碳酸氢钠-连二亚硫酸钠还原法在敌草快和百草枯中毒快速检测中的应用及意义

目的评价碳酸氢钠-连二亚硫酸钠还原法对敌草快(diquat,DQ)和百草枯(paraquat,PQ)中毒快速检测评估的可靠性及临床意义。方法采用高效液相色谱法验证血清敌草快、百草枯浓度,确定其准确性。通过体外配制不同浓度敌草快及百草枯中毒患者的血液样本,以及采用敌草快、百草枯灌胃构建中毒动物模型,运用碳酸氢钠-连二亚硫酸钠还原法观察其颜色变化,并得到标准图谱。结果在碳酸氢钠-连二亚硫酸钠的还原作用下,不同浓度敌草快和百草枯的血清标本呈现出不同的颜色,颜色深度与毒物浓度密切相关,且以中毒后1 h最明显。结论碳酸氢钠-连二亚硫酸钠还原法对早期快速、有效鉴别敌草快与百草枯具有重要的临床意义。     

百草枯中毒患者血清肿瘤坏死因子-α白细胞介素-6及百草枯浓度变化的分析

目的 通过监测百草枯中毒患者血清肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)及百草枯浓度变化,从而探讨百草枯致机体多器官衰竭的发病机制.方法采用酶联免疫吸附法(ELISA)监测15例百草枯中毒患者在中毒4、24及96 h后血清TNF-α、IL-6浓度;应用高效液相色谱法(HPLC)监测同期血清百草枯浓度,选取20例正常人作为对照.结果患者百草枯中毒4 h后血清TNF-α及IL-6浓度即出现异常升高,随着时间延续,百草枯中毒后血清TNF-α及IL-6浓度水平持续进行性升高(P均<0.01),TNF-α与IL-6之间存在高度相关性;血清百草枯浓度持续处于高浓度水平,各阶段血清百草枯浓度之间差异无统计学意义(P>0.05),血清TNF-α及IL-6浓度持续进行性升高与百草枯浓度无明显相关性.结论中到重型百草枯患者血清TNF-α、IL-6浓度持续进行性升高,致机体出现全身炎症反应综合征(SIRS),终致多器官衰竭(MOF).     

28份包装标注为敌草快成分的除草剂检测分析

目的分析国内市场销售的包装标注为敌草快除草剂的确切成分并检测其有效成分浓度,为指导临床急性敌草快中毒的精准化诊治提供实验依据。方法购置28份国内市场销售的包装标注浓度为200.0 g/L的敌草快除草剂,应用高效液相色谱质谱(HPLC-MS)检测样品的确切成分和浓度,并对检测结果以及样品来源进行统计分析。结果 28份包装标注为敌草快的除草剂中有23份(占82.14%)含有敌草快成分,5份(占17.86%)检测出百草枯成分,未检测出同时含有敌草快和百草枯的样品。含有敌草快成分的样品检测浓度明显高于含有百草枯成分的样品浓度(g/L:164.7±27.5比79.4±57.0,P0.05)。23份含有敌草快的样品中有5份浓度达标(≥200.0 g/L),其余样品均不达标。5份含有百草枯的样品中检出最高浓度为179.0g/L,其余4份均显著低于200.0 g/L。按检出浓度不同将样品分为4组,其中50.0 g/L组检出1份百草枯样品,50.0～99.9 g/L组检出3份百草枯样品,100.0～149.9 g/L组检出6份敌草快样品,≥150.0 g/L组检出17份敌草快样品和1份百草枯样品。检测出含有敌草快成分的除草剂生产企业分布于山东省(9家)、河北省(4家)、河南省(3家)、安徽省(2家)、江苏省(2家)、重庆市(2家)、广西壮族自治区(1家)。检测出的含百草枯成分的5家除草剂生产企业分布于安徽省、河北省、广西壮族自治区、浙江省和广东省各1家。结论国内销售包装标注为敌草快的除草剂部分商品确切成分为百草枯,无论是敌草快和百草枯成分,大部分商品的浓度均低于标注的200.0 g/L。我国目前有部分企业存在生产假冒伪劣敌草快除草剂的现象,要实现急性敌草快中毒的精准化诊疗,毒物检测分析必不可少,可以降低该类中毒的误诊率。     

