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Medical management of the traumatic consequences of civil unrest incidents: causation, clinical approaches, needs and advanced planning criteria. 内乱事件创伤后果的医疗管理:原因、临床方法、需求和先进的规划标准。
Toxicological reviews Pub Date : 2006-01-01 DOI: 10.2165/00139709-200625030-00003
Bryan Ballantyne
{"title":"Medical management of the traumatic consequences of civil unrest incidents: causation, clinical approaches, needs and advanced planning criteria.","authors":"Bryan Ballantyne","doi":"10.2165/00139709-200625030-00003","DOIUrl":"https://doi.org/10.2165/00139709-200625030-00003","url":null,"abstract":"<p><p>In the context of this review, civil unrest is defined as disharmony, expressive dissatisfaction and/or disagreement between members of a community, which leads to a situation of competitive aggression that may find expression as disruption of organisation, conflicts, damage to property and injuries. Such a breakdown of harmonious relationships, which may result in property damage and human injuries that may be threatening to life, varies in magnitude from participation of a very few individuals up to the involvement of large crowds of people, which may evolve into a full-scale riot. It is the latter situation often involving demonstrators, opposing groups and law enforcement personnel that can result in multiple casualties and present a very significant challenge to the resources of local healthcare institutions. The causation of civil unrest incidents is multifactorial and has generic, specific and potentiating elements. With the current national and international societal, political and discriminatory problems, it is likely that civil unrest incidents on both small and large scales will continue to occur at a high and possibly increasing rate on a worldwide basis, and for these not infrequent incidents, the medical community should be in a state of informed preparation. The circumstances of civil unrest incidents are very variable with respect to causation, overall magnitude, frequency, timing, geographical location, numbers of persons involved, demographics of participants, influence of extremists, confrontation with opposing groups and control measures used by law enforcement agencies. Methods used by police and security forces for the control of civil unrest incidents, if advanced negotiations with organisers and verbal warnings have failed, fall basically into two categories: physical and chemical measures. Physical methods include restraint holds, truncheons, batons, mounted horses, projectiles (such as bean bags, plastic and rubber bullets), water cannons, tasers and (rarely) live ammunition. All of these physical measures are associated with pain and immobilisation, and there is a high potential for soft tissue and bone injuries. Some of the more severe physical methods, including plastic and rubber bullets, may cause lethal injuries. The basis for using chemicals in civil unrest incidents is that they cause distraction, transient harassment and incapacitation, temporary impairment of the conduct of coordinated tasks and cause a desire to vacate the area of unrest. Although screening smokes and malodors have sometimes been employed, the major group of chemicals used are peripheral chemosensory irritants (PCSIs), which reversibly interact with sensory nerve receptors in exposed skin and mucosal surfaces, resulting in the production of local uncomfortable sensations and associated reflexes. Major effects are on the eye, respiratory tract and (to a lesser degree) skin. Thus, the induced transient pain and discomfort in the eye, respi","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"25 3","pages":"155-97"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200625030-00003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26463691","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}
引用次数: 22
A critical reconsideration of the clinical effects and treatment recommendations for sodium channel blocking drug cardiotoxicity. 对钠通道阻断药物心脏毒性的临床效果和治疗建议的重要重新考虑。
Toxicological reviews Pub Date : 2006-01-01 DOI: 10.2165/00139709-200625040-00008
Donna L Seger
{"title":"A critical reconsideration of the clinical effects and treatment recommendations for sodium channel blocking drug cardiotoxicity.","authors":"Donna L Seger","doi":"10.2165/00139709-200625040-00008","DOIUrl":"https://doi.org/10.2165/00139709-200625040-00008","url":null,"abstract":"<p><p>The cardiac sodium channel is comprised of proteins that span the cardiac cell membrane and form the channel pore. Depolarisation causes the proteins to move and open the sodium channel. Once the channel is open (active conformation), sodium ions move into the cell. The channel then changes from the active conformation to an inactive conformation - the channel remains open, but influx of sodium ions ceases. Recovery occurs as the channel moves from the inactive conformation back to the closed conformation and is then ready