Glyphosate poisoning - a case report.

Glyphosate is the most commonly used broad-spectrum, non-selective herbicide in the world. The toxicity is supposed to be due to uncoupling of oxidative phosphorylation and the surfactant polyoxyethylene amine (POEA)- mediated cardiotoxicity. Clinical features of this herbicide poisoning are varied, ranging from asymptomatic to even death. There is no antidote and aggressive supportive therapy is the mainstay of treatment for glyphosate poisoning. We present a 69-year-old female patient with suicidal consumption of around 500 ml of Glycel®. Initially, gastric lavage was done and intravenous fluids were given. Within two hours of presentation, the patient developed respiratory distress needing intubation, hypotension needing vasopressor support, and severe lactic acidosis. She also developed acute respiratory distress syndrome, hypokalemia, hypernatremia, and aspiration pneumonia. Our patient was critically ill with multiple poor prognostic factors, but with timely aggressive supportive management, the patient gradually recovered.

Serial measurement of glyphosate blood concentration in a glyphosate potassium herbicide-intoxicated patient: A case report.

INTRODUCTION: This report describes changes in blood and urine concentrations of glyphosate potassium over time and their correlations with clinical symptoms in a patient with acute glyphosate potassium poisoning. CASE REPORT: A 67-year-old man visited the emergency center after ingesting 250 mL of a glyphosate potassium-based herbicide 5 h before. He was alert but presented with nausea, vomiting, and bradyarrhythmia with atrial fibrillation (tall T waves). Laboratory findings revealed a serum potassium level of 6.52 mEq/L. After treatment with an injection of calcium gluconate, insulin with glucose, bicarbonate, and an enema with polystyrene sulfonate, the patient's serum potassium level normalized and the bradyarrhythmia converted to a normal sinus rhythm. During admission, the blood and urine concentration of glyphosate and urine aminomethylphosphonic acid (AMPA, a glyphosate metabolite) was measured at regular time intervals. The patient's glyphosate blood concentration on admission was 11.48 mg/L, and it had decreased rapidly by 16 h and maintained about 1mgl/L by 70 h after admission. Urine glyphosate and AMPA levels had also decreased rapidly by 6 h after admission. DISCUSSION: Glyphosate potassium poisoning causes hyperkalemia. Blood concentrations of glyphosate were decreased rapidly by 16 h after admission, and urine concentrations were also decreased by 6 h after admission.

[Analysis of reports of cases of pesticide poisoning in Jiangsu Province, China, from 2006 to 2013].

OBJECTIVE: To investigate the characteristics of pesticide poisoning in Jiangsu Province, China, and to provide a scientific basis for developing effective intervention measures and prevention strategies. METHODS: The data from report cards of pesticide poisoning in Jiangsu Province from 2006 to 2013 were arranged using EXCEL tables, and assessed. Statistical analysis was applied to the epidemiological data using SPSS. RESULTS: From 2006 to 2013, a total of 32672 cases of pesticide poisoning were reported in Jiangsu Province. Most of the cases were caused by non-occupational poisoning (life poisoning) (72.78%). A majority of patients with pesticide poisoning were 35-54 years old (40.85%) or older than 65 years (15.69%). There were more female patients (58.22%) than male patients (41.78%). Among patients with occupational poisoning, male patients (50.90%) were more than female patients. Among patients with non-occupational poisoning, female patients were more than male patients (38.37%). Pesticide poisoning mainly occurred from July to September. The case-fatality rate of occupational poisoning (0.47%) was lower than that of non-occupational poisoning (7.10%). All 13 cities in Jiangsu Province reported cases of pesticide poisoning. There were more cases in the northern regions than in the southern regions. Pesticide poisoning was mainly caused by organophosphorus insecticides including methamidophos, dichlorvos, dimethoate, omethoate, and parathion, which accounted for 65.58%of all cases. Paraquat had the highest case-fatality rate (10.06%) among all pesticides, followed by tetramine (10.00%), dimethoate or omethoate (7.85%), methamidophos (7.79%), and dimehypo (7.68%). CONCLUSION: Pesticide poisoning cannot be ignored. The management and control should be improved in production and usage of highly toxic pesticides including organophosphorus insecticides, rodenticides, and herbicides. More attention should be paid to the protection of vulnerable groups including women, children, and the elderly.

[Oxidative stress and antioxidant therapy with alpha-lipoic acid inclusion in acute poisoning by herbicide based on 2,4-dichlorphenoxyacetic acid].

In patients with acute poisoning amine salt herbicide 2,4-D develops oxidative stress with simultaneous inhibition of intracellular and extracellular antioxidant factors. These changes are more pronounced with neurological disorders that occur in conjunction with a toxic damage of liver or heart. The inclusion of a comprehensive detoxification therapy alpha-lipoic acid not only promotes a more pronounced therapeutic effect but also an earlier recourse cytolytic syndrome, a marked recovery of levels of malondialdehyde and indices of antioxidant system (superoxide dismutase and ceruloplasmin) than for patients in the comparison group.

