Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034069 (pulmonary fibrosis)
 7,050 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Paraquat is a bipyridyl compound with no known chronic toxicity or teratogenicity. It is poorly absorbed when inhaled, but causes severe illness when ingested orally, death usually occurring within 2 days of ingestion of 50 mg/kg. At lower doses death may be delayed for several weeks. The toxic compound accumulates in lung tissue where free radicals are formed, lipid peroxidation is induced and nicotinamide adenine dinucleotide phosphate (NADPH) is depleted. This produces diffuse alveolitis followed by extensive pulmonary fibrosis. The most important prognostic indicator is the quantity of paraquat absorbed, as shown by the plasma paraquat concentration. While renal failure will develop in the majority of those patients who eventually die, it may not, if present alone, indicate a fatal outcome. The absence of caustic burns in the upper digestive tract indicates a good prognosis. Treatment of paraquat poisoning remains ineffective, but Fuller's earth, activated charcoal and resins may prevent some absorption of the toxin. When tubular necrosis occurs, renal excretion of the compound decreases rapidly. A 3-compartment pharmacokinetic model has been described following ingestion of tracer doses including a 'deep' compartment for active pulmonary accumulation. Haemodialysis, haemoperfusion and forced dialysis have been attempted, with no clear improvement in survival rates. Superoxide dismutase, glutathione peroxidase, N-acetylcysteine and other 'free radical scavengers' have failed to alter the outcome in poisoned patients. Other theoretical treatments, such as deferoxamine, immunotherapy, NADPH repletion and lung transplantation still require clinical validation.
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PMID:Paraquat poisoning. An overview of the current status. 219 50

Since a mouthfull of the herbicidal compound Paraquat usually results in death from caustic burns, renal tubular necrosis, circulatory failure of pulmonary fibrosis, the fact that 11 out of 28 people poisoned in the period 1972-1980 survived deserves consideration. The most significant prognostic factors appear to be: (1) the mode of penetration: all 4 patients poisoned through the skin and/or the respiratory tract survived; (2) the volume of Paraquat absorbed: death from circulatory failure occurs within less than 72 hours with more than 50 mg/kg, while 35 to 50 mg/kg produce progressive pulmonary fibrosis; (3) the content of the stomach at the time of ingestion: food can neutralize the compound; (4) the finding of gastric lesions on early endoscopy; (5) evidence of acute renal failure; finally and mostly (6) Paraquat blood levels during the first 24 hours, as measured by radioimmune assays; lethal levels are 2.0, 0.6, 0.3, 0.16 and 0.10 mg/l at 4, 6, 10, 16, and 24 hours respectively. There is no overlapping between values obtained in patients who died and survivors. In this series, the course of the intoxication, as predicted from the initial prognostic factors, was unmodified by the treatments applied (Fuller's earth, dialysis, charcoal haemoperfusion, furosemide, immediate hypooxygenation). The survival of two patients with restrictive respiratory pathology seems to be ascribable to the circumstances of poisoning rather than to the treatment.
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PMID:[Paraquat poisoning. Prognostic and therapeutic evaluation in 28 cases]. 715 25

Paraquat poisoning is very severe. When it is ingested, this herbicide may be responsible for causative lesions of the digestive tract, cytolytic hepatitis, renal tubular necrosis, circulatory failure, and/or pulmonary fibrosis. Since a very low dose (as little as one mouthful) is potentially lethal, it is important to understand why 11 of our 28 patients who entered our department for paraquat poisoning survived. The main prognostic factors appear to be the following: Route of administration. Of four patients who had inhaled paraquat aerosols and/or contaminated their skin with the herbicide, all survived. Ingested amount. Above 50 mg/kg, patients died of circulatory failure within 72 h; between 35 and 50 mg/kg, a progressive pulmonary fibrosis occurred. Delay between ingestion and the last meal. Paraquat is adsorbed and neutralized by foodstuffs. Caustic gastric lesions revealed by early endoscopic examination. The occurrence of an organic renal failure. The plasma paraquat concentrations within the first 24 h. Patients whose plasma concentrations do not exceed 2.0, 0.6, 0.3, 0.16, and 0.1 mg/L at 4, 6, 10, 16, and 24 h, respectively, are likely to survive. The different treatments that have been tested (fuller's earth, forced diarrhea, furosemide, hemodialysis, hemoperfusion, artificial ventilation with hypoxic breathing mixtures) did not modify the initial prognosis. The 11 survivals are only linked to the circumstances of the poisonings (route of administration, ingested amount, delay between ingestion and the last meal, etc.). The treatments did not modify the outcome.
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PMID:Prognosis and treatment of paraquat poisoning: a review of 28 cases. 717 91

The clinical and pathological findings are described in 14 patients who died between 6 hours and 26 days after drinking paraquat. Respiratory failure and delayed pulmonary fibrosis have become the hallmark of this poison, but were not the common mode of death in this series. Toxic myocarditis, renal tubular necrosis and centrilobular liver cell damage were significant factors in the eight deaths which occurred within 5 days of paraquat ingestion. Similar abnormalities plus respiratory failure caused the two deaths which occurred 5 and 6 days after consumption of the poison. Respiratory failure was the sole cause of death in only four patients who died 8 to 26 days after drinking paraquat, although the lungs showed pathological changes in all cases. The patients who died in multisystem failure, with one exception, had drunk larger quantities of paraquat than those who survived for a longer period and died in respiratory failure.
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PMID:The changing pattern of paraquat poisoning in man. 735 46

Acute poisoning with pesticides is a global public health problem and accounts for as many as 300,000 deaths worldwide every year. The majority of deaths occur due to exposure to organophosphates, organochlorines and aluminium phosphide. Organophosphate compounds inhibit acetylcholinesterase resulting in acute toxicity. Intermediate syndrome can develop in a number of patients and may lead to respiratory paralysis and death. Management consists of proper oxygenation, atropine in escalating doses and pralidoxime in high doses. It is Important to decontaminate the skin while taking precautions to avoid secondary contamination of health personnel. Organochlorine pesticides are toxic to the central nervous system and sensitize the myocardium to catecholamines. Treatment involves supportive care and avoiding exogenous sympathomimetic agents. Ingestion of paraquat causes severe inflammation of the throat, corrosive injury to the gastrointestinal tract, renal tubular necrosis, hepatic necrosis and pulmonary fibrosis. Administration of oxygen should be avoided as it produces more fibrosis. Use of immunosuppressive agents have improved outcome in patients with paraquat poisoning. Rodenticides include thallium, superwarfarins, barium carbonate and phosphides (aluminium and zinc phosphide). Alopecia is an atypical feature of thallium toxicity. Most exposures to superwarfarins are harmless but prolonged bleeding may occur. Barium carbonate Ingestion can cause severe hypokalaemia and respiratory muscle paralysis. Aluminium phosphide is a highly toxic agent with mortality ranging from 37% to 100%. It inhibits mitochondrial cytochrome c oxidase and leads to pulmonary and cardiac toxicity. Treatment is supportive with some studies suggesting a beneficial effect of magnesium sulphate. Pyrethroids and insect repellants (e.g. diethyltoluamide) are relatively harmless but can cause toxic effects to pulmonary and central nervous systems. Ethylene dibromide-a highly toxic, fumigant pesticide-produces oral ulcerations, followed by liver and renal toxicity, and is almost uniformly fatal. Physicians working in remote and rural areas need to be educated about early diagnosis and proper management using supportive care and antidotes, wherever available.
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PMID:Pesticide poisoning. 1808 24