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Ann Pharmacother 2002 Jan;36(1):67-71
Canberra Hospital, PO Box 11, Woden ACT 2606, Australia.
OBJECTIVE: To report 2 cases of serotonin syndrome with serious extrapyramidal movement disorders occurring when metoclopramide was coadministered with sertraline or venlafaxine. CASE SUMMARY: A 72-year-old white woman was treated with sertraline for depression for 18 months and was then admitted to the hospital with a fractured tibia. She was administered metoclopramide because of nausea and, within 2 hours, developed agitation, dysarthria, diaphoresis, and a movement disorder. These symptoms recurred following 2 subsequent administrations of metoclopramide. Treatment with diazepam led to resolution of symptoms within 6 hours, and there was no recurrence at 6 weeks' follow-up. A 32-year-old white woman with major depression was treated with venlafaxine for 3 years. She was admitted following a fall and, after being given metoclopramide, developed movement disorder and a period of unresponsiveness. After a second dose of metoclopramide, these symptoms recurred and were associated with confusion, agitation, fever, diaphoresis, tachypnea, tachycardia, and hypertension. She improved with administration of diazepam, but needed repetition of this treatment over the next 16 hours. Symptoms resolved within 2 days, and she continued venlafaxine with no further adverse effects. DISCUSSION: Both cases met Stembach's criteria for serotonin syndrome and had serious extrapyramidal movement disorders. The possible pathophysiologic mechanisms for the adverse reactions include a single-drug effect, a pharmacodynamic interaction, and a pharmacokinetic interaction. We believe that a pharmacodynamic interaction is most likely. CONCLUSIONS: Clinicians should be aware of a risk of serotonin syndrome with serious extrapyramidal reactions in patients receiving sertraline or venlafaxine when metoclopramide is coadministered even in a single, conventional dose.
PMID: 11816261, UI: 21675736
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Ann Pharmacother 2002 Jan;36(1):174
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PMID: 11816252, UI: 21675754
Ann Pharmacother 2002 Jan;36(1):130-47
Division of Nephrology and Hypertension, School of Medicine, University of North Carolina, CB #7155, 348 MacNider Bldg., Chapel Hill, NC 27599-7155, USA.
OBJECTIVE: To evaluate the literature for published cases of drug-induced vasculitis with cutaneous and/or systemic manifestations. DATA SOURCES: The MEDLINE database was searched from 1965 to December 1999 for articles focusing on drugs and vasculitis, using various search terminologies (e.g., Churg-Strauss syndrome, Goodpasture's syndrome, Henoch-Schonlein purpura, various drugs suspected to induce vasculitis). Cases were included when they met the established criteria as described in the methodology. DATA SYNTHESIS: Drugs found to be most frequently associated with vasculitis were propylthiouracil, hydralazine, colony-stimulating factors, allopurinol, cefaclor, minocycline, D-penicillamine, phenytoin, isotretinoin, and methotrexate. The interval between the first exposure and appearance of symptoms was reported to be extremely variable (hours to years). Vasculitis has occurred after drug dosage increases and after rechallenge with the suspected drug. In the majority of cases, vasculitis has resolved after discontinuing the drug. Patients with more severe, often life-threatening, manifestations have required treatment with corticosteroids, plasmapheresis, hemodialysis, or cyclophosphamide. Death was the result in 10% of all published cases, with a predominance in patients in whom multiple organ systems were involved. CONCLUSIONS: Clinicians need to be suspect of drug-induced vasculitis to enable prompt diagnosis and treatment. This should improve patient outcomes based on the data referenced for this article.
PMID: 11816242, UI: 21675745
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BMJ 2002 Jun 22;324(7352):1506-7
Department of Liaison Psychiatry, St James's University Hospital, Leeds LS9 7TF. hakagi@doctors.org.uk
PMID: 12077042, UI: 22071554
Int J Dermatol 2002 Feb;41(2):116-8
Department of Dermatology, University of Miami, Miami, Florida 33101, USA.
