Literature DB >> 9541034

Variation in human plasma cholinesterase activity during low-dose cocaine administration.

R S Hoffman1, T Thompson, G C Henry, D K Hatsukami, P R Pentel.   

Abstract

BACKGROUND: Cocaine is metabolized by a number of enzymes, the activity of one of which, plasma cholinesterase has been associated with dinical manifestations of toxicity. Patients with life-threatening complications of cocaine intoxication have lower plasma cholinesterase activity than less toxic controls. In addition, relatively healthy cocaine users have lower plasma cholinesterase activity than noncocaine using controls. Thus, low plasma cholinesterase activity could be a contributing factor to cocaine toxicity, a consequence of cocaine use, or a confounding variable. The following study was designed to further assess the relationship between cocaine use and plasma cholinesterase activity.
METHODS: We studied fluctuations in plasma cholinesterase activity in nine subjects enrolled in an inpatient study of the behavioral pharmacology of smoked cocaine. Subjects used at least 2 g of cocaine weekly for at least 1 year prior to enrollment. The subjects were admitted to the research unit where they remained drug-free for 2 days. They then received smoked cocaine for 4 days (up to 405 mg over 5 hours daily) and were then drug-free again for 2 days. Plasma cholinesterase activity was measured at 9 AM and 4 PM each day.
RESULTS: Baseline plasma cholinesterase ranged from 265 to 930 U/L (normal > 450 U/L). The mean plasma cholinesterase increased 112+/-100 U/L from day 1 to day 8 (p = 0.025). There was no daily change in plasma cholinesterase levels from 9 AM to 4 PM (15+/-165 U/L, p > 0.6), and there was no difference in the daily change between high- and low-dose cocaine days (-3+/-137 U/L vs 28+/-165 U/L, p = 0.52).
CONCLUSION: These preliminary data suggest that plasma cholinesterase levels do not change over a 7-hour period as a result of cocaine administration, but may increase during a period of inpatient study. Such an increase could potentially influence the pharmacokinetics or effects of cocaine studied in an inpatient setting and may give insight into the etiology of the observed low-plasma cholinesterase activity in cocaine users.

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Year:  1998        PMID: 9541034     DOI: 10.3109/15563659809162576

Source DB:  PubMed          Journal:  J Toxicol Clin Toxicol        ISSN: 0731-3810


  2 in total

1.  Mechanisms of acute cocaine toxicity.

Authors:  Kennon Heard; Robert Palmer; Nancy R Zahniser
Journal:  Open Pharmacol J       Date:  2008

2.  Heart rate variability by triangular index in infants exposed prenatally to cocaine.

Authors:  Sudhir Ken Mehta; Dennis M Super; Ann Salvator; Linda Goetz Fradley; David Connuck; Elizabeth S Kaufman
Journal:  Ann Noninvasive Electrocardiol       Date:  2002-10       Impact factor: 1.468

  2 in total

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