Journal of toxicology. Clinical toxicology最新文献

{"title":"A comparison of the pharmacokinetics of oral and sublingual cyproheptadine.","authors":"Narendra Gunja,&nbsp;Michael Collins,&nbsp;Andis Graudins","doi":"10.1081/clt-120028749","DOIUrl":"https://doi.org/10.1081/clt-120028749","url":null,"abstract":"<p><strong>Background: </strong>Cyproheptadine is reported to be effective in treating serotonin syndrome. It is only available as an oral preparation and administration after SSRI overdose treated with activated charcoal is problematic. Sublingual administration may circumvent this problem. The pharmacokinetics of sublingual cyproheptadine are not characterized. This study compares the pharmacokinetics of cyproheptadine following oral and sublingual administration.</p><p><strong>Methods: </strong>Cross-over, non-blinded, volunteer study using five healthy males. Eight milligrams of oral and sublingual cyproheptadine were administered on separate occasions with a one-week washout period. Sublingual arm subjects were pretreated with 50 g of oral activated charcoal 30 min prior to cyproheptadine, to prevent any gut absorption. Serum cyproheptadine concentration was measured at baseline, 30 min, and 1, 2, 3, 4, 6, 8, and 10 h by liquid chromatography and mass spectroscopy.</p><p><strong>Results: </strong>Mean C(max) for oral and sublingual were 30.0 microg/L and 4.0 microg/L respectively: mean T(max) were 4 h and 9.6 h; mean AUC were 209 and 25 microg x hr/L. Mean +/- SEM within-subject difference between oral and sublingual C(max) was 25.9 +/- 4.1 (p = 0.003) and AUC was 184 +/- 31 (p = 0.004).</p><p><strong>Conclusions: </strong>Serum concentrations after sublingual cyproheptadine are significantly less than after oral administration. At these concentrations, the sublingual route is unlikely to be effective in treating serotonin syndrome.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 1","pages":"79-83"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-120028749","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24467186","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":"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":"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":"Carbon monoxide and cyanide poisoning in fire related deaths in Victoria, Australia.","authors":"Michael J Yeoh,&nbsp;George Braitberg","doi":"10.1081/clt-200035211","DOIUrl":"https://doi.org/10.1081/clt-200035211","url":null,"abstract":"<p><strong>Objective: </strong>This study was undertaken to examine the association of hydrogen cyanide and carboxyhaemoglobin in victims of fire related deaths in Australia. The secondary aim was to document demographic data about Australian fire related deaths.</p><p><strong>Methods: </strong>An observational retrospective study was undertaken of autopsy reports from the Victorian Institute of Forensic Medicine. Reports of fire related deaths were electronically searched using the terms burns, \"smoke\" or \"fire\" as a cause of death in the calender years 1992 to 1998. Data on the circumstances of the fire and results of toxicological screening were obtained on 178 persons. Additional whole blood cyanide levels were determined if blood samples were available in storage. Demographics of the victims were analysed, as well as the relationship between carboxyhaemoglobin and whole blood cyanide levels.</p><p><strong>Results: </strong>Most (82%) of the victims died at the scene, whilst 32 victims died after a period of hospitalisation (hours to weeks). Suicide as a result of self-immolation was the reported cause of death in 32 cases. Most of the fires were in houses (114) and cars (29). The blood ethanol level was zero in 112 cases; the remaining cases (53) had a mean level of 0.17%. Other central nervous system (CNS) depressants were recorded in 49 of the 134 cases that received a complete toxicological screen. Carboxyhaemoglobin levels were measured in only 154 of 178 cases. The carboxyhaemoglobin level was zero in 43 cases. The remaining cases (111) had a mean level of 40%; with 44 cases having a level greater than 50%, a level considered to be potentially lethal. Whole blood hydrogen cyanide levels were measured in only 138 of 178 cases. The hydrogen cyanide level was zero in 52 cases. The remaining cases (86) had a mean level of 1.65 mg/L; with 11 cases having a level greater than 3.0 mg/L (potentially fatal). Blood ethanol levels were significantly correlated with both carboxyhaemoglobin (R = 0.22, P < 0.01) and cyanide (R = 0.36, P < 0.001). In addition, a significant correlation (r = 0.34) between carboxyhaemoglobin and hydrogen cyanide levels was noted.</p><p><strong>Conclusions: </strong>This study showed a correlation between elevated blood ethanol and whole blood cyanide levels (r = 0.36, p < 0.001) and between elevated carboxyhaemoglobin and hydrogen cyanide levels (r = 0.34). Although the mean cyanide level was 1.3 mg/L (above the level some consider potentially toxic) in those cases with a carboxyhaemoglobin level of greater than 10%, there is insufficient data to permit recommendations for clinical care. Further studies are required on those victims that reach hospital alive.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 6","pages":"855-63"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-200035211","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24802978","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,&nbsp;Lakshman Karalliedde,&nbsp;Andrew Dawson,&nbsp;Nimal Senanayake,&nbsp;Michael Eddleston","doi":"10.1081/clt-120028756","DOIUrl":"https://doi.org/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://sci-hub-pdf.com/10.1081/clt-120028756","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":"Diagnostic accuracy of urinary amanitin in suspected mushroom poisoning: a pilot study.","authors":"Raffaella Butera,&nbsp;Carlo Locatelli,&nbsp;Teresa Coccini,&nbsp;Luigi Manzo","doi":"10.1081/clt-200035472","DOIUrl":"https://doi.org/10.1081/clt-200035472","url":null,"abstract":"<p><strong>Background: </strong>Amatoxin-containing species are responsible for the most severe cases of mushroom poisoning, with high mortality rate. Therefore, this poisoning should be ruled out in all patients presenting gastrointestinal symptoms after wild mushroom ingestion.</p><p><strong>Objective: </strong>To determine sensitivity, specificity, positive predictive value, negative predictive value, and diagnostic efficacy (DE) of urinary amanitin analysis in cases of suspected mushroom poisoning.</p><p><strong>Methods: </strong>All cases of mushroom ingestion referred to a Poison Center during a one-month period were analyzed. Amanitin measurements were performed by ELISA method (functional least detectable dose 1.5 ng/ml; cut-off value not clearly established). Gastrointestinal symptoms latency and initial clinical assessment were considered alternative diagnostic tools. Definitive diagnosis was used as the reference standard.</p><p><strong>Results: </strong>Among 61 patients included in the study, amatoxin poisoning was diagnosed in 10 cases. Urine samples were collected 5.5 to 92 hours after mushroom ingestion. Urinary amanitin DE was 91.8%, 93.4%, and 80.3%, based on the cut-off value considered (1.5, 5.0, and 10.0 ng/ml, respectively). Symptoms latency longer than 6 hours and initial clinical assessment DE were 70.5% and 67.2%, respectively. To identify amatoxin poisoning, initial clinical assessment resulted more sensitive and urinary amanitin analysis more specific.</p><p><strong>Conclusions: </strong>Urinary amanitin analysis is a valuable diagnostic tool and may significantly contribute to the management of suspected mushroom poisoning. At present, the best diagnostic accuracy can be obtained taking advantage of both the high sensitivity and negative predictive value of the clinical assessment performed by an experienced toxicologist, and the high specificity and positive predictive value that characterize urinary amanitin analysis.</p>","PeriodicalId":17447,"journal":{"name":"Journal of toxicology. Clinical toxicology","volume":"42 6","pages":"901-12"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1081/clt-200035472","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24802898","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":"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}