连二亚硫酸钠还原法在敌草快中毒诊疗中的临床价值

目的探索用连二亚硫酸钠还原法进行尿液半定量比色在敌草快中毒诊疗中的临床价值。方法回顾性分析2020年12月3日至2022年11月23日在本院救治的49例急性敌草快中毒患者资料, 观察尿比色结果与血浆敌草快浓度相关性;评价尿比色结果对靶器官损伤、及预后的预测价值。结果尿比色结果与血浆敌草快浓度具有显著相关性, 相关系数r=0.89, P <0.01;尿比色结果预测消化道、肝脏、肾脏、及中枢神经系统损伤的临界值分别为2.5、3.5、3.5、5.5,其中尿比色结果预测消化道损伤的敏感性最高[AUC 0.93 (95%CI: 0.89～1.00)];尿比色结果预测死亡结局的临界值为4.5, 阳性预测值为64.2%, 阴性预测值为95.2%。结论尿半定量比色法可用于快速预测入院时血浆敌草快浓度范围;尿比色结果也可有效预测敌草快中毒相关脏器损伤的发生及临床结局, 为临床诊治提供参考。     

应用连二亚硫酸钠判断百草枯中毒的程度和预后

目的 应用连二亚硫酸钠显色法判断百草枯中毒的程度和预后.方法 将不同浓度的百草枯标准品与过量连二亚硫酸钠在碱性条件下反应,建立百草枯检测标准比色卡和标准曲线.应用连二亚硫酸钠显色法前瞻性检测浙江大学医学院附属第一医院2008年1月至2009年5月间收治的22例百草枯中毒患者血、尿液百草枯浓度,回顾性分析了患者就诊即刻血、尿百草枯浓度与患者预后的相关性.结果22例百草枯中毒患者经血液灌流、血浆置换和血液滤过治疗后随访3月以上,存活6例(27.3%).6例存活者就诊即刻百草枯半定量检测显示为极浅(3例)或浅(3例),16例死亡患者就诊即刻百草枯半定量检测显示为浅(1例)、中(2例)、深(2例)、极深(11例).6例存活患者与16例死亡患者就诊即刻尿百草枯质量浓度分别为(1.95±1.76)mg/L和(53.4±45.9)mg/L,P＜0.01.6例存活患者和13例死亡患者就诊即刻血清百草枯质量浓度分别为(1.70±1.39)ng/L和(29.5±22.1)mg/L,P＜0.01.22例百草枯中毒患者存活状况与就诊即刻尿百草枯半定量、定量检测结果 及血清百草枯质量浓度均显著相关(r_s分别为-0.804、-0.772,和-0.593,P＜0.01).结论 应用连二亚硫酸钠可迅速检测患者血、尿百草枯质量浓度,有助于了解患者中毒程度和判断预后.     

敌草快百草枯混合中毒怎么办？

敌草快(diquat, DQ)、百草枯(paraquat, PQ)是我国常用除草剂, 分别于1958年和1962年上市, 具有很好的除草效果, 但同时对人畜有很强的毒性, 可造成多器官功能衰竭, 病死率高达50%～70%[1]。我国在2016年7月1日起禁售百草枯水剂, 在2020年9月26日起全面禁售百草枯所有剂型, 百草枯在生产使用过程中也被敌草快逐步替代。然而, 在市场检测敌草快农药时发现很多敌草快农药中掺有百草枯[2]。临床实际中, 口服敌草快中毒患者体内亦检测到敌草快混合百草枯[3]。百草枯、敌草快均属联吡啶类除草剂, 两者中毒有一定的共性与差异。我国对百草枯、敌草快均有相应的专家共识, 但目前两者混合中毒缺乏文献资料, 更无临床救治规范或共识, 百草枯、敌草快混合中毒已成为"后百草枯时代"下的热点问题, 更需广泛关注[4]。     

尿检百草枯对治疗和预后评估的价值

目的通过回顾分析我科2013年全年救治百草枯中毒病例,分析连二亚硫酸钠还原法尿检百草枯对疗效和预后评估的价值。方法:应用连二亚硫酸钠还原法检测收治的84例百草枯中毒患者尿液百草枯浓度,阳性为血灌指针,阴性者不予灌流。结果:84例百草枯中毒患者经血灌等治疗后90天随访,存活41例(48.8%),死亡43例(51.2%)。存活病例就诊即刻百草枯尿检检测结果明显轻于死亡病例,血灌次数也明显减少。结论:应用连二亚硫酸钠可迅速检测患者尿百草枯浓度,有助于评估患者血药浓度和中毒程度,指导是否给予血灌,尿百草枯持续阳性时间超过72 h,提示预后不良。     

临床需警惕与敌草快中毒伴随的百草枯中毒(附二例报告)

