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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Metabolic pathways have been elucidated for various chemical and solvent exposures in humans. Clinical laboratory analyses in most chemical and solvent exposures are directed toward identification and quantitation of unchanged substance in serum or whole blood. For example, most laboratories routinely screen for unchanged ethylene glycol in suspected poisonings and quantitate ethylene glycol in positive cases even though toxicity from ethylene glycol exposure (including central nervous system depression, acute renal failure, and elevated anion gap metabolic acidosis) is primarily caused by one metabolite-glycolic acid. One objective of this manuscript is to describe the authors' clinical experience with glycolic acid analysis in ethylene glycol human poisonings. Recommended clinical laboratory tests for small hospitals and toxicology reference laboratories are presented to rule out or confirm ethylene glycol exposure. Another concern with laboratory support in ethylene glycol poisoning is correct identification of ethylene glycol because analysis of this substance is often problematic. In one case laboratories incorrectly identified an organic acid from an inherited metabolic disease as ethylene glycol, and in another case the intentional ethylene glycol poisoning of an infant was determined to be the results of an endogenous organic acid. The most robust analytical methods for determining ethylene glycol and glycolic acid are chromatographic methods. Ideally, screening methods for ethylene glycol should be confirmed by another method based on a different principle of analysis or include simultaneous metabolite analysis (glycolic acid). In centers where several ethylene glycol cases present annually, toxicology laboratories supporting these centers should incorporate glycolic acid monitoring in their ethylene glycol screening programs and include analysis of both ethylene glycol and glycolic acid during treatment (hemodialysis) in all confirmed poisonings. Measurement of glycolic acid provides important diagnostic and prognostic information that one cannot correlate with the amount of ethylene glycol in serum or whole blood.
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PMID:Clinical toxicologic implications of ethylene glycol and glycolic acid poisoning. 1189 69

Whole-cell patch clamp recordings were made from neurons in the central nucleus of the inferior colliculus (ICC) in brain slices from rat (8-13 days old). ICC neurons were classified by their discharge pattern in response to depolarizing and hyperpolarizing current injection. Excitatory postsynaptic currents (EPSCs) were elicited by stimulation of synaptic inputs under the condition that the synaptic inhibition was suppressed by strychnine and picrotoxin. EPSCs in all tested types of ICC neurons showed posttetanic, long-term potentiation (LTP) and long-term depression with tetanic stimulation. The potentiated EPSCs consisted of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor and NMDA receptor mediated components. The magnitude of LTP was larger when the intracellular concentration of the calcium buffer ethylene glycol-bis (beta-aminoethyl ether)-N,N,N',N'-tetracetic acid (EGTA) was lower and stimulation frequency was higher in cells with rebound firing patterns. Blocking N-methyl-D-aspartate (NMDA) receptors in rebound cells prevented generation of LTP. These results suggest that excitatory synaptic transmission in ICC neurons can be modified. LTP in the auditory midbrain may be important for activity-dependent, adaptive changes in response to normal and pathological stimulus conditions.
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PMID:Synaptic modification in neurons of the central nucleus of the inferior colliculus. 1211 8

Ingestion of ethylene glycol may be an important contributor in patients with metabolic acidosis of unknown cause and subsequent renal failure. Expeditious diagnosis and treatment will limit metabolic toxicity and decrease morbidity and mortality. Ethylene glycol poisoning should be suspected in an intoxicated patient with anion gap acidosis, hypocalcemia, urinary crystals, and nontoxic blood alcohol concentration. Fomepizole is a newer agent with a specific indication for the treatment of ethylene glycol poisoning. Metabolic acidosis is resolved within three hours of initiating therapy. Initiation of fomepizole therapy before the serum creatinine concentration rises can minimize renal impairment. Compared with traditional ethanol treatment, advantages of fomepizole include lack of depression of the central nervous system and hypoglycemia, and easier maintenance of effective plasma levels.
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PMID:Treatment of ethylene glycol poisoning. 1232 72

Ethylene glycol (EG) toxicosis was diagnosed on postmortem examination in a white leghorn chicken. The clinical signs were sudden onset of depression, ataxia, convulsions and death. Natural cases of EG toxicosis have not been reported in chickens. This report highlights the importance of including EG toxicosis on differential diagnoses lists for sudden onset of depression, ataxia and death in chickens.
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PMID:Ethylene glycol toxicosis in chickens. 1258 96

