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Psychiatric Times. Vol. 23 No. 6
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Psychotropic Drugs: Brain and Plasma Pharmacokinetics and the Therapeutic Window

By Gerhard Gründer | May 1, 2006

Antidepressants

More recently, PET (and SPECT) technology has been applied to the characterization of antidepressant drugs. However, since radioligands for the noradrenaline transporter are still essentially lacking, the selective serotonin reuptake inhibitors (SSRIs) have been characterized with regard to their binding to the serotonin transporter (5- HTT). The quantification of binding of psychotropic drugs to serotonin receptors such as 5-HT2 and 5-HT1A is still somewhat experimental.

Meyer and colleagues10 have demonstrated that clinical doses of various SSRIs occupy more than 80% of the 5- HTT in depressed patients. For patients treated with 20 mg/d of paroxetine(Drug information on paroxetine), the mean 5-HTT occupancy was 83%, and for those treated with 20 mg/d of citalo-pram, it was 77%. The 5-HTT occupancy increased in a nonlinear manner; with paroxetine, 5-HTT occupancy reached a plateau of approximately 85% at serum paroxetine levels above 28 g/mL (Figure 4 [see May 2006 Psychiatric Times, page 61]). Fluvoxamine(Drug information on fluvoxamine) has been shown to lead to 80% 5-HTT occupancy at 50 mg/d or a plasma concentration of approximately 30 ng/mL.11

Assuming that the basic therapeutic principle of treatment with SSRIs is a blockade of 5-HTT, a substantial increase in serum level above the 30 ng/mL threshold (for both paroxetine and fluvoxamine) might lead to a higher incidence of side effects and higher drug costs without increasing clinical effectiveness. Furthermore, saturated 5-HTTs combined with high doses of antidepressants can explain the fact that, in general, relationships between plasma concentrations of SSRIs and clinical treatment response to relatively high oral doses of these drugs cannot be detected. It might also explain the relatively flat dose-response relationship of SSRIs in patients with depression. Increasing the SSRI dose in these nonresponding patients does not substantially increase remission rates (however, the situation might be different with other diseases such as obsessive-compulsive disorder).

It must be noted, however, that individuals differ in their absorption and metabolism of SSRIs. Some patients may require unusually high SSRI doses in order to reach the blood level required for optimal 5-HTT binding. Thus, the notion of a flat response curve is only valid in the aggregate; an individual patient may not fit that model. On the other hand, a rapid metabolizer in the P450 CYP2D6 system might present with very low paroxetine (or any other drug that is metabolized via CYP2D6) plasma concentrations at clinical doses. These patients usually do not respond to treatment because their corresponding 5-HTT occupancy is also too low. Interestingly, the threshold values determined with PET are markedly lower than those of Bauman and associates.9 These discrepancies underline the need for further research with larger clinical samples and in combination with nuclear imaging technology.

Other compounds

Information on the relationship between plasma and brain pharmacokinetics and their relationship to clinical parameters is almost completely lacking for most of the other psychotropic agents. For lithium(Drug information on lithium), carbamazepine(Drug information on carbamazepine), and valproic acid, therapeutic plasma levels have been determined, but their effective brain targets are virtually unknown. Benzodiazepines and nonbenzodiazepine hypnotics, such as zolpidem(Drug information on zolpidem) as receptor agonists, occupy only a small percentage of their target receptors at clinical doses, which makes their measurement with PET or SPECT technology unreliable. Quantification of cholinesterase inhibitor effects in the human brain has not reached clinical importance yet.

Conclusions

Modern nuclear imaging technology has improved our understanding of the relationships between the binding of psychotropic drugs to their molecular targets in the human brain and to their concentrations in plasma and from there to clinical variables such as efficacy and side effects. This is especially true for the class of antipsychotics, and to some extent, for antidepressants. Knowledge of some of these essential relationships helps to decrease the number of patients who are nonresponders, reduce the incidence of side effects, avoid serious toxicity, and decrease the total cost of drug therapy.

Dr Gründer is a professor of psychiatry in the Department of Psychiatry and Psychotherapy at RWTH Aachen University in Aachen, Germany.

Dr Gründer reports that he has served as a consultant for Bristol-Myers Squibb, Janssen, Otsuka, Pfizer, and Astra Zeneca. He has served on the speakers bureau of Bristol- Myers Squibb, Otsuka, Pfizer, Astra Zeneca, Eli Lilly, and Wyeth. He has received grant support from Bristol Myers Squibb, Pfizer, and Sanofi Synthelabo.

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Drugs Mentioned in This Article

Aripiprazole (Abilify)
Carbamazepine (Carbatrol, Tegretol, others)
Citalopram (Celexa)
Clozapine (Clozaril)
Fluvoxamine (Luvox)
Lithium (Eskalith)
Olanzapine (Zyprexa)
Paroxetine (Paxil)
Quetiapine (Seroquel)
Risperidone (Risperdal)
Valproic acid (Depakote, others)
Ziprasidone (Geodon)
Zolpidem (Ambien)

References

1. Hiemke C, Dragicevic A, Gründer G, et al. Therapeutic monitoring of new antipsychotic drugs. Ther Drug Monit. 2004;26:156-160.
2. Farde L, Wiesel FA, Halldin C, Sedvall G. Central D2-dopamine receptor occupancy in schizophrenic patients treated with antipsychotic drugs. Arch Gen Psychiatry. 1988;45:71-76.
3. Gründer G, Landvogt C, Vernaleken I, et al. The striatal and extrastriatal D2/D3 receptor-binding profile of clozapine in patients with schizophrenia. Neuropsychopharmacology. Oct 12, 2005 [E pub ahead of print].
4. Kapur S, Seeman P. Does fast dissociation from the dopamine d(2) receptor explain the action of atypical antipsychotics? A new hypothesis. Am J Psychiatry. 2001;158:360-369.
5. Gründer G, Carlsson A, Wong DF. Mechanism of new antipsychotic medications: occupancy is not just antagonism. Arch Gen Psychiatry. 2003;60:974-977.
6. Cohen ST, Rulf D, Pies R. Extrapyramidal side effects associated with aripiprazole coprescription in 2 patients. J Clin Psychiatry. 2005;66:135-136.
7. Kapur S, Remington G, Zipursky RB, et al. The D2 dopamine receptor occupancy of risperidone and its relationship to extrapyramidal symptoms: a PET study. Life Sci. 1995;57:PL103-PL107.
8. Gefvert O, Eriksson B, Persson P, et al. Pharmacokinetics and D2 receptor occupancy of long-acting injectable risperidone (Risperdal Consta) in patients with schizophrenia. Int J Neuropsychopharmacol. 2005;8:27-36.
9. Baumann P, Hiemke C, Ulrich S, et al; Arbeitsgemeinschaft fur neuropsychopharmakologie und pharmakopsychiatrie. The AGNP-TDM expert group consensus guidelines: therapeutic drug monitoring in psychiatry. Pharmacopsychiatry. 2004;37:243-265.
10. Meyer JH, Wilson AA, Ginovart N, et al. Occupancy of serotonin transporters by paroxetine and citalopram during treatment of depression: a [(11)C]DASB PET imaging study. Am J Psychiatry. 2001;158:1843-1849.
11. Suhara T, Takano A, Sudo Y, et al. High levels of serotonin transporter occupancy with low-dose clomipramine in comparative occupancy study with fluvoxamine using positron emission tomography. Arch Gen Psychiatry. 2003;60:386-391.


 
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