Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case is presented of a fatal ingestion of Furadan (carbofuran), a cholinesterase-inhibiting carbamate insecticide. A 26-year-old white male was found dead with a partially filled 1-gal (3.8-L) container of Furadan 4F insecticide-nematocide (44.9% carbofuran). The individual had ingested approximately 345 mL of the mixture. Analysis of cholinesterase activity in various biological fluids was performed spectrophotometrically using propionylthiocholine and 5,5'-dithiobis-2-nitrobenzoic acid [Sigma Diagnostics, cholinesterase procedure No. 422 (PTC)] which was measured at 405 nm and 30 degrees C in a Gilford Stasar III Spectrophotometer. The cholinesterase activities were as follows: plasma, 245 units (U)/L (93% inhibition/7% normal activity); serum, 208 U/L (95.3% inhibition/4.7% normal activity); whole blood, 297 U/L (92.8% inhibition/7.2% normal activity); erythrocytes, 58 U/L (99% inhibition/1% normal activity); vitreous humor, 7 U/L; and bile, 148 U/L. Carbofuran was detected in the blood and gastric contents by thin-layer chromatography. No alcohol or other drugs were detected in the blood, urine, or gastric contents. Ingestion of the carbofuran produced acute visceral congestion and pulmonary edema. Death was caused by anoxia due to respiratory paralysis produced by cholinesterase inhibition from Furadan (carbofuran) ingestion.
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PMID:Poisoning from oral ingestion of carbofuran (Furadan 4F), a cholinesterase-inhibiting carbamate insecticide, and its effects on cholinesterase activity in various biological fluids. 842 60

Aldicarb toxicosis was diagnosed in 200 sheep that died suddenly. Carbamate insecticide toxicosis was suspected based on observed clinical signs (hypersalivation, diarrhea, urination, paddling, seizures, miosis, and deaths occurring within 1 hour). Tissue samples were submitted from 4 Columbian ewes for pathologic and analytical evaluation. Severe diffuse pulmonary edema was observed on gross and histologic examination. Inhibition of cholinesterase activity in retina (21.2-68.1% of normal activity, n = 3), brain (40.6-45.6% of normal activity, n = 3), and whole blood (27% of normal activity, n = 1) supported a diagnosis of carbamate toxicosis. Reversal of brain and whole blood cholinesterase activities (reactivation factor greater than 1.4) following an in vitro 1 hour incubation at 37 C was also consistent with carbamate poisoning. Aldicarb toxicosis was confirmed following its detection in rumen contents at 1.5, 5.5, and 334 ppm using both high-pressure liquid chromatography with UV detection and gas chromatography with nitrogen/phosphorus detection.
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PMID:Aldicarb toxicosis in a flock of sheep. 155 68