to open following the next depolarisation. Sodium channel blocking drugs (NCBDs) occupy receptors in the channel during the active and inactive conformations. The drug dissociates from most of the channel receptors during recovery, but the time it takes the drug to dissociate slows recovery. The slowed recovery prolongs conduction time, the main toxicity of NCBD overdose. Conduction time is further prolonged if heart rate increases as there are more available active and inactive conformations/unit time, which increases channel receptor binding sites for the NCBD. In addition to prolonging conduction time, NCBDs also decrease inotropy. Treatment of NCBD cardiotoxicity has been based on in vitro and animal experiments, and case reports. Assumptions based on this evidence must now be reassessed. For example, canines consistently develop ventricular tachycardia (VT) when tricyclic antidepressants (TCAs) are administered. Much of the literature discussing NCBD cardiotoxicity assumes that TCA poisoning induces VT in humans with the same regularity that occurs in canines. Seemingly, in support of this assumption was the finding that patients with remote myocardial infarction developed VT when therapeutically ingesting a NCBD. However, conduction is prolonged in myocardium that is or has been ischaemic. NCBD prolong conduction more in previously ischaemic myocardium than in normal myocardium, which causes nonuniform conduction and allows the development of re-entrant arrhythmias such as VT. Although some nonuniform conduction may occur in the healthy heart following a NCBD overdose, there is no evidence that nonuniform conduction occurs to the extent that it will cause re-entrant arrhythmias in this setting. Using various animal models and a variety of NCBDs, sodium ions, bicarbonate ions and alkalosis have been compared for the treatment of ventricular arrhythmias, hypotension and mortality. The results of these experiments have been extrapolated to NCBD overdose in humans. Animal models and single treatment approaches may have narrowed our scope. More recent evidence indicates that properties of each individual NCBD may require unique treatment. There is limited evidence that glucagon, which increases initial sodium ion influx into the cardiac cell, should be considered early in the treatment of cardiotoxicity. Another consideration may be treatment of NCBD with faster kinetics. Conduction time is decreased if a NCBD occupying ","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"25 4","pages":"283-96"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200625040-00008","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26542839","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}
引用次数: 26
Poisoning due to pyrethroids. 拟除虫菊酯引起的中毒。
Toxicological reviews Pub Date : 2005-01-01 DOI: 10.2165/00139709-200524020-00003
Sally M Bradberry, Sarah A Cage, Alex T Proudfoot, J Allister Vale
{"title":"Poisoning due to pyrethroids.","authors":"Sally M Bradberry,&nbsp;Sarah A Cage,&nbsp;Alex T Proudfoot,&nbsp;J Allister Vale","doi":"10.2165/00139709-200524020-00003","DOIUrl":"https://doi.org/10.2165/00139709-200524020-00003","url":null,"abstract":"<p><p>The first pyrethroid pesticide, allethrin, was identified in 1949. Allethrin and other pyrethroids with a basic cyclopropane carboxylic ester structure are type I pyrethroids. The insecticidal activity of these synthetic pyrethroids was enhanced further by the addition of a cyano group to give alpha-cyano (type II) pyrethroids, such as cypermethrin. The finding of insecticidal activity in a group of phenylacetic 3-phenoxybenzyl esters, which lacked the cyclopropane ring but contained the alpha-cyano group (and hence were type II pyrethroids) led to the development of fenvalerate and related compounds. All pyrethroids can exist as at least four stereoisomers, each with different biological activities. They are marketed as racemic mixtures or as single isomers. In commercial formulations, the activity of pyrethroids is usually enhanced by the addition of a synergist such as piperonyl butoxide, which inhibits metabolic degradation of the active ingredient. Pyrethroids are used widely as insecticides both in the home and commercially, and in medicine for the topical treatment of scabies and headlice. In tropical countries mosquito nets are commonly soaked in solutions of deltamethrin as part of antimalarial strategies. Pyrethroids are some 2250 times more toxic to insects than mammals because insects have increased sodium channel sensitivity, smaller body size and lower body temperature. In addition, mammals are protected by poor dermal absorption and rapid metabolism to non-toxic metabolites. The mechanisms by which pyrethroids alone are toxic are complex and become more complicated when they are co-formulated with either piperonyl butoxide or an organophosphorus insecticide, or both, as these compounds inhibit pyrethroid metabolism. The main effects of pyrethroids are