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Ethylene glycol poisoning is an important toxicological problem in medical practice because early diagnosis and treatment can prevent considerable morbidity and mortality. When ingested in the form of antifreeze or other automotive products, ethylene glycol results in central nervous system depression, cardiopulmonary compromise, and renal insufficiency. Metabolism of ethylene glycol to organic acids is required for metabolic derangement and organ damage. Laboratory features of ethylene glycol poisoning include increased anion gap metabolic acidosis, increased osmolal gap, calcium oxalate crystalluria, and detectable ethylene glycol in serum. This Case Conference integrates discussion of the toxicokinetic and analytical variables that affect the laboratory diagnosis of ethylene glycol intoxication.
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PMID:Ethylene glycol poisoning: toxicokinetic and analytical factors affecting laboratory diagnosis. 979 73

Four of approximately 15 dry cows introduced on a 10-acre fescue-clover-orchard grass-Dallis grass pasture in East Tennessee became recumbent. Clinical findings included depression, muscle tremors, increased heart and respiratory rates, hypocalcemia, hypomagnesemia, hyperkalemia, azotemia, and elevated creatinine phosphokinase. Three cows recovered; 1 died. Differential diagnoses considered were hypocalcemia, hypomagnesemia, rabies and toxicoses from Amaranthus retroflexus (pigweed), Quercus spp (oak), Cassia spp (senna) oxalate (Aspergillus niger or flavus), mycotoxicosis, lead, arsenic or insecticides. Pigweed toxicosis was confirmed based on clinical and postmortem findings, partially ingested pigweed in the pasture, and ruling out other possible causes. Several factors probably contributed to this incident: since the cattle were newly introduced to the pasture, the cattle may have been attracted to the pigweed in the new pasture and became addicted to it; their rumen microflora had little time to acclimate to the pigweed; and dry weather produced poor forage quality thus forcing the cows to eat the pigweed.
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PMID:Pigweed (Amaranthus retroflexus) toxicosis in cattle. 968 7

Alpha2-adrenoceptor antagonists, which can enhance synaptic norepinephrine levels by blocking feedback inhibition processes, are potentially useful in the treatment of disease states such as depression, memory impairment, impotence and sexual dysfunction. (10bS)-1,2,3,5,6,10b-Hexahydropyrrolo[2,1-a]isoquinoline oxalate (YSL-3S) was evaluated in several in vitro biological tests to establish its pharmacological profile of activities as an alpha2-adrenoceptor antagonist. Saturation binding assay revealed that [3H]rauwolscine bound to the alpha2-adrenoceptors with a Kd value of 6.3+/-0.5 nM and a Bmax value of 251+/-39 fmol/mg protein in rat cortical synaptic membranes. Competitive binding assay showed that YSL-3S inhibited the binding of [3H]rauwolscine (1 nM) in a concentration-dependent manner with a Ki value of 98.2+/-12.1 nM while it did not inhibit the binding of [3H]cytisine (1.25 nM) to neuronal nicotinic cholinergic receptors. The Ki values of yohimbine, clonidine and norepinephrine for [3H]rauwolscine binding were 15.8+/-1.0, 40.1+/-5.9 and 40.0+/-11.5 nM, respectively. In addition, the binding affinity of YSL-3S for alpha2-adrenoceptors was higher than that of its antipode and the racemic mixture. The functional activity of YSL-3S at the presynaptic alpha2-adrenoceptors was assessed using the prostatic portion of the rat vas deferens. Clonidine inhibited field-stimulated contractions of the vas deference in a dose-dependent manner. The presence of YSL-3S or yohimbine caused a parallel, rightward the dose-response curve of clonidine in a dose-dependent manner, indicating an antagonistic action at the presynaptic alpha2-adrenoceptors. The pA2 values of yohimbine and YSL-3S were 7.66+/-0.13 and 6.64+/-0.18, respectively. The results indicate that YSL-3S acts as a competitive antagonist at presynaptic alpha2-adrenoceptors with a potency approximately ten times lower than yohimbine, but is devoid of binding affinity for neuronal nicotinic cholinergic receptors.
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PMID:Pharmacological characterization of (10bS)-1,2,3,5,6,10b-hexahydropyrrolo[2,1-a]isoquinoline oxalate (YSL-3S) as a new alpha2-adrenoceptor antagonist. 1097 83