PMID: 11982652, UI: 21979427
Int J Dermatol 2002 Feb;41(2):114-6
Servico Medico/Departamento de Doencas Infecciosas, Centro de Pesquisa Hospital Evandro Chagas, Fundacao Oswaldo Cruz, Rio de Janeiro, Brazil. mclara@cpqhec.fiocruz.br
PMID: 11982651, UI: 21979426
Int J Dermatol 2002 Feb;41(2):96-8
Department of Dermatology, New Jersey Medical School, Newark, New Jersey 07103-2714, USA.
BACKGROUND: Fixed drug eruption (FDE) is a common cutaneous disorder which develops within hours of taking the offending drug and recurs at the same site with subsequent exposure to the same drug. Non-steroidal anti-inflammatory drugs (NSAIDs) are common offending drugs. METHODS: A 14-year-old girl initially presented with a 1-year history of a recurrent reddish-brown plaque around her right areola. The lesion became pruritic and raised during menses, and subsided during the remainder of her menstrual cycle with the exception of persistent residual hyperpigmentation. The patient had a pattern of naproxen use during menses for dysmenorrhea. RESULTS: The skin biopsy specimen revealed focal bullae formation and scattered necrotic keratinocytes in epidermis, hydropic degeneration of the basal cell layer, pigmentary incontinence and a perivascular infiltrate composed of lymphocytes and eosinophils. These changes confirmed the diagnosis of fixed drug eruption. CONCLUSION: Fixed drug eruption to nonsteroidal anti-inflammatory drugs is common. However, FDE due to naproxen, one of the NSAIDs, is rarely reported. We describe an unusual case of FDE, which recurred at each menses.
PMID: 11982645, UI: 21979420
J Toxicol Clin Toxicol 2002;40(2):205-6
PMID: 12126198, UI: 22121201
J Toxicol Clin Toxicol 2002;40(2):201-2
PMID: 12126196, UI: 22121199
J Toxicol Clin Toxicol 2002;40(2):199
PMID: 12126195, UI: 22121198
J Toxicol Clin Toxicol 2002;40(2):177-80
Department of Emergency Medicine, Brody Medical School at East Carolina University, Greenville, North Carolina 27858, USA.
BACKGROUND: Metformin is prescribed with an increasing frequency for patients with Type II diabetes mellitus; the increasing availability increases the risk of intentional overdoses. Metformin may cause severe lactic acidosis in overdose, especially when accompanied by co-ingestants or other medical conditions that alter lactate handling or metformin elimination. Though the clearance of therapeutic metformin by hemodialysis is known, the clearance in the setting of a large overdose has not been reported. CASE REPORT: A 58-year-old man with a history of Type II diabetes, hypertension, bipolar disease, and decreased renal function presented after ingestion of approximately 40 500-mg metformin tablets and 20 240-mg diltiazem sustained-release tablets. Clinical manifestations of poisoning included somnolence, hypotension, bradycardia, severe lactic acidosis, and ultimately death. Gastric decontamination was attempted with gastric lavage, multiple dose activated charcoal, and whole bowel irrigation. Hemodynamic support was provided with pressors, glucagon, insulin, and intra-aortic balloon pump. Due to hypotension, continuous renal replacement therapy, rather than hemodialysis, was initiated. Continuous veno-venous hemodialysis was performed with a blood flow of 180 mL/min and dialysate flow of 2.5 L/h. A Multiflow 60 kidney (Cobe) on a Prisma (Cobe) continuous renal replacement therapy machine was used. The initial metformin level was 110 microg/mL (therapeutic range 1-2 microg/mL). By continuous veno-venous hemodialysis, an absolute clearance of 50.4 mL/min was obtained. CONCLUSION: Metformin was cleared by the continuous veno-venous hemodialysis modality of continuous renal replacement therapy in this metformin overdose. Although a fatal outcome occurred in this patient, its utility in other patients with metformin overdose should be investigated.