目的总结敌草快混合百草枯中毒的临床特点和检测方法,以减少临床误漏诊。方法回顾性分析两例除草剂中毒的临床资料,总结单纯敌草快中毒与敌草快混合百草枯中毒的临床表现及预后。结果本文两例敌草快中毒史明确,分别为皮肤接触中毒和口服中毒,分别于中毒后12 h、10 h急诊入院。经皮肤吸收中毒者主要表现为皮肤烧灼样疼痛、肺部条索样改变,给予规范化处理,住院13 d出院。经口服中毒者主要表现为恶心呕吐、意识障碍,入院次日出现呼吸衰竭、弥漫性肺间质病变伴双侧气胸,中毒后45 h因多脏器功能衰竭抢救无效死亡,后向生产厂家追溯药品成分发现其口服的敌草快溶液中含有较高浓度的百草枯。结论目前较多除草剂生产厂家在敌草快溶液中混合有百草枯,故对敌草快中毒患者需高度警惕合并百草枯中毒的可能,此类中毒患者预后不良,应注意鉴别诊断,避免漏诊而延误处理。     

急性敌草快中毒12例诊治分析

正敌草快与百草枯均属于联吡啶类接触性除草剂,规范使用敌草快对人畜少有危害,但意外经皮肤、黏膜或口服吸收,则对人体有较强毒性,可造成中毒,甚至死亡。近年来,由于百草枯水剂在国内禁止生产,敌草快的使用随之增加,其急性中毒的发生率也逐渐增加。迄今为止,对敌草快中毒而言尚无特效解毒剂,也无明确治疗方案~([1])。因此,正确认识敌草快中毒表现,正确诊断和救治敌草快中毒患者,意义重大。本文回顾性分析研究遵义医学院附属医     

血清胱抑素C动态变化在百草枯急性中毒早期肾损伤的意义

目的 探讨血清胱抑素C(Cys-C)动态变化在急性百草枯中毒早期肾损伤的意义.方法 对85例急性百草枯中毒组和50例正常对照组进行血清胱抑素C的浓度测定,中毒组又分为存活组和死亡组.根据血清胱抑素C的动态变化结果进行统计学分析.结果 动态检测血清胱抑素C可以早期发现急性百草枯中毒后导致肾损伤,并且中毒越严重(根据服毒量的多少),升高的越快、越显著,预后越差,死亡率越高.结论 血清胱抑素C是反应急性百草枯中毒早期肾损伤的一项灵敏指标.     

High-dose diquat poisoning: a case report

Diquat is a widely used herbicide that is substituted for paraquat. With paraquat off the market, cases of diquat poisoning have been gradually increasing. The kidney is the most frequently impaired organ in diquat poisoning. Few cases of multiple organ failure caused by diquat have been reported.We herein describe a 30-year-old man who orally ingested about 160 mL of enriched diquat. Despite aggressive treatment, the patient’s condition progressed to multiple organ failure and death. The pulmonary lesions in this patient were different from those previously reported. This patient did not die of renal failure but of severe respiratory failure. He exhibited three different stages of pulmonary disease.The lung lesions in this case were unique. We hope that doctors will pay more attention to the lung lesions in patients with diquat poisoning in future and find new treatment methods to save the lives of such patients.     

A Case of Fatal Diquat Poisoning: Toxicokinetic Data and Autopsy Findings

Case Report: A 37-year-old man ingested in a suicide attempt 300 mL of a diquat solution (equivalent to 60 g diquat ion). The initial diquat serum concentration was 64 μg/mL 4 hours after poisoning. The clinical course was characterized by a progressive anuria and by neurological disorders (coma and seizures). The patient died 26 hours after poisoning from refractory cardiocirculatory collapse. Extracorporeal techniques removed 1.09 g of diquat which could be considered as significant in regard to the total amount that was likely absorbed, but they did not influence the clinical outcome. There was marked renal tubular damage at autopsy and the highest diquat tissue concentration was found in the kidneys.     

