Fluvoxamine and chlorimipramine in endogenous depression

Wilde, J.E.M. De; Doogan, D P

doi:10.1016/0165-0327(82)90009-x

Cited by 70 publications

(21 citation statements)

References 9 publications

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“…The daily dose of 100-150 mg resulted in significantly more improvement than that of 50-75 mg. Many clinical trials (DeWider and Doogan, 1982;Guelfi et al, 1983;Lapierre et al, 1987) testing the efficacy of fluvoxamine in depression have been carried out with a daily dose of 100 mg and over, and those trials showed good results. The results of the present study support those findings.…”

Section: Discussionmentioning

confidence: 96%

Possible predictors of response to fluvoxamine for depression

Morishita¹,

Arita²

2002

Human Psychopharmacology

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Section: Discussionmentioning

confidence: 96%

Possible predictors of response to fluvoxamine for depression

Morishita¹,

Arita²

2002

Human Psychopharmacology

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“…Meanwhile, fluvoxamine decreased the total peripheral resistance, leading to the hypotensive action. Although in vitro vasodilator effect of fluvoxamine has not been reported, the hypotensive action has been observed in patients (de Wilde et al, 1983;de Wilde and Doogon, 1982;Granfors et al, 2004;Guelfi et al, 1983;Rodriguez de la Torre et al, 2001), which was not detected in dogs, cats (Roos, 1983) or healthy human volunteers (Robinson and Doogan, 1982). Importantly, fluvoxamine increased the LVEDP in a dose-related manner; however, the maximum value was 13 ± 1 mmHg at 10 min after the high dose, which still remained within a physiological range.…”

Section: Cardiohemodynamic Effectsmentioning

confidence: 98%

“…) and hypotensive effect (de Wilde et al, 1983;de Wilde and Doogon, 1982;Granfors et al, 2004;Guelfi et al, 1983;Rodriguez de la Torre et al, 2001) have been observed in patients during fluvoxamine treatment. In the present study, we simultaneously assessed the electropharmacological effects of fluvoxamine together with its plasma concentrations using the halothane-anesthetized in vivo canine model under physiologically maintained electrical and mechanical conditions.…”

mentioning

confidence: 99%

Fluvoxamine by itself has potential to directly induce long QT syndrome at supra-therapeutic concentrations

et al. 2015

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-Fluvoxamine is one of the typical selective serotonin-reuptake inhibitors. While its combined use with QT-prolonging drugs has been contraindicated because of the increase in plasma concentrations of such drugs, information is still limited whether fluvoxamine by itself may directly prolong the QT interval. We examined electropharmacological effects of fluvoxamine together with its pharmacokinetic profile by using the halothane-anesthetized dogs (n = 4). Fluvoxamine was intravenously administered in three escalating doses of 0.1, 1 and 10 mg/kg over 10 min with a pause of 20 min between the doses. The low dose provided therapeutic plasma drug concentration, whereas the middle and high doses attained approximately 10 and 100 times of the therapeutic ones, respectively. Supra-therapeutic concentration of fluvoxamine exerted the negative chronotropic, inotropic and hypotensive effects; and suppressed the atrioventricular nodal and intraventricular conductions, indicating inhibitory actions on Ca 2+ and Na + channels, whereas it delayed the repolarization in a reverse use-dependent manner, reflecting characteristics of rapidly activating delayed rectifier K + current channel-blocking property. Fluvoxamine prolonged the terminal repolarization phase at 100 times higher concentration than the therapeutic, indicating its proarrhythmic potential. Thus, fluvoxamine by itself has potential to directly induce long QT syndrome at supra-therapeutic concentrations.

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“…Consequently, higher dosages of fluvoxamine might be needed to treat smokers. However, we previously reported that no differences were found between responders and nonresponders in terms of either daily dosage or plasma concentrations of fluvoxamine [13], and further, fluvoxamine has a broad therapeutic range [1,2] due to the fact that interindividual pharmacokinetic variability caused by factors other than smoking is also significant.…”

Section: Discussionmentioning

confidence: 99%

“…Fluvoxamine, a selective inhibitor of serotonin reuptake, is widely used in the management of depression, obsessive-compulsive disorders, panic disorder, social phobia and eating disorders [1,2]. The specific isozymes involved in fluvoxamine metabolism have not yet been identified.…”

Section: Introductionmentioning

confidence: 99%

Interaction between Fluvoxamine and Cotinine or Caffeine

Yoshimura

Ueda²,

Nakamura³

et al. 2002

Neuropsychobiology

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We examined the relationships between plasma fluvoxamine concentrations and plasma levels of cotinine and caffeine, respectively, under steady-state conditions in 30 patients who met DSM-IV criteria for a major depressive disorder and who were being treated with fluvoxamine. The daily dosages of fluvoxamine ranged from 50 to 200 mg (mean ± SD 108 ± 42 mg). Eleven patients were smokers and the remaining 19 were nonsmokers. The plasma fluvoxamine concentrations were significantly higher in nonsmokers (0.92 ± 0.40 ng/ml/mg) than in smokers (0.56 ± 0.28 ng/ml/mg); in addition, a trend towards negative correlations was observed between the plasma fluvoxamine concentrations and the plasma cotinine levels, although it was not significant. Significant positive correlations were found between the plasma fluvoxamine concentrations and the plasma caffeine levels. These findings are compatible with those in earlier reports that cytochrome P450 1A2 plays a major role in fluvoxamine metabolism.

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Fluvoxamine and chlorimipramine in endogenous depression

Cited by 70 publications

References 9 publications

Possible predictors of response to fluvoxamine for depression

Possible predictors of response to fluvoxamine for depression

Fluvoxamine by itself has potential to directly induce long QT syndrome at supra-therapeutic concentrations

Interaction between Fluvoxamine and Cotinine or Caffeine

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