Acute glyphosate-surfactant poisoning with neurological sequels and fatal outcome

Potrebic, Olivera; Jovic-Stosic, Jasmina; Vučinić, Slavica; Tadić, Jelena; Radulac, Misel

doi:10.2298/vsp0909758p

Cited by 15 publications

(9 citation statements)

References 12 publications

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“…[ 5 ] In a single case report, patient developed neurotoxic sequels of GlySH-surfactant exposure with white matter lesions and development of Parkinsonism. [ 6 ] Our patient had oral ulcers, gastrointestinal involvement, and deteriorated due to development of acute pulmonary edema and respiratory failure.…”

Section: Discussionmentioning

confidence: 99%

Glyphosate poisoning with acute pulmonary edema

Thakur¹,

Khot²,

Pp³

et al. 2014

Toxicol Int

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GlySH-surfactant herbicide (GlySH), one of the most commonly used herbicides worldwide, has been considered as minimally toxic to humans. However, clinical toxicologists occasionally encounter cases of severe systemic toxicity. The US Environmental Protection Agency (EPA) states that ‘GlySH’ is of relatively low oral and acute dermal toxicity. It does not have anticholinesterase effect and no organophosphate-like central nervous system (CNS) effects. The clinical features range from skin and throat irritation to hypotension and death. Severe GlySH-surfactant poisoning is manifested by gastroenteritis, respiratory disturbances, altered mental status, hypotension refractory to the treatment, renal failure, and shock.[1] GlySH intoxication has a case fatality rate 3.2–29.3%. Pulmonary toxicity and renal toxicity seem to be responsible for mortality. Metabolic acidosis, abnormal chest X-ray, arrhythmias, and elevated serum creatinine levels are useful prognostic factors for predicting GlySH mortality.[2] There is no antidote and the mainstay of treatment for systemic toxicity is decontamination and aggressive supportive therapy.We report a case of acute pulmonary edema, which is a rare but severe manifestation of oral GlySH poisoning, where patient survived with aggressive supportive therapy.

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Section: Discussionmentioning

confidence: 99%

Glyphosate poisoning with acute pulmonary edema

Thakur¹,

Khot²,

Pp³

et al. 2014

Toxicol Int

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“…Serum CBZ level was assessed using a biochemical auto analyzer (ARCHITECT c8000 Clinical Chemistry analyzer, Abbott®, U.S., Japan). Total oxidative status (TOS) ( 9 ) and TAS of serum was determined using a novel automated measurement method developed by Erel ( 10 , 11 ). Oxidants present in the sample oxidize the ferrous ion-o-dianisidine complex to ferric ion.…”

Section: Methodsmentioning

confidence: 99%

“…On the other hand, malondialdehyde (MDA) values, an indicator of membrane lipid peroxidation, were found to be unchanged in children with epilepsy ( 8 ). Oxidative stress index ( 9 ) is reported as a valuable parameter indicating oxidative stress level. Furthermore, previously conducted studies revealed that oxidative stress index (OSI) rate indicates oxidative injury, as well ( 10 - 12 ).…”

Section: Introductionmentioning

confidence: 99%

Oxidative Status in Epileptic Children Using Carbamazepine

et al. 2015

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Background:There is an increasing attention towards the relationship between oxidative stress and epilepsy. The effect of antiepileptic drugs on oxidant status is of major interest. Antiepileptic drugs can increase levels of free radicals, which consequently might lead to seizures. Carbamazepine (CBZ) is an antiepileptic drug commonly used in childhood and adolescence.Objectives:Therefore we aimed to investigate the effects of CBZ on total antioxidant status, total oxidant stress, and oxidative stress index.Patients and Methods:The study included 40 epileptic patients and 31 healthy children between 4 and 12 years of age. Serum CBZ level, total antioxidant capacity and total oxidant status were measured. Oxidative stress index was also calculated both in controls and patients.Results:In the epileptic group, decreased levels of total antioxidant capacity, increased total oxidative stress and oxidative stress index levels were found. Positive correlation between plasma CBZ levels and total oxidant status was observed.Conclusions:Antioxidant action could not be playing any role in antiepileptic effect of CBZ. Furthermore, increased oxidative stress induced by CBZ could be the cause of CBZ-induced seizures. Therefore combining CBZ with antioxidants could be beneficial.

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“…The clinical picture of severe GI poisoning may result in some clinical complications such as gastroenteritis, respiratory diseases, alterations in mental status, nephrotoxicity, acute renal failure, shock, neurological sequel, and death. 4,5…”

Section: Introductionmentioning

confidence: 99%

Effects of intralipid and caffeic acid phenyl esther (CAPE) against hepatotoxicity and nephrotoxicity caused by glyphosate isopropylamine (GI)

et al. 2016

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This study was aimed to investigate the protective effects of caffeic acid phenyl esther (CAPE) and Intralipid (IL) against hepatotoxicity and nephrotoxicity caused by acute intoxication of glyphosate (N-phosphonomethyl)glycine) (GI) in rats. Forty-nine Wistar Albino rats were randomly divided into seven groups as: I, Control; II, Intralipid (IL) (18.6 mL/kg, orally); III, CAPE (10 µmol/kg, intraperitoneally); IV, GI (4 mg/kg/day, intraperitoneally); V, GI + IL; VI, GI+CAPE; and VII, GI + IL + CAPE. Total antioxidant status (TAS) and total oxidant status (TOS) levels were measured in serum samples. Tissues were analyzed with hematoxylin and eosin (H&E) staining protocol. Bcl-2, Bax, and caspase-3 were evaluated by immunohistochemical method. The results revealed that, in hepatic tissues, the TAS levels were lower and the TOS levels were higher in the GI group compared to other groups. In renal tissues, the TAS levels were significantly lower in the GI group than in the control, IL, CAPE, and GI + IL + CAPE groups. The TOS levels were significantly higher in the GI group than in the control group. Moreover, histopathological analysis revealed severe hepatotoxicity in the GI group. In the GI + CAPE + IL group, hepatotoxicity recovered significantly. Nephrotoxicity was also observed in the GI group and moderately reduced in the GI + CAPE group. Biochemical results were confirmed by histopathologic examination. The results also revealed that CAPE and IL, due to their antioxidant effects, have a decreasing effect against both hepatotoxicity and nephrotoxicity caused by GI. Therefore, CAPE and IL may function as potential agents for supportive therapy since they decrease organ damage, or may facilitate the therapeutic effects of the routine treatment of patients with GI poisoning.

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Acute glyphosate-surfactant poisoning with neurological sequels and fatal outcome

Cited by 15 publications

References 12 publications

Glyphosate poisoning with acute pulmonary edema

Glyphosate poisoning with acute pulmonary edema

Oxidative Status in Epileptic Children Using Carbamazepine

Effects of intralipid and caffeic acid phenyl esther (CAPE) against hepatotoxicity and nephrotoxicity caused by glyphosate isopropylamine (GI)

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