Hostname: page-component-78c5997874-m6dg7 Total loading time: 0 Render date: 2024-11-17T18:17:34.797Z Has data issue: false hasContentIssue false
  • English
  • Français

Acetylator status and inhibition of platelet monoamine oxidase following treatment with pheneizine

Published online by Cambridge University Press:  09 July 2009

Celia M. Yates  and
J. B. Loudon
Celia M. Yates*
Affiliation:
MRC Brain Metabolism Unit, Department of Pharmacology, University of Edinburgh
J. B. Loudon
Affiliation:
MRC Brain Metabolism Unit, Department of Pharmacology, University of Edinburgh
*
1Address for correspondence: Dr Celia M. Yates, MRC Brain Metabolism Unit, University Department of Pharmacology, I George Square, Edinburgh EH8 9JZ.
Get access Rights & Permissions [Opens in a new window]

Synopsis

The activity of platelet monoamine oxidase(MAO)was measured in 22 severely depressed patients before and after treatment with 45 mg and 60 mg phenelzine. The per cent inhibition of platelet MAO after both doses was not related to acetylator status.

Phenelzine, since it is a hydrazine derivative, is probably metabolized by polymorphic acetylation. Patients who were phenotypically slow acetylators have been reported to show a better clinical response (Johnstone & Marsh, 1973) and more side-effects (Evans et al. 1965) to a given dose of phenelzine than patients who were fast acetylators.

Type
Preliminary Communication
Information
Psychological Medicine , Volume 9 , Issue 4 , November 1979 , pp. 777 - 779
Copyright
Copyright © Cambridge University Press 1979

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Emson, P. C., Bush, B. M. H. & Joseph, M. H. (1976). Transmitter metabolising enzymes and free amino acid levels in sensory and motor nerves and ganglia of the shore crab (carcinus maenas). Journal of Neurochemistry 26, 779–783.CrossRefGoogle Scholar
Evans, D. A. P., Davison, K. & Pratt, R. T. C. (1965). The influence of acetylator phenotype on the effects of treating depression with phenelzine. Clinical Pharmacology and Therapeutics 6, 430–435.CrossRefGoogle ScholarPubMed
Johnstone, E. C. (1976). The relationship between acetylator status and inhibition of monoamine oxidase, excretion of free drug and antidepressant response in depressed patients on pheneizine. Psychopharmacologia (Berlin) 46, 289–294.CrossRefGoogle Scholar
Johnstone, E. C. & Marsh, W. (1973). The relationship between response to phenelzine and acetylator status in depressed patients. Proceedings of the Royal Society of Medicine 66, 947–949.CrossRefGoogle ScholarPubMed
Nies, A., Robinson, D. S., Ravaris, C. L. & Ives, J. O. (1974). The efficacy of the MAO inhibitor phenelzine: dose effects and prediction of response. Journal de Pharmacologie 5, Supplement 1, 100–101.Google Scholar
Ravaris, C. L., Nies, A., Robinson, D. S., Ives, J. O., Lamborn, K. R. & Korson, L. (1976). A multiple-dose, controlled study of phenelzine in depression-anxiety states. Archives of General Psychiatry 33, 347–350.CrossRefGoogle ScholarPubMed
Robinson, D. S., Nies, A., Ravaris, C. L. & Lamborn, K. R. (1973). The monoamine oxidase inhibitor, phenelzine, in the treatment of depressive-anxiety states. Archives of General Psychiatry 29, 407–413.CrossRefGoogle ScholarPubMed
Schröder, H. (1972). Simplified method for determining acetylator phenotype. British Medical Journal iii, 506–507.CrossRefGoogle Scholar