In this review, some common food plants and their toxic or otherwise bioactive components and mycotoxin contaminants have been considered. Crucifers contain naturally occurring components that are goitrogenic, resulting from the combined action of allyl isothiocyanate, goitrin, and thiocyanate. Although crucifers may provide some protection from cancer when taken prior to a carcinogen, when taken after a carcinogen they act as promoters of carcinogenesis. The acid-condensed mixture of indole-3-carbinol (a component of crucifers) binds to the TCDD receptor and causes responses similar to those of TCDD. Herbs contain many biologically active components, with more than 20% of the commercially prepared human drugs coming from these plants. Onion and garlic juices can help to prevent the rise of serum cholesterol. Most herbs used in treatments may have many natural constituents that act oppositely from their intended use. Some herbs like Bishop's week seed contain carcinogens, and many contain pyrrolizidine alkaloids that can cause cirrhosis of the liver. The general phytoalexin response in plants (including potatoes, tomatoes, peppers, eggplant, celery, and sweet potatoes) induced by external stimuli can increase the concentrations of toxic chemical constituents in those plants. In potatoes, two major indigenous compounds are alpha-solanine and alpha-chaconine, which are human plasma cholinesterase inhibitors and teratogens in animals. Because of its toxicity, the potato variety Lenape was withdrawn from the market. Celery, parsley, and parsnips contain the linear furanocoumarin phytoalexins psoralen, bergapten, and xanthotoxin that can cause photosensitization and also are photomutagenic and photocarcinogenic. Celery field workers and handlers continually have photosensitization problems as a result of these indigenous celery furanocoumarins. A new celery cultivar (a result of plant breeding to produce a more pest-resistant variety) was responsible for significant incidences of phytophotodermatitis of grocery employees. Since there is no regulatory agency or body designated to oversee potential toxicological issues associated with naturally occurring toxicants, photodermatitis continues to occur from celery exposure. Sweet potatoes contain phytoalexins that can cause lung edema and are hepatotoxic to mice. At least one of these, 4-ipomeanol, can cause extensive lung clara cell necrosis and can increase the severity of pneumonia in mice. Some phytoalexins in sweet potatoes are hepatotoxic and nephrotoxic to mice. The common mushroom Agaricus bisporus contains benzyl alcohol as its most abundant volatile, and A. bisporus and Gyromitra esculenta both contain hydrazine analogues. Mycotoxins are found in corn, cottonseed, fruits, grains, grain sorghums, and nuts (especially peanuts); therefore, they also occur in apple juice, bread, peanut butter, and other products made from contaminated starting materials.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Natural pesticides and bioactive components in foods. 240 25

In patients poisoned with a cholinesterase inhibitor, the diagnosis may initially be missed especially when no history is available from the patient or his relatives. The predominant respiratory symptoms may suggest pulmonary oedema as illustrated by the two case reports presented here. A high degree of suspicion and a careful clinical examination are necessary to make the correct diagnosis, which eventually can be confirmed by measurement of red cell and serum cholinesterase activity.
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PMID:Acute cholinesterase inhibitor poisoning mimicking pulmonary oedema. 280 Aug 85

Disease secondary to heroin abuse constitutes a rarity in Spain. While there had been no previous cases in earlier years four young heroin addicts were admitted to the Hospital "1st de Octubre" for severe medical complications of their addiction within the last twelve months. Two patients were admitted in deep coma due to drug overdose, being cardiac arrhythmias and pulmonary edema the main associated complications. Cardiac rhythm disturbances are due to a heightened vagal tone, either secondary to inhibition of acetylcholine hydrolysis or to hypoxia, hypercapnia, and acidosis, factors that diminish cholinesterase activity and act synergistically to increase vagal tone. Pulmonary edema secondary to heroin overdose is non-cardiogenic and probably due to hypoxia added to the local action of heroin on the alveolocapillary membrane. The goal of therapy in such cases is to obtain an appropriate alveolar ventilation, the use of continuous positive pressure ventilation being required when there is pulmonary edema. The third patient had staphylococcal pneumonia with multiple abscess formation secondary to venous septic embolization originated peripherally where the drug was injected. Finally, the fourth patient was admitted because of a clinical and biochemical picture of HBsAg negative acute viral hepatitis, having suffered a similar clinical picture three years previously.
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PMID:[Severe medical sequelae in heroin addicts]. 720 89

