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At least 595 records · Page 33Linked to original sources
PubMed1992

Prolonged toxicity with intermediate syndrome after combined parathion and methyl parathion poisoning.

A prolonged type of organophosphate toxicity, previously characterized as the Intermediate Syndrome, has been recognized in 6 out of 7 prospectively studied patients poisoned by insecticide containing parathion and methyl parathion in equal proportions. The clinical characteristics included respiratory paresis, weakness in the territories of several motor cranial nerves, neck flexors and proximal limb muscles, and depressed tendon reflexes, all lasting for several days or weeks. Electromyography in the early stages disclosed diverse types of impaired neuromuscular transmission. EMG normalization preceded clinical recovery. Severe plasma butyrylcholinesterase and erythrocyte acetylcholinesterase inhibition persisted along with the occurrence of Intermediate Syndrome-related symptoms. We conclude that combined parathion and methyl parathion poisoning is more likely to induce Intermediate Syndrome than parathion poisoning alone. The mechanisms underlying this difference remain obscure. The Intermediate Syndrome shows clinical and electromyographic hallmarks of combined postsynaptic impairment of neuromuscular transmission.

Adult↗
PubMed1994

Organophosphate poisoning: peripheral vascular resistance--a measure of adequate atropinization.

We report severe organophosphate poisoning complicated by hypotension and ischemic sequelae in two patients with pre-existing vascular disease. Both patients had a low total peripheral resistance and high cardiac output that were significantly reversed by doses of atropine in excess of those required to control other muscarinic symptoms. Cerebral infarcts and gangrene requiring a below knee amputation were complications of the poisonings. It is proposed that the ischemic complications are due to paradoxical vasoconstriction by acetylcholine at sites of endothelial injury. One patient, who had taken fenthion, also had a significantly delayed peak and prolonged, 2-3 week, systemic toxicity. We propose that stability of the plasma cholinesterase at 6 to 8 h after temporarily suspending oxime provides a rapid guide to the duration of therapy, especially in patients whose complications make clinical assessment difficult.

Acetylcholinesterase↗
PubMed1995

Acute organophosphate poisoning after disulfoton ingestion.

A 75-year-old woman attempted suicide by ingesting a large quantity of granular Di-Syston which is an organophosphate insecticide containing 5% disulfoton (ethylthiometon). On admission, the total plasma phosphorodithioate sulfone concentration (disulfoton and its metabolites, phosphorodithioate sulfoxide and its sulfone) determined by gas chromatography was 1095 ng/mL. After gastric lavage, the concentration gradually decreased to 505 ng/mL. However, it began to increase again 20 h after admission and reached the peak concentration (1322 ng/mL) at 56 h. It was concluded that the secondary elevation of the plasma concentration was due to the prolonged absorption of the organophosphate from the residual granules in the stomach, despite the early gastric lavage. Pralidoxime iodide administration temporarily restored erythrocyte cholinesterase activity to almost normal and inhibited the excessive, delayed reduction of cholinesterase activity. It is recommended that poisoning with the granular form of disulfoton should be treated with repetitive or prolonged gastric and intestinal lavage, charcoal, and a continuous intravenous infusion of pralidoxime iodide in addition to atropine sulfate.

Aged↗
PubMed1996

Pharmacokinetics following a loading plus a continuous infusion of pralidoxime compared with the traditional short infusion regimen in human volunteers.

BACKGROUND: Many authors currently recommend infusing the adult dose (1 g) of pralidoxime over a 15-30 minute period. When administered in this manner, computer simulations predict that plasma pralidoxime concentrations will fall below 4 mg/L as early as one and one half hours after administration. The objective of this study was to assess whether a loading dose followed by a continuous infusion would maintain therapeutic levels longer than the traditional short infusion regimen of pralidoxime if the same total dose was administered. METHODS: Utilizing a randomized, crossover design, healthy volunteers were administered either 16 mg/kg of pralidoxime intravenous over 30 minutes or 4 mg/kg of pralidoxime intravenous over 15 minutes followed by 3.2 mg/kg/h for 3.75 h (for a total dose of 16 mg/kg). Pralidoxime levels were obtained at 0, 10, 20, 30, 60, 120, 180, 240, 300, and 390 minutes and patients were observed for vital sign changes and adverse effects. RESULTS: Seven subjects completed both arms of the study. One subject's data were excluded from pharmacokinetic analysis due to aberrant plasma pralidoxime analysis. The loading dose followed by the continuous infusion maintained therapeutic levels for 257.3 +/- 50.5 minutes whereas the short infusion maintained therapeutic levels for 118.1 +/- 52.1 (p < 0.001). Adverse effects were encountered during the short infusion regimen which did not occur during the continuous infusion. Dizziness or blurred vision occurred in all subjects during the short infusion regimen. Additionally, statistically significant increases in diastolic blood pressure occurred during the short infusion regimen. CONCLUSIONS: The results of this study indicate that a loading dose followed by a continuous infusion of pralidoxime maintains therapeutic concentrations for a longer period of time than the currently recommended short infusion regimen in healthy volunteers.

Adult↗
PubMed1976

Reactivation studies on organophosphate inhibited human cholinesterases by pralidoxime (P-2-AM).

There is biochemical and clinical evidence that P-2-AM (Pyridine-2-Aldoxime Methiodide, Pralidoxime) does not reactive human acetylcholinesterase inhibited by either Malathion or Malaoxon. In vitro studies using Pralidoxime iodide up to ten times the recommended concentrations, produced insignificant reactivation of cholinesterases inhibited by Malathion or Malaoxon. This was observed inspite of prolonged exposure of the inhibited cholinesterases to the oxime. The value of Pralidoxime as a reactivator of phosphorylated cholinesterases is therefore in doubt, and should not be used in preference to large doses of atropine and other supportive treatment in poisoning by organophosphate pesticides.

Acetylcholinesterase↗
PubMed1976

[Reactivation of phosphorylated acetylcholinesterase (AChE): quaternary salts of vinylogous pyridinaldoxims (author's transl)].

Application of Wittig reaction to 4-pyridinecarboxaldehyde leads to 4-beta-formylvinylpyridine (62%). The corresponding oxime (4-(2)) can be quaternized with alpha,alpha'-bis-(chloromegonin), and with methyliodide one to 4-PAM (4-(3)). In this case the formal insertion of an ethylenic double bond between the pyridinium ring and the aldoxime group decreases the ability to reactivate phosphorylated acetylcholinesterase (AChE).

Acetylcholinesterase↗
PubMed1999

Accidental injection of a U.S. Air Force aviator by a pralidoxime chloride auto-injector: a case report.

To counter the threat of organophosphate nerve agents, military personnel may be issued auto-injectors containing pralidoxime chloride. This drug helps to dephosphorylate the nerve agent-acetylcholinesterase complex and, thus, regenerate the enzyme. In non-poisoned persons, pralidoxime chloride is rapidly excreted by the kidneys and is fairly well tolerated. We present the first reported case of an accidental injection of an Air Force aviator by an auto-injector. The patient recovered well with no specific treatment needed. The pharmacology and toxicology of pralidoxime chloride are discussed.

Accidents, Occupational↗