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Dear colleagues,
I found two interesting articles on gastrointestinal motility and CYP2D6
metabolism of codeine. Unfortunately their conclusions are totally
contradictory. Is it codeine or its metabolites (M, M6G, M3G and NM)
that are responsible for the influence on motility?
Ref:
1. Hasselstrom J et al. Eur J of Clin Pharmacol 1997 (n=24)
2. Mikus G et al. Clin Pharmacol & Ther 1997 (n=8)
Erik
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As far as I am aware the effect of codeine on gastrointestinal
activity should be a function of the agonist character of the
individual compound and the effect site concentrations. In this case,
codeine, morphine, and M6G should have activity- don't know about
normorphine or codeine glucuronide, though. M3G definitely should
have no activity unless its rumoured non-opiate action is of
importance.
Steve Graham
s.g.graham.-at-.ncl.ac.uk
http://www.ncl.ac.uk/~nsgg/
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Andrew Sutton
Guildford Clinical Pharmacology.
ASutton.aaa.gcpl.co.uk
It seems that mu receptors are the main site of action (Shook JE et al,
Peptide opiate antagonist separates peripheral and central opioid
antitransit effects. J Pharmacol Exp ther 1987 243: 492-500) and Murphy
DB et al (Anesthesiology, October 1997, vol 84 4 :765-770) showed that it
is mediated largely by peripheral receptors even though rat studies
indicate that central receptors do also have an influence (Parolaro D et
al Effect of intracerebroventricular administration of morphine upon
intestinal motility in rats and its antagonism by naloxone. Eu J
Pharmacol 1977 46 329). Accordingly, it would seem that potency at mu
receptors would be the key indicator of activity of codeine...and its
metabolites
Andrew Sutton
Andrew Sutton
ASutton.-a-.gcpl.co.uk
Guildford Clinical Pharmacology
Telephone +44 (0) 1483 406886
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Copyright 1995-2010 David W. A. Bourne (david@boomer.org)