on sodium and chloride channels. Pyrethroids modify the gating characteristics of voltage-sensitive sodium channels to delay their closure. A protracted sodium influx (referred to as a sodium 'tail current') ensues which, if it is sufficiently large and/or long, lowers the action potential threshold and causes repetitive firing; this may be the mechanism causing paraesthesiae. At high pyrethroid concentrations, the sodium tail current may be sufficiently great to prevent further action potential generation and 'conduction block' ensues. Only low pyrethroid concentrations are necessary to modify sensory neurone function. Type II pyrethroids also decrease chloride currents through voltage-dependent chloride channels and this action probably contributes the most to the features of poisoning with type II pyrethroids. At relatively high concentrations, pyrethroids can also act on GABA-gated chloride channels, which may be responsible for the seizures seen with severe type II poisoning. Despite their extensive world-wide use, there are relatively few reports of human pyrethroid poisoning. Less than ten deaths have been reported from ingestion or following occupational exposure. Occupa","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"24 2","pages":"93-106"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200524020-00003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25619495","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}
引用次数: 524
A clinical and pharmacoeconomic justification for intravenous acetylcysteine: a US perspective. 静脉注射乙酰半胱氨酸的临床和药物经济学依据:美国视角。
Toxicological reviews Pub Date : 2005-01-01 DOI: 10.2165/00139709-200524020-00007
Colleen M Culley, Edward P Krenzelok
{"title":"A clinical and pharmacoeconomic justification for intravenous acetylcysteine: a US perspective.","authors":"Colleen M Culley,&nbsp;Edward P Krenzelok","doi":"10.2165/00139709-200524020-00007","DOIUrl":"https://doi.org/10.2165/00139709-200524020-00007","url":null,"abstract":"<p><p>Paracetamol (acetaminophen) poisoning remains the most common exposure reported to US poison information centres and the leading cause of poisoning-related fatalities, despite the availability of an effective antidote, acetylcysteine. Oral acetylcysteine solution has been approved for the management of acetaminophen poisoning in the US for four decades. Until the recent approval of intravenous acetylcysteine in the US, it was necessary to compound the oral solution for intravenous administration. The effectiveness and tolerability of oral and intravenous acetylcysteine for the prevention of hepatotoxicity induced by paracetamol poisoning are well established in the literature. Intravenous acetylcysteine may be preferred over oral administration based on improved tolerability, ease of administration and the shortened course of therapy (20 hours intravenous vs 72 hours oral). The two intravenous acetylcysteine regimens documented in the literature, 48 hours and 20 hours, have similar efficacy when started within 8-10 hours of ingestion. Although there are no legal concerns with continuing the routine compounding of the oral solution to an intravenous product, new standards for pharmacy compounding of sterile preparations set forth by the US Pharmacopoeia highlight that the risk of compounding products for intravenous use must be assessed carefully. Changing the route of administration of a sterile oral solution to an intravenous preparation, when a commercial sterile and pyrogen-free product is available, may not be advisable. The best cost-containment strategies must be used for introduction of the more costly sterile, pyrogen-free intravenous acetylcysteine formulation by hospitals and healthcare systems. The intravenous acetylcysteine product is more cost effective when given for 20 hours than other treatment protocols based on the costs of acetylcysteine and hospitalisation. If used per protocol, the 20-hour intravenous acetylcysteine regimen may decrease hospital length of stay, thereby, offsetting the increased drug cost. Data conflict on the efficacy and administration of intravenous acetylcysteine for off-label uses, such as radiographic contrast media-induced nephropathy prevention and reperfusion in orthotopic liver transplantation. The costs for the intravenous formulation for these indications is significantly higher than use of the oral formulation for oral administration in radiographic contrast media-induced nephropathy prevention and compounded for intravenous use in orthotopic liver transplantation. The oral solution should be retained by healthcare systems for oral and inhalation applications, such as respiratory conditions, oral administration for radiographic contrast media nephropathy prevention, or the use of the 72-hour oral protocol to treat paracetamol poisoning, when the intravenous preparation cannot be used.</p>","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"24 2","pages":"131-43"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200524020-00007","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25619499","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}
