Toxicological reviews最新文献

{"title":"Tricyclic antidepressant poisoning : central nervous system effects and management.","authors":"D Nicholas Bateman","doi":"10.2165/00139709-200524030-00010","DOIUrl":"https://doi.org/10.2165/00139709-200524030-00010","url":null,"abstract":"<p><p>All tricyclic drugs are potentially able to cause the main acute CNS toxic syndromes of coma and convulsions. Dosulepin (dothiepin) seems more likely to cause convulsions than other drugs in this class, and amitriptyline also appears a more toxic tricyclic agent. Coma is the most useful sign indicative of toxic risk and appears to predict severe toxic complications (fits and arrhythmias) more reliably than ECG changes. Prophylactic therapy against convulsions has not been shown to be effective. Use of an anticholinesterase (physostigmine) is not recommended for management of coma. There is no good evidence base to support a particular anticonvulsant.</p>","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"24 3","pages":"181-6"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200524030-00010","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25781236","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":"Anticoagulant rodenticides.","authors":"Barbara E Watt,&nbsp;Alex T Proudfoot,&nbsp;Sally M Bradberry,&nbsp;J Allister Vale","doi":"10.2165/00139709-200524040-00005","DOIUrl":"https://doi.org/10.2165/00139709-200524040-00005","url":null,"abstract":"<p><p>Anticoagulant pesticides are used widely in agricultural and urban rodent control. The emergence of warfarin-resistant strains of rats led to the introduction of a new group of anticoagulant rodenticides variously referred to as 'superwarfarins', 'single dose' or 'long-acting'. This group includes the second generation 4-hydroxycoumarins brodifacoum, bromadiolone, difenacoum, flocoumafen and the indanedione derivatives chlorophacinone and diphacinone. Most cases of anticoagulant rodenticide exposure involve young children and, as a consequence, the amounts ingested are almost invariably small. In contrast, intentional ingestion of large quantities of long-acting anticoagulant rodenticides may cause anticoagulation for several weeks or months. Occupational exposure has also been reported. Anticoagulant rodenticides inhibit vitamin K(1)-2,3 epoxide reductase and thus the synthesis of vitamin K and subsequently clotting factors II, VII, IX and X. The greater potency and duration of action of long-acting anticoagulant rodenticides is attributed to their: (i) greater affinity for vitamin K(1)-2,3-epoxide reductase; (ii) ability to disrupt the vitamin K(1)-epoxide cycle at more than one point; (iii) hepatic accumulation; and (iv) unusually long biological half-lives due to high lipid solubility and enterohepatic circulation. Substantial ingestion produces epistaxis, gingival bleeding, widespread bruising, haematomas, haematuria with flank pain, menorrhagia, gastrointestinal bleeding, rectal bleeding and haemorrhage into any internal organ; anaemia may result. Spontaneous haemoperitoneum has been described. Severe blood loss may result in hypovolaemic shock, coma and death. The first clinical signs of bleeding may be delayed and patients may remain anticoagulated for several days (warfarin) or days, weeks or months (long-acting anticoagulants) after ingestion of large amounts. There are now sufficient data in young children exposed to anticoagulant rodenticides to conclude that routine measurement of the international normalised ratio (INR) is unnecessary. In all other cases, the INR should be measured 36-48 hours post exposure. If the INR is normal at this time, even in the case of long-acting formulations, no further action is required. If active bleeding occurs, prothrombin complex concentrate (which contains factors II, VII, IX and X) 50 units/kg, or recombinant activated factor VII 1.2-4.8 mg or fresh frozen plasma 15 mL/kg (if no concentrate is available) and phytomenadione 10mg intravenously (100 microg/kg bodyweight for a child) should be given. If there is no active bleeding and the INR is < or =4.0, no treatment is required; if the INR is > or =4.0 phytomenadione 10mg should be administered intravenously.</p>","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"24 4","pages":"259-69"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200524040-00005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25872295","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":"Treatment of US crotalidae bites: comparisons of serum and globulin-based polyvalent and antigen-binding fragment antivenins.","authors":"Donna Seger,&nbsp;Stephen Kahn,&nbsp;Edward P Krenzelok","doi":"10.2165/00139709-200524040-00002","DOIUrl":"https://doi.org/10.2165/00139709-200524040-00002","url":null,"abstract":"<p><p>In the US, two antivenins are marketed for the treatment of snake envenomation. The horse-derived serum-globulin-based Antivenin (Crotalidae) Polyvalent (ACP) has been available since 1954. There are few data on the efficacy and incidence of adverse events that occur following the administration of ACP. Most of the data are retrospective, anecdotal, or case reports. In 2000, ovine-derived serum-globulin-based ACP (Crofab) became available. Crofab is said to cause fewer reactions than ACP, but there are few comparative data to substantiate this claim. Although both antivenins ameliorate the systemic symptoms following snake envenomation, the efficacy of either antivenin in decreasing oedema and swelling is unknown for a number of reasons. Clinical trials are small and have not included control arms. The degree of oedema, as well as the efficacy of the antivenin in decreasing oedema, may depend on the genera of the snake (usually unknown) that envenomated the patient. This article compares available data on clinical aspects of the two antivenins. More prospective data are needed to determine the comparative efficacy of the two antivenins, or the efficacy of Crofab in preventing tissue oedema. There are still unanswered questions regarding the optimal dosing regimen of Crofab.