Where ferroptosis inhibitors and paraquat detoxification mechanisms intersect, exploring possible treatment strategies.

Paraquat (PQ) is a fast-acting and effective herbicide that is used throughout the world to eliminate weeds. Over the past years, PQ was considered one of the most popular poisoning substances for suicide, and PQ poisoning accounts for about one-third of suicides around the world. Poisoning with PQ may cause multiorgan failure, pulmonary fibrosis, and ultimately death. Exposure to PQ results in the accumulation of PQ in the lungs, causing severe damage and, eventually, fibrosis. Until now, no effective antidote has been found to treat poisoning with PQ. In general, the toxicity of PQ is due to the formation of high energy oxygen free radicals and the peroxidation of unsaturated lipids in the cell. Ferroptosis is the result of the loss of glutathione peroxidase 4 (GPX4) activity that transforms iron-dependent lipid hydroperoxides to lipid alcohols, which are inert in the biological environment. Impaired iron metabolism and lipid peroxidation are increasingly known as the driving agents of ferroptosis. The contribution of ferroptosis to the development of cell death during poisoning with PQ has not yet been addressed. There is growing evidence about the relationship between PQ poisoning and ferroptosis. This raises the possibility of using ferroptosis inhibitors for the treatment of PQ poisoning. In this hypothesis-driven review article, we elaborated how ferroptosis inhibitors might circumvent the toxicity induced by PQ and may be potentially useful for the treatment of PQ toxicity.

Can early hemodialysis affect the outcome of the ingestion of glyphosate herbicide?

The ingestion of small amounts of glyphosate herbicide usually causes only mild symptoms. However, when large volumes of concentrates are ingested intentionally, it can generate potentially fatal symptoms that are refractory to treatment. It also is well known that the treatment for glyphosate poisoning is primarily of a supportive nature. We report two patients who intentionally ingested glyphosate herbicide, and both exhibited cardiovascular collapse and complicated renal failure despite the use of aggressive supportive therapy. Hemodialysis was conducted and the results were satisfactory; both patients were discharged without any sequelae. After analyzing these cases, we suggest that hemodialysis might have contributed to the favorable outcomes of our patients, and that there are several mechanisms that might justify the use of hemodialysis in these patients. In conclusion, physicians may wish to consider the early use of hemodialysis to improve the prognosis of patients exhibiting refractory hypotension and oliguria, despite vigorous supportive treatment in glyphosate herbicide intoxication.

Prospects for treatment of paraquat-induced lung fibrosis with immunosuppressive drugs and the need for better prediction of outcome: a systematic review.

BACKGROUND: Acute paraquat self-poisoning is a significant problem in parts of Asia, the Pacific and the Caribbean. Ingestion of large amounts of paraquat results in rapid death, but smaller doses often cause a delayed lung fibrosis that is usually fatal. Anti-neutrophil ('immunosuppressive') treatment has been recommended to prevent lung fibrosis, but there is no consensus on efficacy. AIM: To review the evidence for the use of immunosuppression in paraquat poisoning, and to identify validated prognostic systems that would allow the use of data from historical control studies and the future identification of patients who might benefit from immunosuppression. DESIGN: Systematic review. METHODS: We searched PubMed, Embase and Cochrane databases for 'paraquat' together with 'poisoning' or 'overdose'. We cross-checked references and contacted experts, and searched on [www.google.com] and [www.yahoo.com] using 'paraquat', 'cyclophosphamide', 'methylprednisolone' and 'prognosis'. RESULTS: We found ten clinical studies of immunosuppression in paraquat poisoning. One was a randomized controlled trial (RCT). Seven used historical controls only; the other two were small (n = 1 and n = 4). Mortality in controls and patients varied markedly between studies. Three of the seven non-RCT controlled studies measured plasma paraquat; analysis using Proudfoot's or Hart's nomograms did not suggest that immunosuppression increased survival in these studies. Of 16 prognostic systems for paraquat poisoning, none has been independently validated in a large cohort. DISCUSSION: The authors of the RCT have performed valuable and difficult research, but their results are hypothesis-forming rather than conclusive; elsewhere, the use of historical controls is problematic. In the absence of a validated prognostic marker, a large RCT of immunosuppression using death as the primary outcome is required. This RCT should also prospectively test and validate the available prognostic methods, so that future patients can be selected for this and other therapies on admission.

Accident insurance, sickness, and science: New Zealand's no-fault system.

This article explores the process of seeking compensation for occupational illness under a no-fault accident insurance scheme. The author uses two case studies--firefighters who attended a fire at a chemical storage depot and timbermill workers who worked with pentachlorophenol--to illustrate how science can be used to deny compensation to sick and dying workers. The results of the studies suggest that a no-fault accident compensation scheme, considered to be a victory for workers, offers no guarantee of just outcomes for working people. And science can be co-opted and used to support business and state interests against workers; this ideological support is increasingly hidden behind the development of "objective" systems of assessing compensation claims.

