INTERACTION BETWEEN CARBAMAZEPINE AND FLUVOXAMINE - INFLUENCE ON PLASMA CARBAMAZEPINE LEVELS

The current practices concerning psychotropic drugs use plasma levels for the therapeutic adaptation and for the prevention of overdose and side effects. We observed, among two patients treated with constant dosages of carbamazepine (CBZ), that the addition of fluvoxamine (FLV) has increased significantly plasma levels of CBZ. The first patient, suffering of an affective bipolar trouble (ICD-10), was hospitalized for major depression. His admission treatment was CBZ (800 mg/day) and cyamemazine (75 mg/day). The introduction of the FLV (200 mg/day) was justified by the symptomatology. Then, plasma levels of CBZ increased progressively. No clinic or biological side effect was observed. Rapidly, CBZ oral dosages were decreased, but the plasma levels of CBZ reached the therapeutic window only when the FLV prescription was definitively stopped. The other patient was hospitalized for an acute exacerbation of a paranoiac disorder. He was treated with haloperidol for this episode. For five years, he received CBZ for neuralgia of the Trigeminus. The emergence of a depressive disorder justified a FLV treatment. From the introduction of FLV, plasma levels of CBZ were significantly increased. The reduction, then the stop of the FLV treatment, has allowed the standardization of plasma concentrations of CBZ. Three similar studies were found in the literature. The danger of this interaction was notified in two studies (one case each). Furthermore, in the third study (three cases) was put forward the hypothesis of a new therapeutic pathway. This hypothesis was suggested by the fact that these two medications were proposed independently to treat impulsive behaviors. It appears clearly that this interaction is dangerous, and must be pointed out. Nevertheless, we have observed no side effect (probably because of the supervision of the plasma levels and the low dosage taken). Furthermore, we have not been able to demonstrate therapeutic efficiency of this association on impulsive behaviors. We can notice the absence of efficiency on the depressive symptoms. The most probable biological hypothesis to explain this drug interaction could be a pharmacokinetic interaction. It is conceivable, therefore, that there was a competition between these two molecules in their common hepatic oxidative pathway. In conclusion, this interaction must be pointed out. Our experience has not brought us the proof of a better clinic efficiency. However, the description of these cases appears to us important to allow more consequent investigations.