Journal of toxicology. Clinical toxicology最新文献

{"title":"Epidemiology of lindane exposures for pediculosis reported to Poison Centers in Texas, 1998-2002.","authors":"Mathias B Forrester,&nbsp;Jennifer S Sievert,&nbsp;Sharilyn K Stanley","doi":"10.1081/clt-120028745","DOIUrl":"https://doi.org/10.1081/clt-120028745","url":null,"abstract":"<p><strong>Background: </strong>Lindane (gamma-benzene hexachloride), commonly used as a treatment for pediculosis, has been associated with adverse reactions and has recently undergone increased regulation.</p><p><strong>Objective: </strong>We sought to describe the patterns of a large number of lindane exposures reported to poison centers in Texas during 1998-2002.</p><p><strong>Methods: </strong>Data on all lindane exposures for pediculosis reported to the Texas Poison Center Network were analyzed.</p><p><strong>Results: </strong>There were 528 reported human exposures to lindane for pediculosis. The incidence of lindane exposures has decreased by 52% from 1998 to 2002. Misuse or abuse of lindane was reported in at least 87% of the cases. Of those cases with a known patient age, 45% were less than age 6 yrs, 23% age 6-19 yrs, and 32% over age 19 yrs. Female patients accounted for 55% of reported cases. Of those cases with a known medical outcome, 61% reported no effects. The most frequently reported symptoms were vomiting, nausea, and ocular irritation or ocular pain.</p><p><strong>Conclusion: </strong>The number of reported lindane exposures in Texas is decreasing. The majority of reported exposures involve misuse or abuse of the product. The pattern of symptoms reported in Texas was consistent with the literature.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 1","pages":"55-60"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-120028745","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24467283","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"N-acetylcysteine for the treatment of clove oil-induced fulminant hepatic failure.","authors":"Jeffrey S Eisen,&nbsp;Gideon Koren,&nbsp;David N Juurlink,&nbsp;Vicky L Ng","doi":"10.1081/clt-120028751","DOIUrl":"https://doi.org/10.1081/clt-120028751","url":null,"abstract":"<p><p>We present a 3-month-old female who developed fulminant hepatic failure after ingesting less than 8 mL of clove oil. Initial treatment involved gastrointestinal decontamination, supportive measures, and admission to hospital. She subsequently developed fulminant hepatic failure and was treated with intravenous N-acetylcysteine (N-AC) according to a protocol used for acetaminophen poisoning. Over the next 72 h her liver synthetic function and clinical status improved, and she made a complete recovery. Previous reported cases of clove oil toxicity and the potential role of N-AC therapy are reviewed.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 1","pages":"89-92"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-120028751","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24467188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A rare ingestion of the Black Locust tree.","authors":"Alan Hui,&nbsp;Jeanna M Marraffa,&nbsp;Christine M Stork","doi":"10.1081/clt-120028752","DOIUrl":"https://doi.org/10.1081/clt-120028752","url":null,"abstract":"<p><strong>Background: </strong>The Black Locust (Robinia Pseudoacacia) tree contain toxalbumins, robin and phasin, that exert their toxic effects by inhibition of protein synthesis. Despite the potential dangers of Black Locust intoxication, reports of human toxicity after ingestion are rare. We report the first human intoxication of Black Locust bark in North America in over one hundred years.</p><p><strong>Case report: </strong>An eight-year-old male was brought to the emergency department 6 hours after chewing and expelling the Black Locust bark. He presented with emesis, which began approximately 2.5 hours after exposure. His vital signs were as follows: oral temperature, 97.5 degrees F; blood pressure, 128/75 mmHg; heart rate, 114 beats per minute; respiratory rate, 15 breaths per minute. Initial treatment included 4 mg i.v. ondansetron, which resolved the vomiting, one dose of activated charcoal, and intravenous fluids. He was then admitted to the intensive care unit (ICU) for observation of signs of toxicity. Laboratory findings were unremarkable except for a white blood cell of 18.4 K/uL and an elevated alkaline phosphatase of 183 U/L. The patient remained asymptomatic throughout his stay in the ICU and was discharged on the fifth day of admission with a normal white blood cell of 4.1 K/uL and an alkaline phosphatase of 251 U/L.</p><p><strong>Conclusion: </strong>Patients with clinical toxicity following the ingestion of Black Locust are expected to do well with supportive care and observation.