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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

One characteristic of ethylene glycol overdose is a cardiopulmonary syndrome including hypertension and pulmonary edema with pathology indicating damage to the endothelium of heart, lung and brain vessels. The mechanism of the cardiopulmonary toxicity is unknown, but has been linked with accumulation of the metabolite calcium oxalate monohydrate (COM) in the endothelium. These studies have evaluated the hypothesis that COM or the oxalate ion produces endothelial damage in vitro and that damage is linked with induction of reactive oxygen species (ROS). In cultured human umbilical vein endothelial cells (HUVEC), COM, but not the oxalate ion, produced cytotoxicity in a dose- and time-dependent manner. Using three ROS-sensitive dyes, HUVEC exposed to COM did not significantly increase ROS production. Additionally, co-treatment with three antioxidants that operate by different mechanisms did not reduce COM cytotoxicity. As such, an increase in ROS production does not explain cell death in endothelial cells. Aluminum citrate, uniquely among citrate compounds, significantly reduced COM cytotoxicity to endothelial cells and thus may act as an adjunct therapy for ethylene glycol poisoning to reduce endothelial damage. These results imply that accumulation of COM in endothelial cells is an important aspect of the cardiopulmonary toxicity from ethylene glycol.
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PMID:Calcium Oxalate Monohydrate is Associated with Endothelial Cell Toxicity But Not with Reactive Oxygen Species Accumulation. 3258 15