引用次数: 14
Tricyclic antidepressant poisoning : cardiovascular toxicity. 三环类抗抑郁药物中毒:心血管毒性。
Toxicological reviews Pub Date : 2005-01-01 DOI: 10.2165/00139709-200524030-00013
H K Ruben Thanacoody, Simon H L Thomas
{"title":"Tricyclic antidepressant poisoning : cardiovascular toxicity.","authors":"H K Ruben Thanacoody,&nbsp;Simon H L Thomas","doi":"10.2165/00139709-200524030-00013","DOIUrl":"https://doi.org/10.2165/00139709-200524030-00013","url":null,"abstract":"<p><p>Tricyclic antidepressants remain a common cause of fatal drug poisoning as a result of their cardiovascular toxicity manifested by ECG abnormalities, arrhythmias and hypotension. Dosulepin and amitriptyline appear to be particularly toxic in overdose. The principal mechanism of toxicity is cardiac sodium channel blockade, which increases the duration of the cardiac action potential and refractory period and delays atrioventricular conduction. Electrocardiographic changes include prolongation of the PR, QRS and QT intervals, nonspecific ST segment and T wave changes, atrioventricular block, right axis deviation of the terminal 40 ms vector of the QRS complex in the frontal plane (T 40 ms axis) and the Brugada pattern (downsloping ST segment elevation in leads V1-V3 in association with right bundle branch block). Maximal changes in the QRS duration and the T 40 ms axis are usually present within 12 hours of ingestion but may take up to a week to resolve. Sinus tachycardia is the most common arrhythmia due to anticholinergic activity and inhibition of norepinephrine uptake by tricyclic antidepressants but bradyarrhythmias (due to atrioventricular block) and tachyarrhythmias (supraventricular and ventricular) may occur. Torsade de pointes occurs uncommonly. Hypotension results from a combination of reduced myocardial contractility and reduced systemic vascular resistance due to alpha-adrenergic blockade. Life-threatening arrhythmias and death due to tricyclic antidepressant poisoning usually occurs within 24 hours of ingestion. Rapid deterioration is common. Level of consciousness at presentation is the most sensitive clinical predictor of serious complications. Although a QRS duration >100 ms and a rightward T 40 ms axis appear to be better predictors of cardiovascular toxicity than the plasma tricyclic drug concentration, they have at best moderate sensitivity and specificity for predicting complications.</p>","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"24 3","pages":"205-14"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200524030-00013","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25781182","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}
引用次数: 154
Is electric arc welding linked to manganism or Parkinson's disease? 电弧焊与锰中毒或帕金森症有关吗?
Toxicological reviews Pub Date : 2005-01-01 DOI: 10.2165/00139709-200524040-00004
Grant McMillan
{"title":"Is electric arc welding linked to manganism or Parkinson's disease?","authors":"Grant McMillan","doi":"10.2165/00139709-200524040-00004","DOIUrl":"https://doi.org/10.2165/00139709-200524040-00004","url":null,"abstract":"<p><p>Manganese and its inorganic compounds are widely used in many industries and have been accepted as occupational neurotoxins that have caused a distinct and disabling clinical entity, manganism, in several types of work, notably where exposure is by way of dust. There is inconclusive and inconsistent evidence that, in these occupations, subclinical neurological effects, detectable only by neurobehavioural studies, may be caused by low doses. This has prompted a re-evaluation of occupational exposure limits. Some countries, including the UK, already demand much higher levels of protection against exposure than 5 years ago. Welding is the most common source of occupational exposure as manganese is an essential component of steel and so its compounds are inevitable components of fume emitted from steel welding processes. There it is found in respirable particles, often as complex oxides (spinels), sometimes within a core protected by a silicon oxide shell - as distinct from the much simpler form of particle formed by disintegration in processes such as mining and ore milling where manganism has been diagnosed convincingly. Millions of workers are at risk of exposure to manganese-containing compounds in fumes from electric arc welding of steel. In recent years it has been asserted that neurological and neurobehavioural disorders may develop consequent to exposure to steel welding fumes and that employment as a welder is associated with the unusually early onset of Parkinson's disease. Causal relationships have been postulated. Welders have been recorded as having been exposed to high levels of manganese-containing fume, especially where they have worked in confined, unventilated spaces, although this