Alcohol intoxication is the principal drug addiction in many countries of the world. It affects all age groups, both sexes and almost all social groups. Mortality associated with acute alcohol poisoning on its own is exceptional, but it can be an important factor if it coexists with recreational drugs. It is directly responsible for more than half of traffic accidents. Diagnosis is easy by means of anamnesis and clinical examination, and can be confirmed by determining the level of ethanol in the bloodstream. Supportive care is the best therapy in order to protect the patient from secondary complications. Methanol, or alcohol fuel, is used as a solvent, and can also be found as an adulterant of alcoholic drinks. Poisoning by oral means is the most frequent. Oxidized in the liver through dehydrogenase enzyme alcohol, toxicity is due to its metabolites, formaldehyde and formic acid. The clinical picture basically consists of cephalea, nausea, vomiting, hypotension and depression of the central nervous system. The optic nerve is especially sensitive, with total and irreversible blindness as a possible result. Ethylenglicol is used as a solvent and as an antifreeze; toxicity is due to an accumulation of its metabolites. The clinical picture includes symptoms that are held in common with methylalcohol intoxication. Kidney failure due to tubular necrosis and the deposit of oxalate crystals can occur.
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PMID:[Alcohol intoxication]. 1281 81

Responses of Melaleuca leucadendra (L.) L., Melaleuca cajuputi Powell, Acacia auriculiformis A. Cunn. ex Benth. and Eucalyptus camaldulensis Dehnh. to aluminum (Al) toxicity at low pH are poorly understood. We investigated effects of low pH and exudation of ligands by roots on Al tolerance of these species. Seedlings were grown hydroponically in nutrient solutions at pH 4.2 or 3.5 containing AlCl3 at concentrations ranging from 0 to 4 mM Al. The presence of 4 mM Al at pH 3.5 depressed growth in all species. Growth depression was greatest in E. camaldulensis, least in A. auriculiformis. In the low Al treatment (0.5 mM Al), roots of M. cajuputi tended to have the highest Al concentration among species, whereas in the 4 mM Al treatment, the highest Al concentration was found in roots of E. camaldulensis. Aluminum application enhanced root exudation of citrate in all species, with the enhancement in M. cajuputi, M. leucadendra and A. auriculiformis being similar and much greater than in E. camaldulensis. Exudation of oxalate and phenolic compounds was greater in E. camaldulensis than in the other species. The presence of Al enhanced phosphate exudation in all species, particularly in A. auriculiformis. Acacia auriculiformis was tolerant to low pH, probably because the presence of an unknown substance increased the pH. Application of 0.38 mM Al alleviated the toxicity of the pH 3.5 treatment in E. camaldulensis and M. cajuputi, whereas low pH alleviated Al toxicity in A. auriculiformis. We conclude that exudation of ligands such as citrate and phosphate only partly accounts for interspecific differences in Al tolerance among the tropical woody plants studied, whereas the reciprocal alleviation of Al toxicity and low pH differed considerably among the species.
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PMID:Role of exudation of organic acids and phosphate in aluminum tolerance of four tropical woody species. 1297 28

Severe ethylene glycol toxicity can cause profound morbidity and is almost universally fatal if untreated. Central nervous system depression with intoxication, pulmonary edema, and acute oliguric renal failure with crystalluria are among the most commonly encountered complications of ingestion. The previously reported gastrointestinal side effects of ethylene glycol toxicity are mostly nonspecific, including nausea, abdominal pain, and cramping. In addition, hepatic damage due to calcium oxalate deposition has been reported. We describe a patient who developed acute colonic ischemia following ethylene glycol intoxication. Three months after the ingestion, the patient presented with severe abdominal pain secondary to a colonic stricture and perforation, necessitating emergent colectomy. Histology of the resected colon revealed polarizable polyhedral crystals suggestive of oxalate deposition. The pathophysiology underlying ethylene glycol intoxication, treatment strategies, and gastrointestinal toxicity are discussed.
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PMID:Ethylene glycol toxicity associated with ischemia, perforation, and colonic oxalate crystal deposition. 1510 May 24

