(2)-adrenoceptor binding occupancy after an ordinary dose of propranolol. CONCLUSIONS: The sleep disorder and nightmares experienced by this patient had been induced by elevation of central beta(2)-adrenoceptor binding occupancy at night as the result of improper use of carvedilol.

PMID: 12398570, UI: 22285936


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Ann Pharmacother 2002 Nov;36(11):1727-1732

Octreotide for Sulfonylurea-Induced Hypoglycemia Following Overdose.

Carr R, Zed PJ

Roxane Carr BSc BSc(Pharm), PharmD, at time of writing, PharmD student, Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, British Columbia, Canada; now, Education Supervisor, Department of Pharmacy, Children's and Women's Health Centre of British Columbia; Assistant Professor, Faculty of Pharmaceutical Sciences, University of British Columbia.

[Record supplied by publisher]

OBJECTIVE: To describe the use of octreotide in the management of 2 cases of sulfonylurea-induced hypoglycemia following overdose and to review the literature on the use of octreotide in the management of sulfonylurea overdose. CASE SUMMARY: Case 1 describes a 27-year-old woman who ingested 500 mg of glyburide; case 2 describes a 22-year-old woman following ingestion of glyburide 1000 mg. Despite administration of bolus doses of dextrose 50% and infusions of dextrose 10%, both patients demonstrated refractory hypoglycemia. Three doses of octreotide 50 micro g were administered subcutaneously spaced 8 hours apart to both patients, resulting in a reduction of hypoglycemic episodes and a reduced need for dextrose administration. DISCUSSION: In addition to the 2 cases described, 8 citations involving 23 patients with sulfonylurea overdose in which octreotide was used were identified in the literature. As with our patients, episodes of hypoglycemia and the need for bolus doses of dextrose 50% were reduced following administration of octreotide. CONCLUSIONS: The use of octreotide appears to reduce the number of hypoglycemic episodes and glucose requirements, with no reported toxicities associated with its use for sulfonylurea-induced hypoglycemia following overdose.

PMID: 12398568


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BMJ 2002 Oct 26;325(7370):922

Coroner highlights prescribing error after patient dies from warfarin overdose.

Eaton L

[Medline record in process]

PMID: 12399335, UI: 22285980


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Int J Dermatol 2001 Dec;40(12):774-6

Generalized lichenoid drug eruption following Blaschko lines.

Krasowska D, Schwartz RA, Lecewicz-Torun B

Department of Dermatology, Medical University of Lublin, Lublin, Poland.

PMID: 11903676, UI: 21901340


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Lancet 2002 Oct 12;360(9340):1163

Pesticide poisoning in the developing world-a minimum pesticides list.

Eddleston M, Karalliedde L, Buckley N, Fernando R, Hutchinson G, Isbister G, Konradsen F, Murray D, Piola JC, Senanayake N, Sheriff R, Singh S, Siwach SB, Smit L

Centre for Tropical Medicine, University of, Oxford, UK

[Medline record in process]

In parts of the developing world, pesticide poisoning causes more deaths than infectious diseases. Use of pesticides is poorly regulated and often dangerous; their easy availability also makes them a popular method of self-harm. In 1985, the UN Food and Agriculture Organisation (FAO) produced a voluntary code of conduct for the pesticide industry in an attempt to limit the harmful effects of pesticides. Unfortunately, a lack of adequate government resources in the developing world makes this code ineffective, and thousands of deaths continue today. WHO has recommended that access to highly toxic pesticides be restricted-where this has been done, suicide rates have fallen. Since an Essential Drugs List was established in 1977, use of a few essential drugs has rationalised drug use in many regions. An analogous Minimum Pesticides List would identify a restricted number of less dangerous pesticides to do specific tasks within an integrated pest management system. Use of safer pesticides should result in fewer deaths, just as the change from barbiturates to benzodiazepines has reduced the number of deaths from pharmaceutical self-poisoning.

PMID: 12387969, UI: 22276433


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Lancet 2002 Oct 12;360(9340):1151

Effect of acetylcysteine on prothrombin index in paracetamol poisoning without hepatocellular injury.

Schmidt LE, Knudsen TT, Dalhoff K, Bendtsen F

Departments of Hepatology, Rigshospitalet University Hospital, Blegdamsvej 9, DK-2100, Copenhagen, Denmark

[Medline record in process]

Acetylcysteine treatment reduces liver damage after paracetamol overdose, but can affect the prothrombin index, which is used to assess the progress of overdose patients. We aimed to assess retrospectively the effect of intravenous acetylcysteine on the prothrombin index in patients with paracetamol poisoning without signs of hepatocellular injury. Prothrombin index had been recorded before, and serially during, acetylcysteine treatment in 87 patients. After initiation of treatment, prothrombin index decreased (mean 0.33, 95% CI 0.29-0.38) in all patients, and was strongly associated with the start of acetylcysteine infusion. In patients with uncomplicated paracetamol poisoning, a fall in this index might be misinterpreted as a sign of liver failure, leading to prolonged treatment time.

PMID: 12387966, UI: 22276430


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Lancet 2002 Oct 12;360(9340):1115

N-acetylcysteine for paracetamol poisoning: effect on prothrombin.

Pol S, Lebray P

Unite d'Hepatologie et INSERM U-370, Hopital Necker, 75015, Paris, France

[Medline record in process]

PMID: 12387954, UI: 22276418


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