Controlled comparison of paroxetine and fluvoxamine in major depression

Ansseau, Marc; Gabriëls, A.; Loyens, J.; Bartholomé, F.; Evrard, Jean-Luc; Nayer, André; Linhart, R.; Wirtz, Janina; Bruynooghe, F; Surinx, K.; Clarysse, H.; Marganne, R.; Papart, Patrick

doi:10.1002/hup.470090502

Cited by 19 publications

(6 citation statements)

References 12 publications

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“…Two previous prospective studies with no genetic variants considered have demonstrated no significant differences in clinical response to treatment of depression between the two SSRIs [49,50] . In our previous report, we hypothesized that the reasons for the different responses of the two in SERTPR s/s genotype carriers were related to their differences in potential serotonin uptake inhibition [9] .…”

Section: Discussionmentioning

confidence: 99%

Effects of the Serotonin Type 2A, 3A and 3B Receptor and the Serotonin Transporter Genes on Paroxetine and Fluvoxamine Efficacy and Adverse Drug Reactions in Depressed Japanese Patients

et al. 2006

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In this study, we tested the influence of the serotonin type 2A, 3A and 3B receptor genes (HTR2A, HTR3A, HTR3B) in addition to a polymorphism in the promoter region of the serotonin transporter (SERTPR), and investigated the different characteristics of clinical responses to paroxetine and fluvoxamine. A total of 100 Japanese patients affected by major recurrent depression were enrolled in a randomized 6-week study. The clinical response was evaluated using the Hamilton Rating Scale for Depression (HAM-D), and adverse drug reactions were assessed at each visit. Patients with the l allele of SERTPR showed a better response to SSRIs than s/s genotype carriers (p = 0.015–0.042), more significantly to fluvoxamine. The –1438G/G genotype of HTR2A was associated with a good response to SSRIs (p = 0.010–0.039), especially to fluvoxamine, and significantly with severe nausea in paroxetine-treated patients (p = 0.013). The 178C/C genotype of the HTR3A was associated with an antidepressant response (p = 0.022–0.042), and more significantly in paroxetine-treated patients (p = 0.002–0.042). These effects were independent of one another. We replicated the finding that the SERPTR polymorphism was associated with a response to SSRIs. We additionally found that HTR2A and HTR3A polymorphisms are associated with the efficacy, and the HTR2A polymorphism is also associated with adverse drug reactions. Furthermore, the effects of these polymorphisms varied from one SSRI to another and thus may depend on the characteristics of each SSRI.

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Section: Discussionmentioning

confidence: 99%

Effects of the Serotonin Type 2A, 3A and 3B Receptor and the Serotonin Transporter Genes on Paroxetine and Fluvoxamine Efficacy and Adverse Drug Reactions in Depressed Japanese Patients

et al. 2006

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“…One study suggested that paroxetine has a more rapid onset of action and may be more effective in relieving associated anxiety than fluoxetine (28), although the differences in the onset of action and in anxiolytic activity were not confirmed in another study (107). No significant differences between paroxetine to fluvoxamine were reported in two other studies (4,60). The only study comparing paroxetine and sertraline involved hospitalized patients with delusional depression; no significant differences between the two drugs were found in patients who completed the trial (109,113).…”

Section: Clinical Studies Depressionmentioning

confidence: 99%

Paroxetine: A Review

Bourin

Chue

Guillon³

2001

CNS Drug Reviews

369

122

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Paroxetine is a potent and selective serotonin reuptake inhibitor (SSRI) with currently approved indications for the treatment of depression, obsessive-compulsive disorder, panic disorder and social phobia. It is also used in the treatment of generalized anxiety disorder, post traumatic stress disorder, premenstrual dysphoric disorder and chronic headache.Paroxetine, a phenylpiperidine derivative, is the most potent inhibitor of the reuptake of serotonin (5-hydroxytryptamine, 5-HT) of all the currently available antidepressants including the class of SSRIs. It is a very weak inhibitor of norepinephrine (NE) uptake but it is still more potent at this site than the other SSRIs. The selectivity of paroxetine, i.e., the ratio of inhibition of uptake of norepinephrine to serotonin (NE/5-HT) is amongst the highest of the SSRIs. Paroxetine has little affinity for catecholaminergic, dopaminergic or histaminergic systems and by comparison with tricyclic antidepressants (TCAs) has, therefore, has a reduced propensity to cause central and autonomic side effects. Paroxetine exhibits some affinity for the muscarinic cholinergic receptor but much less than the TCAs. In addition, the adaptive changes of somatodendritic (5-HT 1A ) and terminal (5-HT 1B/1D ) autoreceptors observed with paroxetine are different to those observed with TCAs; it also inhibits nitric oxide synthase. It is both a substrate and an inhibitor of cytochrome isoenzyme P450 2D6. Paroxetine is well absorbed orally and undergoes extensive first pass metabolism that is partially saturable. Its metabolites are pharmacologically inactive in vivo. Steady state levels are achieved after 4-14 days and an elimination half-life of 21 h is consistent with once-daily dosing. There is wide inter-individual variation in the pharmacokinetics of paroxetine in adults as well as in the young and the elderly with higher plasma concentrations and slower elimination noted in the latter. Elimi- 25

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“…In the only other direct comparison of paroxetine with an SSRI in major depression (Ansseau et al. 1994).…”

Section: (Hamd Montgomery Asberg Depression Rating Scalementioning

confidence: 99%

Paroxetine: a Review of Clinical Experience

Dunner¹,

Kumar²

1998

Pharmacopsychiatry

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The selective serotonin reuptake inhibitor paroxetine has been extensively studied and is now an established therapy for the treatment of depressive disorders. Paroxetine has demonstrated efficacy in major depression in both young and elderly patients, with an improved tolerability profile over conventional antidepressants. Paroxetine is effective across a continuum of anxiety and depressive disorders, including severe depression, depression with anxiety, comorbid depression and obsessive-compulsive disorder. The first agent of its class licensed for use in panic disorder, paroxetine has been shown to be effective in reducing the number of panic attacks and preventing relapse. A worldwide clinical database has established that paroxetine has a benign adverse event profile. Paroxetine therefore offers an effective and well tolerated treatment for a broad spectrum of psychiatric disorders.

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Controlled comparison of paroxetine and fluvoxamine in major depression

Cited by 19 publications

References 12 publications

Effects of the Serotonin Type 2A, 3A and 3B Receptor and the Serotonin Transporter Genes on Paroxetine and Fluvoxamine Efficacy and Adverse Drug Reactions in Depressed Japanese Patients

Effects of the Serotonin Type 2A, 3A and 3B Receptor and the Serotonin Transporter Genes on Paroxetine and Fluvoxamine Efficacy and Adverse Drug Reactions in Depressed Japanese Patients

Paroxetine: A Review

Paroxetine: a Review of Clinical Experience

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