Correlating the severity of paraquat poisoning with specific hemodynamic and oxygen metabolism variables

OBJECTIVE: To investigate the hemodynamics and oxygen metabolism of patients with varying degrees of severity of paraquat poisoning. DESIGN: Prospective, observational, clinical study. SETTING: Intensive care unit in a university hospital. PATIENTS: Forty-three consecutive patients with paraquat and/or diquat poisoning were classified into three groups by the severity index of paraquat poisoning (SIPP; hr/mg/L). INTERVENTIONS: Standard treatments included specific respiratory management, fluid resuscitation, and aggressive circulatory support. MEASUREMENTS AND MAIN RESULTS: Serum paraquat and diquat levels were measured at arrival, and SIPP was calculated. The cardiac index (CI), left ventricular stroke work index (LVSWI), systemic vascular resistance index (SVRI), oxygen delivery index (DO2I), oxygen consumption index (VO2I), and oxygen extraction ratio (O2ER) were measured at 6, 12, 24, 36, 48, 72, and 96 hrs postadmission. A significant inverse correlation between SIPP and survival time was found in 31 fatal cases (r = .85; p < .001). In the SIPP 10-50 group, CI, DO2I, VO2I, and O2ER were maintained at higher levels than in the SIPP group of <10 (p < .05), whereas SVRI decreased significantly (p < .05). In the SIPP group of >50, CI, LVSWI, SVRI, DO2I, and VO2I decreased, whereas O2ER had a tendency to increase progressively. There was a significant correlation between SVRI and SIPP, O2ER and SIPP, and O2ER and SVRI 24 hrs after admission, respectively (p < .001). CONCLUSIONS: Paraquat poisoning is characterized by high oxygen consumption with high oxygen extraction, with the degree of derangement based on the severity index. The development of a marked imbalance between increased oxygen demand and decreased oxygen supply because of myocardial depression might be a possible cause of death in circulatory failure.     

Mechanisms of Toxicity,Clinical Features,and Management of Diquat Poisoning: A Review

Uses: Diquat (1,1′-ethylene-2,2′-bipyridilium) is a nonselective bipyridyl herbicide, related structurally to paraquat, which is used both as a contact herbicide and a preharvest desiccant. In comparison to paraquat, diquat is used much less widely in agriculture. Mechanisms of Toxicity: Diquat is a potent redox cycler and is readily converted to a free radical which, in reaction with molecular oxygen, generates superoxide anions and subsequently other redox products. These products can induce lipid peroxidation in cell membranes, and potentially cause cell death. Features: Over the period 1968–1999, only 30 cases of diquat poisoning were reported in detail in the literature, of which 13 (43%) were fatal. Local and systemic effects have been reported following diquat exposure, with systemic features being invariably associated with ingestion. In severe and usually fatal cases, gastrointestinal mucosal ulceration, paralytic ileus, hypovolemic shock, acute renal failure, and coma have been reported. Management: After rapid confirmation of the diagnosis using a qualitative urine test, gut decontamination may be considered in patients who present within 1 hour of a life-threatening ingestion (>6 g). Supportive measures including fluid and electrolyte replacement should then be employed. Although hemofiltration and hemodialysis are of proven value if renal failure supervenes, there is no clinical evidence that hemodialysis or hemoperfusion removes toxicologically significant amounts of diquat, thereby reducing the risk of organ failure and preventing a fatal outcome in severe cases.     

Liver Necrosis and Lipid Peroxidation in the Rat as the Result of Paraquat and Diquat Administration: EFFECT OF SELENIUM DEFICIENCY

Paraquat and diquat facilitate formation of superoxide anion in biological systems, and lipid peroxidation has been postulated to be their mechanism of toxicity. Paraquat has been shown to be more toxic to selenium-deficient mice than to controls, presumably as the result of decreased activity of the selenoenzyme glutathione peroxidase. The present study was designed to measure lipid peroxidation and to assess toxicity in control and selenium-deficient rats given paraquat and diquat. Lipid peroxidation was measured by determining ethane production rates of intact animals; toxicity was assessed by survival and by histological and serum enzyme evidence of liver and kidney necrosis. Paraquat and diquat were both much more toxic to selenium-deficient rats than to control rats. Diquat (19.5 μmol/kg) caused rapid and massive liver and kidney necrosis and very high ethane production rates in selenium-deficient rats. The effect of paraquat (78 μmol/kg) was similar to that of diquat but was not as severe. Acutely lethal doses of paraquat (390 μmol/kg) and diquat (230 μmol/kg) in control rats caused very little ethane production and no evidence of liver necrosis. These findings suggest that paraquat and diquat exert their acute toxicity largely through lipid peroxidation in selenium-deficient rats. Selenium deficiency had no effect on superoxide dismutase activity in erythrocytes or in 105,000 g supernate of liver or kidney. Glutathione peroxidase, which represents the only well-characterized biochemical function of selenium in animals, was dissociated from the protective effect of selenium against diquat-induced lipid peroxidation and toxicity by a time-course study in which selenium-deficient rats were injected with 50 μg of selenium and later given diquat (19.5 μmol/kg). Within 10 h, the selenium injection provided significant protection against diquat-induced lipid peroxidation and mortality even though this treatment resulted in no rise in glutathione peroxidase activity of liver, kidney, lung, or plasma at 10 h. This suggests that a selenium-dependent factor in addition to glutathione peroxidase exists that protects against lipid peroxidation.     