Aflatoxin (AF)-contaminated and fumonisin B1 (FB1)-contaminated (culture material from Fusarium moniliforme) diets were fed singly and in combination to growing cross-bred barrows. Six barrows (3 replicates of 2 each; mean body weight, 17.5 kg) per group were fed: 0 mg of AF and 0 mg of FB1/kg of feed (control); 2.5 mg of AF/kg of feed; 100 mg of FB1/kg of feed; or 2.5 mg of AF plus 100 mg of FB1/kg of feed for 35 days. The effects on production performance, serum biochemical, hematologic, immunologic, and pathologic measurements were evaluated. Body weight, gain, and feed consumption were significantly (P < 0.05) decreased by AF and AF plus FB1 diets. The FB1 diet decreased feed consumption, and although body weight was numerically decreased, it was not statistically significant. Aflatoxin increased serum gamma-glutamyltransferase (GGT) activity and total iron concentration and decreased urea nitrogen concentration and unsaturated iron-binding capacity. The FB1-alone diet increased serum GGT activity, whereas the AF plus FB1 diet increased serum aspartate transaminase, cholinesterase, alkaline phosphatase, and GGT activities, increased RBC count, triglycerides, and total iron concentrations, and decreased unsaturated iron-binding capacity and urea nitrogen concentration. For the most part, the effects of the AF plus FB1 diet on body weight and hematologic measurements could be considered additive. However, the effect of the AF plus FB1 diet on cholinesterase and alkaline phosphatase activities was greater than additive and was a synergistic response. One pig in the FB1-diet group and 2 pigs in the combination-diet group died. Postmortem lesions in pigs of the FB1-diet group consisted of ascites and increased liver weight. Observations at necropsy for pigs of the AF plus FB1-diet group consisted of hydrothorax, ascites, pulmonary edema, gastric erosions and ulceration, and increased liver and spleen weights. The AF diet increased relative liver weight and resulted in liver that was pale, rubbery, and resistant to cutting. Histologic lesions consisted of hepatic necrosis or degeneration, or both, with variable degrees of bile duct proliferation in barrows of the AF-diet groups. Renal tubular nephrosis was observed in barrows of the FB1-diet group, but this was not consistent in the AF plus FB1-diet group. Cell-mediated immunity, as measured by mitogen-induced lymphoblastogenic stimulation index, was decreased in barrows of the AF and FB1-diet groups, and values in barrows given the combination diet were significantly decreased from those in barrows given the single toxin diets. It was concluded that AF and FB1 (from culture material), singly or in combination, can adversely affect clinical performance, serum biochemical, hematologic, and immunologic values and induce lesions in growing barrows. For most of the variables we evaluated under our study conditions and dosages of toxins, measurements were affected more by the combination diet than by either single toxin diet, and the toxic responses could be described as additive or more than additive, particularly for induction of liver disease.
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PMID:Influence of aflatoxin and fumonisin B1-containing culture material on growing barrows. 859 31

Inhalation, skin absorption or ingestion of insecticides containing organic phosphorus may result in abrupt onset of serious illness several hours following exposure. Because of the acute onset, often at night, the patients usually are observed by the first available physician rather than by an industrial physician. Prompt recognition and adequate treatment are essential to prevent death. The organic phosphorus radical has the specific effect of inactivating cholinesterase in the body. When cholinesterase is reduced below a critical level continuous stimulation of the entire parasympathetic nervous system results. The major symptoms are diarrhea, vomiting, pulmonary edema, respiratory difficulty and tonic convulsions. Myosis is frequently present and when found is almost pathognomonic, especially if associated with other symptoms. Treatment consists essentially of heroic doses of atropine or a similar parasympathetic inhibitor, plus supportive therapy. Patients who do not die recover rapidly and completely, but they should not risk re-exposure until cholinesterase activity in the blood reaches a static level which may take as long as ten weeks.
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PMID:Organic phosphorus poisoning in general practice; parathion, TEPP, HEPT, EPN and others. 1305 22

