Abstract
TDM was introduced in Sweden in the early 1970's for monitoring treatment of depression with TCAs, characterized by large interindividual differences in pharmacokinetics, narrow therapeutic range, concentration-dependent adverse effects, and slow onset of action. For antipsychotics, TDM started in the late 1980's, coinciding with the re-introduction of clozapine, to improve its safety with respect to CNS toxicity. Today, SSRIs and SNRIs have largely replaced TCA in the treatment of depression and anxiety disorders and most psychotropic drugs have a spectrum of approved indications. Polytherapy is common. Thus, establishing concentration-effect relationships is increasingly challenging. TDM is still equally valid for assessing whether the patient has reasonable, high or low serum concentrations in relation to dose, for identification of drug interactions, or for follow-up over time in relation to individually determined “target concentrations” (1).
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