Upon ingestion ethylene glycol (EG, monoethylene glycol) is rapidly absorbed from the gastrointestinal tract, and depending on the severity of exposure signs of toxicity may progress through three stages. Neurological effects characterize the first step consisting of central nervous depression (intoxication, lethargy, seizures, and coma). The second stage, usually 12-24 h after ingestion, is characterized by metabolic acidosis due to the accumulation of acidic metabolites of EG, primarily glycolic acid (GA), contributing to the ensuing osmolal and anion gaps. Stage 3, generally 24-72 h after ingestion, is determined mainly by oxalic acid excretion, nephropathy, and eventual renal failure. Because the toxicity of EG is mediated principally through its metabolites, adequate analytical methods are essential to provide the information necessary for diagnosis and therapeutic management. The severe metabolic acidosis and multiple organ failure caused by ingestion of high doses of EG is a medical emergency that usually requires immediate measures to support respiration, correct the electrolyte imbalance, and initiate hemodialysis. Since metabolic acidosis is not specific to EG, whenever EG intoxication is suspected, every effort should be made to determine EG as well as its major metabolite GA in plasma to confirm the diagnosis and to institute special treatment without delay. A number of specific and sensitive analytical methods (GC, GC-MS, or HPLC) are available for this purpose. Due to the rapid metabolism of EG, the plasma concentration of GA may be higher than that of EG already upon admission. As toxicity is largely a consequence of metabolism of EG to GA and oxalic acid, the simultaneous quantification of EG and GA is important. Formation of calcium oxalate monohydrate in the urine may be a useful indicator of developing oxalate nephrosis although urine crystals can result without renal injury. The pathways involved in the metabolism of EG are qualitatively similar in humans and laboratory animals, although quantitative differences have been reported. Comparison between species is difficult, however, because the information on humans is derived mainly from acute poisoning cases whereas the effects of repeated exposures have been investigated in animal experiments. Based on published data the minimum human lethal dose of EG has been estimated at approx. 100 ml for a 70-kg adult or 1.6 g/kg body weight (calculation of dose in ml/kg to mg/kg based in EG density=1.11 g/l). However, human data from case reports are generally insufficient for the determination of a clear dose-response relationship and quantification of threshold doses for systemic toxicity, in particular renal effects, is limited. As toxicity is largely a consequence of metabolism of EG to GA, it is important to note that no signs of renal injury have developed at initial plasma glycolate concentrations of up to 10.1 mM (76.7 mg/dl). Plasma EG levels of 3.2 mM (20 mg/dl) are considered the threshold of toxicity for systemic exposure, if therapeutic strategy is based on the EG concentration alone.
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PMID:Ethylene glycol: an estimate of tolerable levels of exposure based on a review of animal and human data. 1537 38

Ethylene glycol (EG) can be found in many agents, such as antifreeze. Ingestion of EG may cause serious poisoning. Adults are typically exposed when EG is ingested as a cheap substitute for ethanol or in suicide-attempts. Children may be exposed by accidental ingestion caused by decantation of EG to unlabeled bottles. EG has in itself a low toxicity, but is in vivo broken down to four organic acids: glycoaldehyde, glycolic acid, glyoxylic acid and oxalic acid. The metabolites are cell toxins that cause central nervous system depression, and cardio-pulmonary and renal failure. Glycolic acid causes severe acidosis, and oxalate is precipitated as calcium oxalate in the kidneys and other tissues. We present five case reports of fatal EG-poisoning, and review the literature concerning clinical presentation and diagnosis, pathological findings, treatment and prevention.
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PMID:Ethylene glycol poisoning. 1622 55

Inadvertent ingestion of thiafentanil oxalate by a captive adult female mountain lion (Puma concolor) caused a prolonged clinical syndrome that included sedation and depression, muscle tension, and myopathy that was incompletely antagonized by naltrexone HCl. A serum chemistry profile revealed markedly elevated creatinine phosphokinase (CK; 490,450 IU/l), alanine aminotransferase (ALT; 1,896 IU/l), and aspartate aminotransferase (AST; 4,321 IU/l) 2 days after onset. The affected animal's condition gradually improved over the next 15 days in response to supportive therapy that included diazepam (5 mg as needed), Normasol R (3 l/day), dexamethasone (tapering dose starting at 1 mg/kg), and ketoprofen (1 mg/kg). She eventually recovered completely. Based on these observations, carcasses of animals immobilized with thiafentanil should be marked and disposed of properly to preclude opportunities for secondary exposure and potential intoxication in scavenging species. In addition, caution is advised when using thiafentanil in animals that could be preyed upon before full metabolism of the drug.
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PMID:Suspected secondary thiafentanil intoxication in a captive mountain lion (Puma concolor). 1645 79

We report a case of a 75-year-old hypertensive, diabetic man who presented to the emergency room with symptoms and signs of nausea, acute intoxication, significant alteration in mental status with rapid neurologic deterioration, and blunt impact injuries sustained during a recent altercation with a 36-year-old female companion-caretaker. He denied a history of ethanol abuse or other recent toxic ingestion and had not been diagnosed with or treated for depression. Hospital laboratory tests revealed a metabolic acidosis and a negative urine toxicology screen. He was diagnosed with toxic encephalopathy with metabolic acidosis secondary to metformin. Despite treatments including hemodialysis, he expired after approximately 28 hours of hospitalization. A postmortem anatomic examination revealed recent blunt-impact injuries and cardiac and renal pathology. A subsequent histologic examination revealed the presence of calcium oxalate crystals in the kidneys and brain, in addition to cardiac and renal pathology. Comprehensive forensic toxicologic testing was performed on antemortem and postmortem samples and revealed lethal levels of ethylene glycol. The cause of death was as a result of acute intoxication by ethylene glycol with another condition of multiple blunt impacts to the head, trunk, and extremities. The manner of death was ruled as homicide. A trial by jury, involving the female companion-caretaker, resulted in her conviction, and she was sentenced to 23 years to life in prison. In this report, we present an unusual case of homicidal ethylene glycol intoxication in which legal proceedings have occurred.
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PMID:Homicidal ethylene glycol intoxication: a report of a case. 1673 34


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