</p>","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"24 4","pages":"217-27"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200524040-00002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25872942","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":"Hyperbaric oxygen for carbon monoxide poisoning : a systematic review and critical analysis of the evidence.","authors":"Nicholas A Buckley, Geoffrey K Isbister, Barrie Stokes, David N Juurlink","doi":"10.2165/00139709-200524020-00002","DOIUrl":"10.2165/00139709-200524020-00002","url":null,"abstract":"<p><p>Poisoning with carbon monoxide (CO) is an important cause of unintentional and intentional injury worldwide. Hyperbaric oxygen (HBO) enhances CO elimination and has been postulated to reduce the incidence of neurological sequelae. These observations have led some clinicians to use HBO for selected patients with CO poisoning, although there is considerable variability in clinical practice. This article assesses the effectiveness of HBO compared with normobaric oxygen (NBO) for the prevention of neurological sequelae in patients with acute CO poisoning. The following databases were searched: MEDLINE (1966 to present), EMBASE (1980 to present), and the Controlled Trials Register of the Cochrane Collaboration, supplemented by a manual review of bibliographies of identified articles and discussion with recognised content experts. All randomised controlled trials involving people acutely poisoned with CO, regardless of severity, were examined. The primary analysis included all trials from which data could be extracted. Sensitivity analysis examined trials with better validity (defined using the validated instrument of Jadad) and those enrolling more severely poisoned patients. Two reviewers independently extracted from each trial, including information on the number of randomised patients, types of participants, the dose and duration of the intervention, and the prevalence of neurological sequelae at follow-up. A pooled odds ratio (OR) for the presence of neurological symptoms at 1-month follow-up was calculated using a random effects model. Bayesian models were also investigated to illustrate the degree of certainty about clinical effectiveness. Eight randomised controlled trials were identified. Two had no evaluable data and were excluded. The remaining trials were of varying quality and two have been published only as abstracts. The severity of CO poisoning varied among trials. At 1-month follow-up after treatment, sequelae possibly related to CO poisoning were present in 242 of 761 patients (36.1%) treated with NBO, compared with 259 of 718 patients (31.8%) treated with HBO. Restricting the analysis to the trials with the highest quality scores or those that enrolled all patients regardless of severity did not change the lack of statistical significance in the outcome of the pooled analysis. We found empiric evidence of multiple biases that operated to inflate the benefit of HBO in two positive trials. In contrast, the interpretation of negative trials was hampered by low rates of follow-up, unusual interventions for control patients and inclusion of less severely poisoned patients. Collectively, these limitations may have led negative trials to overlook a real and substantial benefit of HBO (type II error). There is conflicting evidence regarding the efficacy of HBO treatment for patients with CO poisoning. Methodological shortcomings are evident in all published trials, with empiric evidence of bias in some, particularly those that suggest ","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"24 2","pages":"75-92"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25619494","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":"Hyperbaric oxygen or normobaric oxygen?","authors":"Kent R Olson","doi":"10.2165/00139709-200524030-00003","DOIUrl":"https://doi.org/10.2165/00139709-200524030-00003","url":null,"abstract":"","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"24 3","pages":"151; discussion 159-60"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200524030-00003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25781230","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":"The potential adverse health effects of dental amalgam.","authors":"Amy M Brownawell,&nbsp;Stanley Berent,&nbsp;Robert L Brent,&nbsp;James V Bruckner,&nbsp;John Doull,&nbsp;Eric M Gershwin,&nbsp;Ronald D Hood,&nbsp;Genevieve M Matanoski,&nbsp;Raphael Rubin,&nbsp;Bernard Weiss,&nbsp;Meryl H Karol","doi":"10.2165/00139709-200524010-00001","DOIUrl":"https://doi.org/10.2165/00139709-200524010-00001","url":null,"abstract":"<p><p>There