Single and Multiple Oral Dose Fluvoxamine Kinetics in Young and Elderly Subjects

Vries, M. Hugo de; Raghoebar, M.; Mathlener, I S; Harten, J. Van

doi:10.1097/00007691-199212000-00010

Cited by 59 publications

(29 citation statements)

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“…Venous blood samples (5 ml) for the determination of alprazolam and metabolites were collected into heparinized tubes (Vacutainer ®) at the following times: day 7-before and at 1,2,4,5,6,7,9,10,11,12,14,15, and 20 h after the 08.00 h dose of alprazolam; days 8-9 -before the morning dose of alprazolam; day 10 -before and at 1,2,4,5,6,7,8,9,10,11,12,14,15,16,17,19,21,24,29, and36 h after the 08.00 h dose of alprazolam. Plasma was harvested and frozen until analysed.…”

Section: Methodsmentioning

confidence: 99%

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A pharmacokinetic and pharmacodynamic evaluation of the combined administration of alprazolam and fluvoxamine

Fleishaker

Hulst

1994

Eur J Clin Pharmacol

125

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We have assessed the pharmacokinetic and pharmacodynamic interaction between fluvoxamine, a serotonin reuptake inhibitor, and alprazolam, a triazolobenzo-diazepine. Healthy men took fluvoxamine maleate daily for 10 days (50 mg on days 1-3, 100 mg on days 4-10) (n = 20), 1 mg of alprazolam four times daily for four days (days 7-10 of the study period) (n = 20), or a combination of the two (n = 20), according to a parallel study design. Alprazolam and fluvoxamine concentrations were measured in serial plasma samples by HPLC and gas chromatography respectively, and psychomotor performance and memory were assessed on days 1, 7, and 10. Fluvoxamine increased plasma alprazolam concentrations by 100%. The mean apparent half-life of alprazolam was increased from 20 h to 34 h after fluvoxamine co-administration. The increased plasma concentrations of alprazolam resulted in significantly greater reductions in psychomotor performance evident on day 10. Mean fluvoxamine plasma concentrations were about 25% lower in those who took the combination than in those who took only fluvoxamine; this was more likely due to heterogeneity between the treatment groups than to an effect of alprazolam. The dosage of alprazolam should be reduced during co-administration with fluvoxamine.

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Section: Methodsmentioning

confidence: 99%

“…The apparent volume of distribution (Vz/f) was calculated as CLm/2 z. Neither value was calculated for fluvoxamine, because steady-state fluvoxamine pharmacokinetics are poorly predicted from single-dose kinetics [9].…”

Section: Methodsmentioning

confidence: 99%

A pharmacokinetic and pharmacodynamic evaluation of the combined administration of alprazolam and fluvoxamine

Fleishaker

Hulst

1994

Eur J Clin Pharmacol

125

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“…Platelets are produced by megacaryocytes with dense granules devoid of serotonin. Platelets from patients treated with high doses of fluoxetine (40 mg/day) [91], fluvoxamine (300 mg/day) [92], paroxetine (60 mg/day), sertraline (250 mg/day) or citalo-162 E. Maurer-Spurej SSRIs and cardiovascular diseases pram (60 mg/day) [93] for 6 weeks are therefore highly depleted of intracellular serotonin. Interestingly, based on platelet immunocytochemistry, this acquired serotonin deficiency is indistinguishable from congenital serotonin disorders such as Hermansky-Pudlak syndrome [41].…”

Section: Ssris Block Serotonin Uptakementioning

confidence: 99%

Serotonin reuptake inhibitors and cardiovascular diseases: a platelet connection

Maurer‐Spurej

2005

CMLS, Cell. Mol. Life Sci.

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Selective serotonin reuptake inhibitors (SSRIs) are a heterogeneous group of new antidepressants that cause a well documented acquired but reversible serotonin deficiency in blood platelets. Platelets are small, anucleate cells and are the only blood cells specialized in storing peripheral serotonin. Platelets are also an integral part of the hemostatic process that is initiated during pathologic thrombus formation in cardiovascular diseases. Serotonin release from platelets is important for functional hemostasis as indicated by congenital diseases with serotonin-deficient platelets that can lead to life-threatening bleeding problems. The postulate that SSRIs should have an impact on cardiovascular diseases is therefore well founded. Cardiovascular effects of SSRIs have indeed been shown in a number of studies investigating the effect of SSRIs in patients with psychosomatic comorbidity. SSRIs reduce the incidence of recurrent myocardial infarction (MI) in patients suffering from post-MI depression. In addition, SSRIs inhibit tight clot formation of platelets in vitro, which points to a direct anti-thrombotic or pro-fibrinolytic effect of SSRIs.

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“…With the exception of fluoxetine, the half-lives of the SSRIs under steady-state conditions are all close to 24 h: citalopram and escitalopram 1.5 days (Milne and Goa 1991), fluvoxamine 0.5-1 day (de Vries et al 1992), paroxetine 1 day (at 20 mg/day) (Preskorn 1993(Preskorn , 1996, and sertraline 1 day (Preskorn 1993(Preskorn , 1996. For this reason, it is recommended that all but fluvoxamine be dosed once a day (Janicak et al 2001;Preskorn 1993).…”

Section: Chemistry Pharmacology and Metabolismmentioning

confidence: 99%

Selective Serotonin Reuptake Inhibitors

Preskorn

Ross²,

Stanga³

2004

Antidepressants: Past, Present and Future

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Single and Multiple Oral Dose Fluvoxamine Kinetics in Young and Elderly Subjects

Cited by 59 publications

References 0 publications

A pharmacokinetic and pharmacodynamic evaluation of the combined administration of alprazolam and fluvoxamine

A pharmacokinetic and pharmacodynamic evaluation of the combined administration of alprazolam and fluvoxamine

Serotonin reuptake inhibitors and cardiovascular diseases: a platelet connection

Selective Serotonin Reuptake Inhibitors

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