百草枯中毒患者血清基质金属蛋白酶-9水平及其临床意义

目的：探讨百草枯中毒患者血清基质金属蛋白酶-9的变化，以及其变化与肺纤维化的相关程度。方法：采用酶联免疫吸附法对32例百草枯中毒患者和24例健康人（健康对照组）血清基质金属蛋白酶-9进行测定。结果：百草枯中毒患者第1天和第28天血清基质金属蛋白酶-9均高于健康对照组，差异有显著性意义（P〈0．01）；中毒患者第1天血清基质金属蛋白酶-9高于第28天，比较差异有显著性意义（P〈0．01）。结论：基质金属蛋白酶-9在百草枯中毒致肺纤维化发病机制中起着重要作用。     

分光光度法检测血清百草枯质量浓度及意义

目的 评价分光光度法测定血清百草枯(paraquat,PQ)质量浓度的可靠性及其临床意义。方法 验证普通分光光度法和二阶导数分光光度法测定血清PQ质量浓度的检测波长后,采用二阶导数分光光度法测定血清PQ质量浓度,确定其线性范围并评价其准确性;采用该法测定8例PQ中毒患者血清PQ质量浓度并与高效液相色谱法测定值比较分析其可靠性;对上海市第十人民医院肾病免疫科2008年10月至2010年9月收治的口服PQ4h以上人院的21例急性PQ中毒患者的资料行回顾性统计分析,根据该法测定患者入院时血清PQ质量浓度是否大于1.8 μ.g/mL分为两组,采用成组t检验和Fisher精确概率法对两组患者的临床特征进行统计分析。结果 (1)普通分光光度法检测含PQ血清样本时在257 nm波长处未见明显吸收峰;(2)二阶导数分光光度法测定血清PQ质量浓度在0.4～8.0 μg/mL范围内呈现良好的线性关系,相关系数为0.996;回收率为95.0％～99.5％,相对标准差(RSD)为1.35％～5.41％ (n=6),检出下限为0.05 μg/mL;(3)8例PQ中毒患者血清PQ质量浓度二阶导数分光光度法测定值与HPLC法检测值相吻合,r=0.995,P＜0.01;(4)血清PQ质量浓度＞1.8 μg/mL组患者存活率为22.2％,酸中毒和少尿发生率55.6％,纵膈气肿发生率77.8％,与血清PQ质量浓度＜1.8 μg/mL组比较差异均有统计学意义(P＜0.05)。结论 (1)普通分光光度法用于测定血清PQ质量浓度不能采用257 rn为检测波长;(2)二阶导数分光光度法用于检测血清百草枯质量浓度可靠性高;(3)二阶导数分光光度法测定值可用于中毒患者的临床严重程度判断,口服PQ中毒4h后血清质量浓度＞1.8 μg/mL是患者预后不良的重要指标。     

急性百草枯中毒患者预后影响因素的分析

目的：探讨影响百草枯中毒患者预后的因素,为其临床治疗提供救治依据。方法收集我院2011年3月至2013年3月百草枯中毒病例66例对其进行回顾性分析,其中死亡48例,存活18例;男26例,女40例。分析患者服药剂量、洗胃时间、APACHEⅡ评分、血清白细胞计数、血清肌酐、谷丙转氨酶、肌酸激酶同工酶与患者的预后关系,然后采用Logistic逐步向前回归筛选出有效指标,并通过ROC曲线评价其在百草枯中毒预后的诊断价值。结果两组患者在口服剂量、血白细胞计数、肌酐、谷丙转氨酶、肌酸激酶同工酶存在统计学意义。通过Logistic向前逐步分析后,口服剂量、APACHEⅡ评分进入Logistic回归方程。口服剂量、APACHEⅡ评分对患者死亡风险评价具有显著影响。不同时间段的APACHEⅡ评分对于患者预后的评价相关程度不同。对口服剂量、APACHEⅡ评分、口服剂量联合APACHEⅡ评分进行曲线下面积分析,其各自的曲线下面积为0.923、0.945、0.957。结论中毒剂量、APACHEⅡ评分可作为判断急性百草枯中毒病情严重程度及预后的可靠指标,口服剂量联合APACHEⅡ评分对预后评价更有意义。