For survival in adverse environments where there is drought, high salt concentration or low temperature, some plants seem to be able to synthesize biochemical compounds, including proteins, in response to changes in water activity or osmotic pressure. Measurement of the water activity or osmotic pressure of simple aqueous solutions has been based on freezing point depression or vapor pressure deficit. Measurement of the osmotic pressure of plants under water stress has been mainly based on vapor pressure deficit. However, differences have been noted for osmotic pressure values of aqueous polyethylene glycol (PEG) solutions measured by freezing point depression and vapor pressure deficit. For this paper, the physicochemical basis of freezing point depression and vapor pressure deficit were first examined theoretically and then, the osmotic pressure of aqueous ethylene glycol and of PEG solutions were measured by both freezing point depression and vapor pressure deficit in comparison with other aqueous solutions such as NaCl, KCl, CaCl(2), glucose, sucrose, raffinose, and bovine serum albumin (BSA) solutions. The results showed that: (1) freezing point depression and vapor pressure deficit share theoretically the same physicochemical basis; (2) theoretically, they are proportional to the molal concentration of the aqueous solutions to be measured; (3) in practice, the osmotic pressure levels of aqueous NaCl, KCl, CaCl(2), glucose, sucrose, and raffinose solutions increase in proportion to their molal concentrations and there is little inconsistency between those measured by freezing point depression and vapor pressure deficit; (4) the osmotic pressure levels of aqueous ethylene glycol and PEG solutions measured by freezing point depression differed from the values measured by vapor pressure deficit; (5) the osmotic pressure of aqueous BSA solution measured by freezing point depression differed slightly from that measured by vapor pressure deficit.
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PMID:Theoretical and experimental studies on freezing point depression and vapor pressure deficit as methods to measure osmotic pressure of aqueous polyethylene glycol and bovine serum albumin solutions. 1496 46

As a response to recent expression of concern about possible unreliability of vapor pressure deficit measurements (K. Kiyosawa, Biophys. Chem. 104 (2003) 171-188), the results of published studies on the temperature dependence of the osmotic pressure of aqueous polyethylene glycol solutions are shown to account for the observed discrepancies between osmolality estimates obtained by freezing point depression and vapor pressure deficit osmometry--the cause of the concern.
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PMID:Reappraisal of disparities between osmolality estimates by freezing point depression and vapor pressure deficit methods. 1283 36

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

Chronic hepatitis C (HCV) infection affects more than 170 million people throughout the world and 2 to 3 million Americans. End-stage liver disease secondary to chronic HCV infection is the most frequent indication for liver transplantation in this country. Currently, the gold standard for treatment for immunocompetent patients is a combination of peginterferon (PEG-IFN) and ribavirin for 6 to 12 months depending on the genotype. This treatment achieves a sustained virological response (SVR) in 54% to 61% of patients overall. Almost 50% of patients do not respond or have recurrences posttreatment and progress in over 10 to 20 years into chronic liver disease and its complications. Liver transplantation is the only therapeutic modality that impacts on quality of life and survival of these patients. However, recurrence of HCV in the new allograft is universal with accelerated progression to cirrhosis in 5 to 10 years. Response to treatment is usually low (20% to 30%), and associated with significant side effects and depression. A significant percentage of patients with recurrent HCV after transplantation require retransplantation to control the complications of end-stage liver disease. Other solid organ transplants recipients already HCV-positive, or infected at the time of transplantation from blood transfusions or an infected graft, develop accelerated, progressive liver disease facilitated by the adverse effects of immunosuppression in addition to HCV replication. To prevent morbidity, mortality, and high costs related to the consequences of HCV infection, all solid organ transplant candidates should be tested for HCV infection and treated appropriately with PEG-IFN and ribavirin prior to transplantation.
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PMID:Should patients with chronic hepatitis C infection be transplanted? 1525 56

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

A 34-year-old male with a long-standing history of polysubstance abuse and depression was admitted for acute renal failure and hemodialysis secondary to ethylene glycol ingestion that occurred two days prior. The patient was admitted with documented ethylene glycol levels of 41.2 mg/dl, which fell to 25.0 mg/dl after 8 hours and to 6 mg/dl after 12 hours. One week later the patient presented to the outpatient eye clinic complaining of headaches and diplopia. On exam, vision in both eyes was 20/20. No afferent papillary defect was present. The patient had a left abducens palsy. The remainder of the anterior segment exam was normal. On dilated fundus exam the patient was found to have 3+ disc edema with hemorrhages in both eyes. A lumbar puncture revealed elevated intracranial pressure. In our opinion, the patient developed a left abducens nerve palsy and bilateral disc edema secondary to a transient rise in intracranial pressure after ingestion of ethylene glycol.
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PMID:Papilledema and abducens nerve palsy following ethylene glycol ingestion. 1559 May 39


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