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In ten subjects with various affective disorders, phenytoin (100 mg orally three times a day) decreased the mean steady-state peak plasma concentration (Cmax), trough plasma concentration (Cmin) and area under the concentration-time curve (AUC) of quetiapine (250 mg orally three times a day) by 66%, 89% and 80%, respectively, compared to administration of quetiapine alone. The mechanism is phenytoin induction of CYP450 3A4, the isoenzyme responsible for the metabolic clearance of quetiapine. Caution is advised in administering quetiapine to patients who will be experiencing conditions that may contribute to an elevation in core body temperature, such as strenuous exercise, exposure to extreme heat, dehydration, or concomitant treatment with anticholinergic medications {01}. However, disopyramide, procainamide, and quinidine have the potential to add to the possible QT-interval–prolonging effects of quetiapine overdosage {01}. , clozapine, risperidone, olanzapine, quetiapine, ziprasidone) are at an increased risk of developing hyperglycemia and/or diabetes mellitus. For these reasons, quetiapine should be used only in those patients with chronic illness that is responsive to antipsychotic medication, and for whom potentially less harmful treatments are unavailable or inappropriate {01}. Also, changes in the lenses of the eyes have been observed in patients during long-term quetiapine therapy, although a causal relationship to quetiapine has not been established {01}. These effects were still present 2 weeks after discontinuation of quetiapine in the rats that had received 1. The effectiveness of quetiapine for more than 6 weeks has not been evaluated in controlled trials {01}{02}. However, the mean plasma clearance of quetiapine in elderly patients was 30 to 50% less than in younger patients {01}. Also, bretylium may add to the hypotensive effect of quetiapine, due to additive alpha-adrenergic receptor blockade {01}. Also, the smallest effective dose of quetiapine should be used and the need for continuing treatment should be assessed periodically {01}. In a 1-year quetiapine toxicity study, median serum prolactin concentrations were increased a maximum of 32-fold in male rats, and 13-fold in female rats {01}. In ten subjects with various affective disorders, the 3A4 inducer phenytoin (100 mg orally three times a day) decreased the mean steady-state peak plasma concentration (Cmax), trough plasma concentration (Cmin) and area under the concentration-time curve (AUC) of quetiapine (250 mg orally three times a day) by 66%, 89% and 80%, respectively. If signs and symptoms of tardive dyskinesia appear, discontinuation of quetiapine treatment should be considered if clinically feasible {01}{02}. Eleven months later, quetiapine was introduced and the patient once again developed acute symptoms of cholestasis which later resolved after quetiapine discontinuation. Although clinical data are lacking, the possibility of prolonged and/or increased pharmacologic effects of quetiapine should be considered. Quetiapine has no significant affinity for cholinergic muscarinic or benzodiazepine receptors {01}. If discontinuation has been for less than one week, quetiapine may be reinstituted at the previous maintenance dosage {01}. However, the possibility of a diminished therapeutic response to quetiapine should be considered in patients receiving concomitant therapy with these agents.


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