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 1","pages":"93-5"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-120028752","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24467189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Position paper: whole bowel irrigation.","authors":"","doi":"10.1081/clt-200035932","DOIUrl":"https://doi.org/10.1081/clt-200035932","url":null,"abstract":"<p><p>Whole bowel irrigation (WBI) should not be used routinely in the management of the poisoned patient. Although some volunteer studies have shown substantial decreases in the bioavailability of ingested drugs, no controlled clinical trials have been performed and there is no conclusive evidence that WBI improves the outcome of the poisoned patient. Based on volunteer studies, WBI should be considered for potentially toxic ingestions of sustained-release or enteric-coated drugs particularly for those patients presenting greater than two hours after drug ingestion. WBI should be considered for patients who have ingested substantial amounts of iron as the morbidity is high and there is a lack of other options for gastrointestinal decontamination. The use of WBI for the removal of ingested packets of illicit drugs is also a potential indication. WBI is contraindicated in patients with bowel obstruction, perforation, ileus, and in patients with hemodynamic instability or compromised unprotected airways. WBI should be used cautiously in debilitated patients or in patients with medical conditions that may be further compromised by its use. The concurrent administration of activated charcoal and WBI may decrease the effectiveness of the charcoal. The clinical relevance of this interaction is uncertain. A review of the literature since the preparation of the 1997 Whole Bowel Irrigation Position Statement revealed no new evidence that would require a revision of the conclusions of the Statement.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 6","pages":"843-54"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-200035932","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24802977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Severe bone marrow depression induced by an anticancer herb Cantharanthus roseus.","authors":"Ming-Ling Wu,&nbsp;Jou-Fang Deng,&nbsp;Jaw-Ching Wu,&nbsp;Frank S Fan,&nbsp;Ching-Fen Yang","doi":"10.1081/clt-200026963","DOIUrl":"https://doi.org/10.1081/clt-200026963","url":null,"abstract":"<p><p>We report a 67-yr-old woman with hepatitis C-related liver cirrhosis and hepatoma who had developed severe bone marrow suppression after taking Cantharanthus roseus as an alternative anticancer treatment. The patient developed severe pancytopenia with initial presentations of vomiting, diarrhea, oral ulcer, and fever about 1 week after taking 5-days' course of Cantharanthus roseus. Bone marrow biopsy showed autolysis, which indicated massive necrosis of the hematopoietic cells. There was no malignant cell infiltration. The patient also had severe gastrointestinal disturbances, bacteremia, urinary tract infection, and impaired renal and liver function. Supportive care with broad-spectrum antibiotics, granulocyte colony-stimulating factor, repeated blood transfusions, and albumin supplement was given. She recovered and was discharged after 48 days hospitalization. Coadministration of Cantharanthus roseus and cisapride was noted, and these two drugs are both substrates of cytochrome P450 3A4 enzymes (CYP 3A4). Because the vinca alkaloids are extensively metabolized by the liver cytochrome P450 enzymes, poor hepatic function and drug-herb interaction might predispose the patient to develop the bone marrow toxicity. This case report demonstrated possible effect of oral dose of vinca alkaloids and also hinted that all the substrates and inhibitors of CYP 3A4 have propensity to interfere with metabolism of vinca alkaloids.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 5","pages":"667-71"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-200026963","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40900206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Where is the evidence for treatments used in pesticide poisoning? Is clinical toxicology fiddling while the developing world burns?","authors":"Nicholas A Buckley, Lakshman Karalliedde, Andrew Dawson, Nimal Senanayake, Michael Eddleston","doi":"10.1081/clt-120028756","DOIUrl":"10.1081/clt-120028756","url":null,"abstract":"","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 1","pages":"113-6"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2295213/pdf/ukmss-1632.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24467192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relative toxicity of selective serotonin reuptake inhibitors (SSRIs) in overdose.","authors":"Geoffrey K Isbister,&nbsp;Steven J Bowe,&nbsp;Andrew Dawson,&nbsp;Ian M Whyte","doi":"10.1081/clt-120037428","DOIUrl":"https://doi.org/10.1081/clt-120037428","url":null,"abstract":"Background: Selective serotonin reuptake inhibitors (SSRIs) have increasingly replaced tricyclic antidepressants (TCAs) in the treatment of depression. They appear to be safer in overdose, but there is little information on their spectrum of toxicity in overdose, or relative toxicity of each agent. Objective: To determine the effect of SSRIs in overdose, as a group, and the relative toxicity of five different SSRIs. Methods: A review of consecutive SSRI poisoning admissions to a single toxicology unit. Outcomes examined were length of stay [LOS], intensive care [ICU] admission rate, coma, seizures, electrocardiographic [ECG] abnormalities, and presence of serotonin syndrome [SS]. Logistic regression was used to model the outcome QTc > 440 msec. Results: There were 469 SSRI poisoning admissions analyzed after exclusions. The median LOS for all SSRI overdose admissions was 15.3 h (IQR: 10.5–21.3) and 30 of 469 (6.4%; 95% CI 4.3–9.0%) cases were admitted to ICU. The incidence of seizures was 1.9% and coma was 2.4%. Serotonin syndrome occurred in 