[A case of acute poisoning caused by the inhalation of a nonselective herbicide REBIN GT SC (butafenacil and glyphosate isopropylamine)].

REBIN GT SC (glyphosate isopropylamine and butafenacil, hereinafter referred to as "REBIN") is a nonselective herbicide which was developed by Syngenta Japan K. K. and was registered in July 2001 as a herbicide. We report the first case of acute poisoning by REBIN. In this case (Age 67, male), high fever and general fatigue developed immediately after REBIN inhalation. Furthermore, urine sugar, urine protein, high LDH and high GPT were observed. But the patient showed a tendency of recovery after the lapse of 48 hours by the intravenous fluid replacement, hydrocortisone sodium succinate (Solu-Cortef), glycyrrhizin (Stronger Neo-Minophagen C) and glutathione (Tathion). He recovered satisfactorily. It is necessary to respect the instructions for the use of REBIN. In addition, in order to prevent inhalation of REBIN, the proper use of instruments and spray at about 30 cm under knee are essential.

The value of plasma paraquat concentration in predicting therapeutic effects of haemoperfusion in patients with acute paraquat poisoning.

OBJECTIVE: This study was aimed to analyze the scavenging effect of haemoperfusion on plasma paraquat (PQ) and to evaluate the clinical significance of PQ examination in the treatment of patients with acute paraquat poisoning. METHODS: 85 patients with acute paraquat intoxication by oral ingestion were admitted in West China Hospital from Jun, 2010 to Mar, 2011. A standardized therapeutic regimen including emergency haemoperfusion was given on all subjects. A total of 91 whole blood samples were taken before (0 h), underway (1 h after haemoperfusion beginning) and at the end (2 h) of the haemoperfusion therapy. The clearance rate was calculated and related factors were analyzed. RESULTS: As heamoperfusion was going on, the plasma paraquat concentration of the patients kept falling down. After 1 hour of haemoperfusion, the average clearance rate (R(1)) was 37.06±21.81%. After 2 hours of haemoperfusion, the average clearance rate (R(2)) was 45.99±23.13%. The average of R(1)/R(2) ratio was 76.61±22.80%. In the high paraquat concentration group (plasma paraquat concentration (C(0)) >300 ng/mL), both the averages of R(1) and R(2) were significantly higher than those of the low paraquat concentration group (C(0)≤200 ng/mL) (p<0.05), and there was no significant difference of R(1)/R(2) between these two groups (p>0.05). CONCLUSIONS: The dynamic monitoring of plasma PQ concentration was not only critical in the clinical evaluation but also helpful in guiding the treatment of patients with acute PQ intoxication. Haemoperfusion can effectively eliminate paraquat from the plasma in patients with high initial plasma PQ concentration, while in patients with low initial plasma PQ concentration (<200 ng/ml), the clearance effect of harmoperfusion was very limited. Increasing HP time might improve the overall clearance rate of HP on plasma PQ yet decrease the elimination efficiency of HP, while repeated HP treatment was helpful against the rebound phenomena.

Successful treatment of patients with paraquat intoxication: three case reports and review of the literature.

OBJECTIVE: To report on three patients with paraquat (PQ) intoxication surviving after combined therapy with hemoperfusion (HP), cyclophosphamide (CTX), and glucocorticoid. METHODS: Three patients suffered acute renal failure in a few days after ingesting a lethal amount of PQ. Chest computed tomography (CT) scans revealed obvious pulmonary inflammation, pleural effusion, and fibrous lesions several days after ingestion. HP was performed immediately, followed by large doses of glucocorticoid (methylprednisolone, 500 g/d) and CTX (approximately 4 g). RESULTS: After 50 d of treatments, all three patients were discharged in healthy condition, with chest CT showing small fibrous lesions, exudation, and both lungs clear of auscultation. CONCLUSIONS: The protective effect of the lungs may have been due to timely treatment at adequate doses.

Inadvertent poisoning of seven teenagers with monosodium methanearsonate.

INTRODUCTION: Monosodium methanearsonate (MSMA) is an organo-arsenic containing herbicide. There is scant information available concerning the toxicity of this chemical in humans. CASE REPORT: Seven male teenagers, 15-18 years of age, inadvertently used a MSMA herbicide as cooking oil to fry fish. All had early gastrointestinal (GI) symptoms. Whole blood arsenic concentrations ranged from 348 to 613 µg/L and initial urine levels ranged from 81 400 to 226 300 µg-arsenic/g-creatinine. They were all treated with dimercaprol for 1 day and succimer for 19 days. They were followed for 15-months and had no evidence of any serious toxicity. CONCLUSION: MSMA produces early GI symptoms and very high levels of arsenic in blood and urine, but no evidence of long-term toxicity.

Acute diquat poisoning with intracerebral bleeding.

A case of severe diquat poisoning complicated by the development of aggressive behaviour, oliguric renal failure, and intracerebral bleeding is described. The patient was successfully managed and made a complete recovery. In this paper special attention has been given to the major clinical differences between diquat and paraquat intoxication.