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Abstract
Patients with acute cocaine poisoning present with life-threatening symptoms involving several organ systems. While the effects of cocaine are myriad, they are the result of a limited number of cocaine-protein interactions, including monoamine transporters, neurotransmitter receptors and voltage-gated ion channels. These primary interactions trigger a cascade of events that ultimately produce the clinical effects. The purpose of this article is to review the primary interactions of cocaine and the effects that these interactions trigger. We also describe the progression of symptoms observed in cocaine poisoning as they relate to serum cocaine concentrations.
Highlights
Introduction/BackgroundCocaine use contributes to tens of thousands of emergency department (ED) visits and hundreds of deaths each year
Patients who die of acute cocaine poisoning overdose likely have peak serum cocaine concentrations exceeding 10 microM, this estimation is limited by the quality of available data
It is important to note that the increase in serum concentrations for each of these factors is less than 60%, well within the inter-subject variation reported in dosing studies and well below the 20-fold increase that would be required to achieve the mean cocaine concentrations reported in post-mortem samples from overdose patients
Summary
Cocaine use contributes to tens of thousands of emergency department (ED) visits and hundreds of deaths each year. While cocaine use is coincident in most cases, (e.g. trauma, psychiatric or infections), cocaine poisoning accounts for many of these visits. The major effects of cocaine poisoning include CNS effects such as agitation, seizures and psychosis, and cardiovascular effects such as dysrhythmias, myocardial infarction and cardiovascular collapse. The pharmacology of cocaine is complex with effects occurring simultaneously in several organ systems. The initial event for all of these systems is simple; cocaine binds to membrane bound proteins including transporters, receptors and voltage gated ion channels. A specific signal is triggered (or inhibited), and the combination of these effects produces the clinical manifestations of cocaine poisoning. By describing serum cocaine concentrations and the affinity of cocaine for relevant proteins, we will describe the mechanisms of acute cocaine poisoning to assist clinicians to understand the progression of cocaine poisoning and to suggest potential treatments for acute cocaine poisoning
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