14% of overdoses. Comparison of median QTc intervals of the five SSRIs was significantly different (p = 0.0002); citalopram (450 IQR: 436–484) was individually different to fluoxetine (p = 0.045), fluvoxamine (p = 0.022), paroxetine (p = 0.0002), and sertraline (p = 0.001). The proportion of citalopram overdoses with a QTc > 440 msec was 68%, differing significantly from sertraline (adjusted OR: 5.11 95% CI 2.32–11.27). Comparison of median QT intervals of the five SSRIs was statistically different (p = 0.026); citalopram (400 IQR: 380–440) was individually different from sertraline (p = 0.023). Conclusions: This study shows SSRIs are relatively safe in overdose despite serotonin syndrome being common. The exception was citalopram, which was significantly associated with QTc prolongation. We believe that cardiac monitoring should be considered in citalopram overdose, particularly with large ingestions and patients with associated cardiac disease.","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 3","pages":"277-85"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-120037428","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24678088","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Position paper: cathartics.","authors":"","doi":"10.1081/clt-120039801","DOIUrl":"https://doi.org/10.1081/clt-120039801","url":null,"abstract":"<p><p>The administration of a cathartic alone has no role in the management of the poisoned patient and is not recommended as a method of gut decontamination. Experimental data are conflicting regarding the use of cathartics in combination with activated charcoal. No clinical studies have been published to investigate the ability of a cathartic, with or without activated charcoal, to reduce the bioavailability of drugs or to improve the outcome of poisoned patients. Based on available data, the routine use of a cathartic in combination with activated charcoal is not endorsed. If a cathartic is used, it should be limited to a single dose in order to minimize adverse effects of the cathartic. A review of the literature since the preparation of the 1997 Cathartics Position Statement revealed no new evidence that would require a revision of the conclusions of the Statement.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 3","pages":"243-53"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-120039801","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24677033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Toxicity following unintentional DDT ingestion.","authors":"D Niyazi Ozucelik,&nbsp;Ozgur Karcioglu,&nbsp;Hakan Topacoglu,&nbsp;John R Fowler","doi":"10.1081/clt-120037432","DOIUrl":"https://doi.org/10.1081/clt-120037432","url":null,"abstract":"<p><strong>Introduction: </strong>Dichlorodiphenyltrichloroethane (DDT) ingestion is an uncommon cause of poisoning worldwide. To date, no cases of renal impairment after oral intake of DDT in humans have been reported. We describe the clinical course and management of two patients presenting after DDT ingestion, one of whom developed acute oliguric renal failure.</p><p><strong>Case report: </strong>A father and son mistook DDT powder for flour while preparing fish for a meal, and after eating they developed symptoms compatible with acute organochlorine insecticide poisoning. Both were intubated endotracheally due to recurrent convulsions and loss of consciousness followed by admission to the intensive care unit. Both cases developed severe metabolic acidosis. Acute oliguric renal failure (ARF) was diagnosed in the son in the second day, with a blood urea nitrogen level of 47 mg/dl and creatinine 6.4 mg/dl. Urinalysis disclosed abundant RBCs on the third day. Vigorous fluid resuscitation and strict monitoring helped reverse its clinical course by the tenth day. Both patients recovered within two weeks and were discharged without sequelae.</p><p><strong>Conclusion: </strong>Clinicians should not overlook the possibility of DDT poisoning in the differential diagnosis of acute renal failure and seizures. More strict measures should be taken to prohibit misidentification of DDT and similar products, particularly in the developing world.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 3","pages":"299-303"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-120037432","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24678091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Skin toxicity from glyphosate-surfactant formulation.","authors":"Paolo Amerio, Angela Motta, Paola Toto, Saman Mohammad Pour, Reza Pajand, Claudio Feliciani, Antonello Tulli","doi":"10.1081/clt-120038769","DOIUrl":"10.1081/clt-120038769","url":null,"abstract":"<p><p>Glyphosate (N-[phosphonomethyl]glycine) is a nonselective herbicide used in agriculture as a foliage spray for the control and the destruction of herbaceous plants. Adverse skin reactions due to contact with this compound have been rarely described. We report a case of a 78-year-old woman presenting with extensive chemical burns on her trunk and legs caused by accidental contact with a glyphosate-surfactant formulation. The lesions healed in four weeks without scarring.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 3","pages":"317-9"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-120038769","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24678095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}