Platelet MAO and amitriptyline treatment

Giller, Earl L.; Jatlow, Peter; Bialos, Donald; Harkness, Laurie; Docherty, John P.

doi:10.1016/0165-1781(80)90018-9

Cited by 11 publications

(4 citation statements)

References 17 publications

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“…7). This inhibition confirms previous studies with phenelzine (Nies, 1982) and selegiline (Giller and Lieb, 1980) and has also been reported after other MAO inhibitors such as clorgyline (Murphy, Sunderland and Cohen, 1984), tranylcypromine and isocarboxazid (Giller and Lieb, 1980). Platelet MAO is a pure source of the B form of the isoenzyme (Sandler, Reveley and Glover 1981) and clearly moclobemide differs from existing MAO inhibitors in that it does not affect platelet activity.…”

Section: Resultssupporting

confidence: 87%

Clinical pharmacology of moclobemide, a new reversible monoamine oxidase inhibitor

Warrington¹,

Turner

Mant

et al. 1991

J Psychopharmacol

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The clinical pharmacology of the new reversible monoamine oxidase (MAO) inhibitor, moclobemide, was examined in three separate studies in healthy male volunteers. In a single oral dose study, moclobemide (25-150 mg) was rapidly absorbed from the gastrointestinal tract and had a relatively short plasma half-life (mean 1.3 h after 150 mg). A decrease in the plasma concentrations of the noradrenaline metabolite 4- hydroxy-3-methoxyphenylglycol (HMPG), however, indicated a longer time to peak pharmacodynamic effect and longer duration of activity. Assay of platelet MAO activity did not reveal any evidence of irreversible inhibition of the B form of the isoenzyme. Single oral doses of moclobemide (150 and 300 mg) significantly lowered the threshold to the cardiovascular effects ('cheese reaction') of intravenous tyramine. However, after repeated administration of 100 mg three times daily for over 2 weeks, moclobemide caused significantly less potentiation than did phenelzine (15 mg three times per day) on the cardiovascular effects of oral tyramine, a clinically more relevant model. The MAO-B inhibitor, selegiline (5 mg once daily), also lowered the oral tyramine threshold significantly. Moclobemide was generally well tolerated by these healthy volunteers.

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Section: Resultssupporting

confidence: 87%

Clinical pharmacology of moclobemide, a new reversible monoamine oxidase inhibitor

Warrington¹,

Turner

Mant

et al. 1991

J Psychopharmacol

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“…According to Sullivan et al (31), sedative-hypnotic effects of tricyclics correlate closely with the magnitude of platelet MA0 inhibition by these drugs. Giller et al (32) showed that platelet MA0 activity in depressed patients responsive to treatment with amitriptyline was reduced after such treatment. Kammen et al (33) examined unipolar patients whose mania developed during clomipramine treatment for depression.…”

mentioning

confidence: 99%

Studies on biogenic amine metabolizing enzymes (DBH, COMT, MAO) and pathogenesis of affective illness

Pużyński¹,

Hauptmann²,

Załuska³

1983

Acta Psychiatr Scand

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Platelet MAO activity was determined in blood from 31 healthy persons and 43 persons with endogenous depressive syndrome. It was found that the enzyme activity is significantly higher in women than in men, both in healthy controls and in affective illness groups. Statistically significant lowering of the enzyme activity was found in the group of women with affective illness as compared with healthy women controls (P less than 0.05). Although the latter phenomenon is true of all three diagnostic subgroups of affective disorder (bipolar, unipolar, undifferentiated), it is most pronounced, and statistically significant only in the group of women with an undifferentiated course of disease. A small rise in the enzyme activity was noticed in some patients during remission, as compared with a period of depression, but this was not statistically significant. Analysis of the possible links between MAO activity and the clinical picture, or the severity of depression, revealed no significant correlations. No correlation was found between the level of MAO activity and a family history of psychiatric disturbances in general, and affective disorders in particular--in either women or in men.

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“…Finally, the present work clearly shows that imipramine administered at the dose of 50 mg/day has no MAO inhibitory effect. MAO inhibition by tricyclic antidepressants has been reported in vitro (see Roth, 1976) but the contribution of such mechanism in the in vivo action of these drugs at pharmacological doses is still controversial (Bruinvels, 1972;Giller, Jatlow, Bialos, Harkness & Docherty, 1980;Halaris, Lovell & Freedman, 1973;Honecker & Hill, 1977;Kivalo, Rinne & Karinkanta, 1961;Meek & Werdinius, 1970;Roth, 1976;Schildkraut, Winokur & Applegate, 1970;Von Voigtlander & Losey, 1976). To our knowledge, the only work that reports MAO inhibition in man by tricyclic antidepressants (Sullivan, Zung, Stanfield & Cavenar, 1978) is hardly comparable with the present one because of differences in subjects, dose, parameters analysed and substrate used for platelet MAO.…”

Section: Discussionmentioning

confidence: 54%

Effect of caroxazone, a new antidepressant drug, on monoamine oxidases in healthy volunteers.

Moretti¹,

Caccia²,

Martini³

et al. 1981

Brit J Clinical Pharma

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1 Caroxazone is a new antidepressant drug with a reversible inhibitory effect on monoamine oxidases (MAO) as previously shown experimentally in animals. 2 The effect of caroxazone on MAO was explored in healthy volunteers and compared with that of tranylcypromine and imipramine. Daily urinary excretion of tryptamine and MAO activity in platelets were assayed at various times during and after treatment and the differences from basal values were statistically analysed. In addition, caroxazone plasma levels were determined. 3 Caroxazone administered orally at doses of 300 or 600 mg/day for 12 days induced a significant, dose-dependent increase in urinary tryptamine excretion. Tranylcypromine (20 mg/day for 8 days) was even more active in this respect; imipramine (50 mg/day for 12 days) was completely inactive. 4 MAO activity in platelets was not affected by caroxazone or imipramine, but was completely inhibited by tranylcypromine.5 Mean steady-state plasma levels of caroxazone were about 6 ,ug/ml and 11-12 ,ug/ml with the dose of 300 mg/day and 600 mg/day respectively. 6 It can be concluded that caroxazone is a MAO inhibitor in man too, at a clinically effective dose such as 600 mg/day. The fact that its MAO inhibition is not apparent in platelet preparation may be explained by its reversibility. 7 Tranylcypromine -confirmed its potent irreversible MAO inhibitory effect, while imipramine lacked any effect at the tested dose.

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Platelet MAO and amitriptyline treatment

Cited by 11 publications

References 17 publications

Clinical pharmacology of moclobemide, a new reversible monoamine oxidase inhibitor

Clinical pharmacology of moclobemide, a new reversible monoamine oxidase inhibitor

Studies on biogenic amine metabolizing enzymes (DBH, COMT, MAO) and pathogenesis of affective illness

Effect of caroxazone, a new antidepressant drug, on monoamine oxidases in healthy volunteers.

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