From 1982 to 1989, inclusive, 20 poisonings were investigated by the Ontario Ministry of Agriculture and Food following ingestion by domestic livestock of granular insecticides including terbufos (13 poisonings), disulfoton (two poisonings), fonofos (two poisonings), phorate (two poisonings), and carbofuran (one poisoning); all are used for rootworm (Diabrotica spp.) control in corn. A further three poisonings of livestock occurred following the ingestion of the foliar insecticide, endosulfan (two poisonings), and the seed protectant insecticides diazinon plus lindane (one poisoning). There were six poisoning cases as a result of excessive topical applications of the three insecticides coumpahos, fenthion, and lindane as dusts or sprays to control external parasites. Together, these events caused the deaths of 258 domestic animals of which 200 were cattle, 23 were swine, and 35 were sheep. Not all deaths are reported to the Ministry and the cases reported here may only represent 30-50% of the actual deaths over the period. Based on total populations of livestock, the percent losses were very small but they represent serious losses to individual growers. The economic loss is estimated at $160,000 over the eight years, or $20,000 per annum, and this does not include veterinary costs.Some of the poisoned animals died within as little as three to four hours of ingestion while others were sick but survived for several days. Lethal doses of insecticide were found in the rumen, abomasum, or stomach of dead animals. Signs typical of cholinesterase inhibition caused by organophosphorus poisoning were observed in most cases. Cholinesterase readings were found to be zero in dying animals. Necropsy findings were rarely more than pulmonary edema or myocardial hemorrhage. Where organochlorine insecticides were ingested, convulsions were the major manifestation.Contamination of feed was most often accidental, and chemical analysis was most helpful in identifying both potent and minor sources, thus facilitating cleanup procedures.
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PMID:A review of insecticide poisonings among domestic livestock in southern Ontario, Canada, 1982-1989. 1742 67

Cardiac complications often accompany poisoning with organophosphates. These may be serious and often fatal, being represented by cardiac arrhythmias, electrocardiographic abnormalities and conduction defects, as well as myocardial infarction, a rarely reported complication of acute pesticide poisoning. The extent and pathogenesis of cardiac toxicity from these compounds is not yet clearly defined. We report the case of a 57-year-old woman who presented to our emergency department with coma and acute non-cardiogenic pulmonary edema, as a result of organophosphates ingestion. She was resuscitated for asystole presented shortly after admission; prolonged QTc interval, ST-T changes, right bundle branch block, ventricular tachycardia were recorded. Finally she developed acute anteroseptal myocardial infarction and died despite serum cholinesterase normalization. We believe that admission in an intensive care unit, careful electrocardiographic and enzymatic monitoring of all patients is important for the diagnosis and treatment of cardiac complications of organophosphates poisoning.
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PMID:[Electrocardiographic changes in acute organophosphate poisoning]. 1838 78

Organophosphorus chemical warfare agents (nerve agents) are to be feared in military operations as well as in terrorist attacks. Among them, VX (O-ethyl-S-[2-(diisopropylamino)ethyl] methylphosphonothioate) is a low volatility liquid that represents a percutaneous as well as an inhalation hazard if aerosolized. It is a potent irreversible cholinesterase (ChE) inhibitor that causes severe signs and symptoms, including respiratory dysfunction that stems from different mechanisms. VX-induced pulmonary oedema was previously reported in dogs but mechanisms involved are not well understood, and its clinical significance remains to be assessed. An experimental model was thus developed to study VX-induced cardiovascular changes and pulmonary oedema in isoflurane-anaesthetized swine. In the course of this study, we observed a fast and unexpected rebound of plasma ChE activity following inhibition provoked by the intravenous injection of 6 and 12 microg kg(-1) of VX. In whole blood ChE activity, the rebound could stay unnoticed. Further investigations showed that the rebound of plasma esterase activity was neither related to spontaneous reactivation of ChE nor to VX-induced increase in paraoxonase/carboxylesterase activities. A bias in Ellman assay, haemoconcentration or severe liver cytolysis were also ruled out. All in all, these results suggest that the rebound was likely due to the release of butyrylcholinesterase into the blood stream from ChE producing organs. Nature of the organ(s) and mechanisms involved in enzyme release will need further investigations as it may represent a mechanism of defence, i.e. VX scavenging, that could advantageously be exploited.
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PMID:An unexpected plasma cholinesterase activity rebound after challenge with a high dose of the nerve agent VX. 1845 Mar 56


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