is significant public concern about the potential health effects of exposure to mercury vapour (Hg(0)) released from dental amalgam restorations. The purpose of this article is to provide information about the toxicokinetics of Hg(0), evaluate the findings from the recent scientific and medical literature, and identify research gaps that when filled may definitively support or refute the hypothesis that dental amalgam causes adverse health effects. Dental amalgam is a widely used restorative dental material that was introduced over 150 years ago. Most standard dental amalgam formulations contain approximately 50% elemental mercury. Experimental evidence consistently demonstrates that Hg(0) is released from dental amalgam restorations and is absorbed by the human body. Numerous studies report positive correlations between the number of dental amalgam restorations or surfaces and urine mercury concentrations in non-occupationally exposed individuals. Although of public concern, it is currently unclear what adverse health effects are caused by the levels of Hg(0) released from this restoration material. Historically, studies of occupationally exposed individuals have provided consistent information about the relationship between exposure to Hg(0) and adverse effects reflecting both nervous system and renal dysfunction. Workers are usually exposed to substantially higher Hg(0) levels than individuals with dental amalgam restorations and are typically exposed 8 hours per day for 20-30 years, whereas persons with dental amalgam restorations are exposed 24 hours per day over some portion of a lifetime. This review has uncovered no convincing evidence pointing to any adverse health effects that are attributable to dental amalgam restorations besides hypersensitivity in some individuals.</p>","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"24 1","pages":"1-10"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200524010-00001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25209921","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":"The myth.","authors":"Donna Seger","doi":"10.2165/00139709-200524030-00005","DOIUrl":"https://doi.org/10.2165/00139709-200524030-00005","url":null,"abstract":"","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"24 3","pages":"155-6; discussion 159-60"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200524030-00005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25781232","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 dioxide poisoning.","authors":"Nigel J Langford","doi":"10.2165/00139709-200524040-00003","DOIUrl":"https://doi.org/10.2165/00139709-200524040-00003","url":null,"abstract":"<p><p>Carbon dioxide is a physiologically important gas, produced by the body as a result of cellular metabolism. It is widely used in the food industry in the carbonation of beverages, in fire extinguishers as an 'inerting' agent and in the chemical industry. Its main mode of action is as an asphyxiant, although it also exerts toxic effects at cellular level. At low concentrations, gaseous carbon dioxide appears to have little toxicological effect. At higher concentrations it leads to an increased respiratory rate, tachycardia, cardiac arrhythmias and impaired consciousness. Concentrations >10% may cause convulsions, coma and death. Solid carbon dioxide may cause burns following direct contact. If it is warmed rapidly, large amounts of carbon dioxide are generated, which can be dangerous, particularly within confined areas. The management of carbon dioxide poisoning requires the immediate removal of the casualty from the toxic environment, the administration of oxygen and appropriate supportive care. In severe cases, assisted ventilation may be required. Dry ice burns are treated similarly to other cryogenic burns, requiring thawing of the tissue and suitable analgesia. Healing may be delayed and surgical intervention may be required in severe cases.</p>","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"24 4","pages":"229-35"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200524040-00003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25872293","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":"What does the present state of knowledge tell us about the potential role of hyperbaric oxygen therapy for the treatment of carbon monoxide poisoning?","authors":"Jeffrey Brent","doi":"10.2165/00139709-200524030-00001","DOIUrl":"https://doi.org/10.2165/00139709-200524030-00001","url":null,"abstract":"","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"24 3","pages":"145-7"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200524030-00001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25781228","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":"Hyperbaric therapy for carbon monoxide poisoning : to treat or not to treat, that is the question.","authors":"John A Henry","doi":"10.2165/00139709-200524030-00002","DOIUrl":"https://doi.org/10.2165/00139709-200524030-00002","url":null,"abstract":"","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"24 3","pages":"149-50; discussion 159-60"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200524030-00002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25781229","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}