Suppressive effect of citalopram on plasma concentrations of thromboxane B2.

BACKGROUND: Citalopram, a selective serotonin reuptake inhibitor (SSRi), is widely used to treat major depression. Patients treated with SSRIs suffer more frequently from bleeding disorders caused by the antiplatelet effect of SSRIs. METHODS: To investigate the potential suppressive effect of citalopram treatment on plasma thromboxane B2 levels and its possible correlation with actual plasma concentration of citalopram. Plasma concentrations of thromboxane B2 and citalopram were examined in a cohort of 77 aspirin-treated geriatric patients before and in the third week of citalopram therapy. RESULTS: Citalopram therapy led to a significant decrease of plasma concentrations of thromboxane B2 compared to its levels before initiation of the therapy. Furthermore, we have shown negative correlation in thromboxane B2 levels and actual plasma concentration of citalopram. Actual plasma concentrations of citalopram were significantly higher compared to younger adult patients treated with similar dose. CONCLUSIONS: In this study we have shown that even short-term citalopram therapy led to a suppression of thromboxane B2 production in aspirin-treated patients. This suppressive effect correlates with actual plasma concentration of citalopram.

Routine therapeutic monitoring of the active metabolite of carbamazepine: Is it really necessary?

OBJECTIVES: Carbamazepine (CBZ) is primarily used in the treatment of epilepsy as well as trigeminal neuralgia. It is metabolised by the liver to its pharmacologically active metabolite carbamazepine-10,11-epoxide (CBZ-E), which is potentially toxic. The aim of our study was to measure CBZ and CBZ-E in our patient set and to consider the introduction of CBZ-E to routine therapeutic drug monitoring (TDM). High-performance liquid chromatography (HPLC) and Chemiluminescence Microparticle Immuno Assay (CMIA) methods for the measurement of CBZ were compared. DESIGN AND METHODS: We simultaneously measured serum concentrations of CBZ and CBZ-E using HPLC. Serum concentrations of CBZ were also analysed by CMIA. For the measurements we chose patients (ages 5-67years) on monotherapy (n=51), patients taking CBZ with antiepileptic drugs (AEDs) susceptible to pharmacokinetic interaction including phenytoin, phenobarbital, primidone and valproic acid (n=56) and patients taking other AEDs (n=44). RESULTS: Patient's serum levels of CBZ-E ranged from 1.38-27.79µmol/L with a mean value of 6.96±4.07µmol/L. The CBZ-E/CBZ ratio increased significantly in patients taking phenytoin, phenobarbital, primidone and valproic acid. CBZ concentrations measured by CMIA were lower than those obtained by HPLC (mean difference of 3.8µmol/L). The Passing and Bablok regression showed acceptable agreement between these two methods. CONCLUSIONS: Based on our results, we do not consider the introduction of the active metabolite of CBZ to routine TDM to be necessary. However, it might be beneficial in patients taking CBZ with AEDs susceptible to pharmacokinetic interaction to avoid any potential adverse effects. A close correlation between CMIA and HPLC method was found for the measurement of CBZ serum concentrations.