Summary
A patient showed excessive concentrations of desmethylclomipramine after receiving normal daily doses of clomipramine (Anafranil) and the elimination kinetics of the desmethylated metabolite was zero-order/saturable. Investigation showed that she was a poor metabolizer of debrisoquine and that, in addition, she had been treated with allopurinol, an inhibitor of hepatic drug metabolism.
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References
Brösen K, Gram LF, Klysner R, Bech P (1986) Steady-state levels of imipramine and its metabolites: Significance of dose-dependant kinetics. Eur J Clin Pharmacol 30: 43–49
Dayer P, Balant L, Kupfer A, Striberni R, Leemann T (1985) Effect of oxidative polymorphism (debrisoquine/Sparteine type) on hepatic first-pass metabolism of bufurarol. Eur J Clin Pharmacol 28: 317–320
Faravelli C, Ballerini A, Ambronetti A, Broadhurst AD, Das M (1984) Plasma levels and clinical response during treatment with clomipramine. J Affective Disord 6: 95–107
Reisby N, Gram LF, Bech P et al. (1979) Clomipramine: Plasma levels and clinical effects. Commun. Psychopharmacol., 3: 341–351
Prescorn SH, Irwin HA (1982) Toxicity of tricyclic antidepressants-kinetics, mechanism, intervention: a review. J. Clin. Psychiat., 43: 151–156
Evans DAP, Mahgoub A, Sloan TP, Idle JR, Smith RL (1980) A family and population study of the genetic polymorphism of debrisoquine oxidation in a white British population. J Med Genet., 17: 102–105
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Balant-Gorgia, A.E., Balant, L. & Zysset, T. High plasma concentrations of desmethylclomipramine after chronic administration of clomipramine to a poor metabolizer. Eur J Clin Pharmacol 32, 101–102 (1987). https://doi.org/10.1007/BF00609967
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DOI: https://doi.org/10.1007/BF00609967