appears from limited data to be the exception rather than the rule. Even then the dose received is generally less than in mining or ore crushing. When care is taken to exclude exposures from hardfacing and burning and cutting arc processes, where manganese may form a high percentage of the fume, manganese compounds usually form a relatively low percentage of the composition of welding fume particles, <2.0%, much outweighed by iron. Although these manganese-compound-containing welding fume particles are insoluble in water, the manganese compounds in particles that are retained in the alveoli may be absorbed, at least in part. Manganese concentrations in biological material samples in some exposed groups reflect this relative to unexposed workers. Some of the transfer systems for absorption and transport, including across the blood-brain barrier, are used in competition with iron which is present in abundance in welding fume. This may reduce absorption of manganese in welders and thus reduce the opportunity for sufficient doses to cause neurotoxicological consequences. Scrutiny of the literature covering the last 40 years has revealed only five cases that meet sufficient criteria for manganism to just cross the diagnostic threshold, and even then they","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"24 4","pages":"237-57"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200524040-00004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25872294","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}
引用次数: 36
Organophosphate-induced delayed polyneuropathy. 有机磷诱导的迟发性多发性神经病。
Toxicological reviews Pub Date : 2005-01-01 DOI: 10.2165/00139709-200524010-00003
Marcello Lotti, Angelo Moretto
{"title":"Organophosphate-induced delayed polyneuropathy.","authors":"Marcello Lotti,&nbsp;Angelo Moretto","doi":"10.2165/00139709-200524010-00003","DOIUrl":"https://doi.org/10.2165/00139709-200524010-00003","url":null,"abstract":"<p><p>Organophosphate-induced delayed polyneuropathy (OPIDP) is a rare toxicity resulting from exposure to certain organophosphorus (OP) esters. It is characterised by distal degeneration of some axons of both the peripheral and central nervous systems occurring 1-4 weeks after single or short-term exposures. Cramping muscle pain in the lower limbs, distal numbness and paraesthesiae occur, followed by progressive weakness, depression of deep tendon reflexes in the lower limbs and, in severe cases, in the upper limbs. Signs include high-stepping gait associated with bilateral foot drop and, in severe cases, quadriplegia with foot and wrist drop as well as pyramidal signs. In time, there might be significant recovery of the peripheral nerve function but, depending on the degree of pyramidal involvement, spastic ataxia may be a permanent outcome of severe OPIDP. Human and experimental data indicate that recovery is usually complete in the young. At onset, the electrophysiological changes include reduced amplitude of the compound muscle potential, increased distal latencies and normal or slightly reduced nerve conduction velocities. The progression of the disease, usually over a few days, may lead to non-excitability of the nerve with electromyographical signs of denervation. Nerve biopsies have been performed in a few cases and showed axonal degeneration with secondary demyelination. Neuropathy target esterase (NTE) is thought to be the target of OPIDP initiation. The ratio of inhibitory powers for acetylcholinesterase and NTE represents the crucial guideline for the aetiological attribution of OP-induced peripheral neuropathy. In fact, pre-marketing toxicity testing in animals selects OP insecticides with cholinergic toxicity potential much higher than that to result in OPIDP. Therefore, OPIDP may develop only after very large exposures to insecticides, causing severe cholinergic toxicity. However, this was not the case with certain triaryl phosphates that were not used as insecticides but as hydraulic fluids, lubricants and plasticisers and do not result in cholinergic toxicity. Several thousand cases of OPIDP as a result of exposure to tri-ortho-cresyl phosphate have been reported, whereas the number of cases of OPIDP as a result of OP insecticide poisoning is much lower. In this article, we mainly discuss OP pesticide poisoning, particularly when caused by chlorpyrifos, dichlorvos, isofenphos, methamidophos, mipafox, trichlorfon, trichlornat, phosphamidon/mevinphos and by certain carbamates. We also discuss case reports where neuropathies were not convincingly attributed to fenthion, malathion, omethoate/dimethoate, parathion and merphos. Finally, several observational studies on long-term, low-level exposures to OPs that sometimes reported mild, inconsistent and unexplained changes of unclear significance in peripheral nerves are briefly discussed.</p>","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"24 1","pages":"37-49"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200524010-00003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25209923","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}