PMID: 12126190, UI: 22121193
J Toxicol Clin Toxicol 2002;40(2):137-43
Emergency Medicine and Toxicology, Carolinas Medical Center, Charlotte, North Carolina 28232-2861, USA. rkerns@carolinashealthcare.org
OBJECTIVE: We sought to describe the kinetics, dialysis clearance, and laboratory markers of formate (FA), the toxic metabolite of methanol (meOH). METHODS: Data were obtained from a prospective, multicenter study of fomepizole +/- dialysis for methanol poisoning. Inclusion criteria confirmed methanol exposure or suspicion of exposure plus either acidemia or abnormal osmolar gap. Dialysis indications were [meOH] > 50 mg/dL, pH < 7.1, refractory acidosis, or visual toxicity. Serial plasma formate, methanol, pH, and electrolyte measurements were made. Formate was determined by gas chromatography. Endogenous and dialysis elimination half-lives were calculated as t(1/2) = 0.693/Ke, with Ke (elimination constant) derived from the slope of log (FA) vs. time. Half-lives were compared with an unpaired Student's t-test. Dialysis clearance was calculated using the Fick Principle. Pearson correlation analysis compared initial formate with initial pH, serum bicarbonate, and anion gap. RESULTS: Eleven patients were treated in the study. Eight had detectable formate with mean [FA] of 15.1 mmol/L (range 0.5-34.8). Endogenous elimination half-life was 205 +/- 90 minutes. Elimination half-life during dialysis (n = 5) was 150 +/- 37 minutes, which was not different (t = 0.22; NS). The overall dialysis formate clearance rate was 223 +/- 25 mL/min. Correlation coefficients were: pH vs. formate r2 = 0.93; bicarbonate vs. formate r2 = 0.81; and anion gap vs. formate r2 = 0.76 (all p < 0.05). CONCLUSIONS: Although dialysis clears formate, it did not significantly enhance endogenous elimination in our series of patients. Low pH, low bicarbonate, and elevated anion gap correlate independently with formate presence.
PMID: 12126185, UI: 22121188
J Toxicol Clin Toxicol 2002;40(2):107-13
Poison Center and Department of Internal Medicine, Pulmonary and Critical Care Medicine, Chang Gung Memorial Hospital, Chang Gung University, Taipei, Taiwan.
BACKGROUND: Forty-eight patients poisoned with insecticide formulations containing permethrin (a Type I pyrethroid insecticide), xylene, and surfactants are reported here. These patients were diagnosed and treated in the Chang Gung Memorial Hospital in Taiwan from January 1987 to June 1999. Ten patients ingested permethrin in error and 38 patients attempted suicide. Gastrointestinal tract signs and symptoms were most common (35/48; 73%), and included sore throat, mouth ulcerations, dysphagia, epigastric pain, and vomiting. Pulmonary abnormalities were documented in 29% (14/48) of patients. Aspiration pneumonitis occurred in eight patients, including onefatal case. Pulmonary edema was observed in two patients. Sixteen patients (33%) had central nervous system involvement including confusion (6/48; 13%), coma (10/48; 21%), and seizures (4/48; 8%). Cardiovascular symptoms in 3/48 (7%) patients were limited to arrhythmias and shock. Mild renal and hepatic dysfunction was found in 5/48 (10%) and 3/48 (6%) of patients, respectively. Leukocytosis occurred in 16 patients (33%) but was not associated with infection. Only one death occurred during this 12.5-year period. CONCLUSION: Poisoning caused by ingesting insecticides containing permethrin, xylene, and surfactant manifests primarily gastrointestinal tract symptoms and signs. The involvement of the central nervous system and lungs were less common, but clinically more significant. The relative contributions of the 20% permethrin, 70% xylene, and 10% surfactant to these toxic manifestations, however, is uncharacterized.
PMID: 12126181, UI: 22121184
Med J Aust 2002 Jun 3;176(11):562; discussion 562-3
PMID: 12116963, UI: 22108647
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