引用次数: 193
Toxicological aspects of the South American herbs cat's claw (Uncaria tomentosa) and Maca (Lepidium meyenii) : a critical synopsis. 南美草药猫爪(Uncaria tomentosa)和玛卡(Lepidium meyenii)的毒理学方面:一个关键的概要。
Toxicological reviews Pub Date : 2005-01-01 DOI: 10.2165/00139709-200524010-00002
Luis G Valerio, Gustavo F Gonzales
{"title":"Toxicological aspects of the South American herbs cat's claw (Uncaria tomentosa) and Maca (Lepidium meyenii) : a critical synopsis.","authors":"Luis G Valerio,&nbsp;Gustavo F Gonzales","doi":"10.2165/00139709-200524010-00002","DOIUrl":"https://doi.org/10.2165/00139709-200524010-00002","url":null,"abstract":"<p><p>Recent exceptional growth in human exposure to natural products known to originate from traditional medicine has lead to a resurgence of scientific interest in their biological effects. As a strategy for improvement of the assessment of their pharmacological and toxicological profile, scientific evidence-based approaches are being employed to appropriately evaluate composition, quality, potential medicinal activity and safety of these natural products. Using this approach, we comprehensively reviewed existing scientific evidence for known composition, medicinal uses (past and present), and documented biological effects with emphasis on clinical pharmacology and toxicology of two commonly used medicinal plants from South America with substantial human exposure from historical and current global use: Uncaria tomentosa (common name: cat's claw, and Spanish: uña de gato), and Lepidium meyenii (common name: maca). Despite the geographic sourcing from remote regions of the tropical Amazon and high altitude Andean mountains, cat's claw and maca are widely available commercially in industrialised countries. Analytical characterisations of their active constituents have identified a variety of classes of compounds of toxicological, pharmacological and even nutritional interest including oxindole and indole alkaloids, flavonoids, glucosinolates, sterols, polyunsaturated fatty acids, carbolines and other compounds. The oxindole alkaloids from the root bark of cat's claw are thought to invoke its most widely sought-after medicinal effects as a herbal remedy against inflammation. We find the scientific evidence supporting this claim is not conclusive and although there exists a base of information addressing this medicinal use, it is limited in scope with some evidence accumulated from in vitro studies towards understanding possible mechanisms of action by specific oxindole alkaloids through inhibition of nuclear factor (NF)-kappaB activation. Although controlled clinical studies have demonstrated reduction in pain associated with cat's claw intake in patients with various chronic inflammatory disorders, there is insufficient clinical data overall to draw a firm conclusion for its anti-inflammatory effects. An important observation was that experimental results were often dependent upon the nature of the preparation used. It appears that the presence of unknown substances has an important role in the overall effects of cat's claw extracts is an important factor for consideration. The available animal toxicological studies did not indicate severe toxicity from oral intake of cat's claw preparations but rather were suggestive of a low potential for acute and subacute oral toxicity, and a lack of evidence to demonstrate genotoxic potential and mutagenic activity. Maca is a clear example of a herb with substantial medicinal use in traditional herbal medicine by indigenous cultures in South America since the first recorded knowledge of it in the seventeenth ","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"24 1","pages":"11-35"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200524010-00002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25209922","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}
引用次数: 141
Editorial announcement. 编辑公告。
Toxicological reviews Pub Date : 2005-01-01 DOI: 10.2165/00139709-200524020-00001
Jeffrey Brent, Allister Vale
{"title":"Editorial announcement.","authors":"Jeffrey Brent,&nbsp;Allister Vale","doi":"10.2165/00139709-200524020-00001","DOIUrl":"https://doi.org/10.2165/00139709-200524020-00001","url":null,"abstract":"","PeriodicalId":87031,"journal":{"name":"Toxicological reviews","volume":"24 2","pages":"73"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2165/00139709-200524020-00001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25599167","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}
引用次数: 0
Poisoning due to urea herbicides. 尿素除草剂引起的中毒。
Toxicological reviews Pub Date : 2005-01-01 DOI: 10.2165/00139709-200524030-00008
Barbara E Watt, Alex T Proudfoot, Sally M Bradberry, J Allister Vale
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引用次数: 17
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