Associations Between Baseline Plasma MHPG (3-methoxy-4-hydroxyphenylglycol) Levels and Clinical Responses With Respect to Milnacipran Versus Paroxetine Treatment

Shinkai, Koji; Yoshimura, Reiji; Ueda, Nobuhisa; Okamoto, Keitaro; Nakamura, Jun

doi:10.1097/01.jcp.0000104904.75206.19

Cited by 42 publications

(64 citation statements)

References 35 publications

(36 reference statements)

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“…A trend for a positive correlation was found between the change of plasma MHPG and the HAMD17 score in the SNRI responders. These results are essentially in agreement with our previous findings [3]: the responders adsorbed materials were eluted with 200 μL of methanol to a 0.1 M phosphate buffer (pH 4.8) mixture (40:60, v/v). A 20-μL portion of this solution was injected into the HPLC system.…”

Section: Discussionsupporting

confidence: 93%

“…The values of each patient's the HAMD17 and plasma MHPG at to paroxetine showed significantly decreased plasma MHPG at week 4, whereas responders to milnacipran had significantly increased plasma MHPG at week 4 [3].…”

Section: Resultsmentioning

confidence: 89%

“…When administered to patients with MDD, some antidepressants increase plasma MHPG, whereas other antidepressants decrease or do not change the plasma MHPG level. We demonstrated that paroxetine, an SSRI, decreased plasma MHPG, and that the SNRI milnacipran increased plasma MHPG; we also reviewed the effects of several antidepressants on plasma MHPG levels [3][4][5][6][7][8][9]. We also found that plasma MHPG is useful for predicting relapse to a major depressive episode in MDD patients [8].…”

Section: Introductionmentioning

confidence: 88%

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Can Plasma Level of 3-methoxy-4-hydroxyphenylglycol Predict the Response for Selective Serotonin Reuptake Inhibitor and Serotonin Noradrenaline Reuptake Inhibitor in Major Depressive Disorder?

Yoshimura¹,

Katsuki²,

Atake³

et al. 2017

J Depress Anxiety

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IntroductionDepression is a serious mental illness requiring treatment. Major depressive disorder (MDD) is a complex disorder confounded by many bio psychosocial factors. Treatment with selective serotonin reuptake inhibitors (SSRIs) or serotonin noradrenaline reuptake inhibitors (SNRIs) is useful for MDD. The treatment of MDD requires collaborative efforts and holistic approaches by healthcare providers, public health interventions, and a reform in policies as well as the allocation of resources for the effective management of individuals with MDD, especially those with geriatric depression [1,2].A major metabolite of noradrenaline, 3-methoxy-4-hydroxyphenylglycol (MHPG), passes the blood-brain barrier. It is thought that 30% to 60% of plasma MHPG originates in the brain. When administered to patients with MDD, some antidepressants increase plasma MHPG, whereas other antidepressants decrease or do not change the plasma MHPG level. We demonstrated that paroxetine, an SSRI, decreased plasma MHPG, and that the SNRI milnacipran increased plasma MHPG; we also reviewed the effects of several antidepressants on plasma MHPG levels [3][4][5][6][7][8][9]. We also found that plasma MHPG is useful for predicting relapse to a major depressive episode in MDD patients [8]. Another of our studies showed that switching from paroxetine to milnacipran did not alter plasma MHPG levels [9]. We conducted the present study to investigate whether MDD patients' responses to an SSRI and an SNRI can be predicted based on plasma MHPG. Patients and MethodsPatients (n=240) with MDD diagnosed based on DSM-IV-TR were enrolled. All participants were undergoing monotherapy with the SSRI paroxetine (n=81), duloxetine, a selective serotonin and norepinephrine reuptake inhibitor antidepressant (SSNRI) (n=49), the SNRI milnacipran (n=48), the SSRI fluvoxamine (n=63), or the SSRI escitalopram (n=27). Only benzodiazepines were permitted during the study period. The patients (102 males, 138 females) were 42 ± 19 years old (mean ± SD). The severity of each patient's depressive state was evaluated with the 17-item Hamilton Rating Scale for Depression (HAMD17). The end-point point of the present study was week 8.Patients whose HAMD17 scores had decreased by ≥50% at the study end-point were defined as responders; others were considered non-responders. Blood was drawn twice before and 8 weeks after the start of treatment. Plasma MHPG levels were measured using highperformance liquid chromatography (HPLC) with electrochemical detection according to the method reported by Minegishi and Ishizaki [10]. Briefly, the plasma was separated by centrifugation at 600 g at 4°C. Extraction was performed under a vacuum using Bond-Elut columns (Varian, Palo Alto, CA) pre packed with 100 mg of C18-bonded silica (40 μm) in a 1 mL capacity disposable syringe. The columns, which were inserted into a vacuum chamber connected to an aspirator, were prepared by washing with 1 mL methanol followed by 1 mL of water.After the addition of 50 μL of a solution of vanillyl alcohol (in...

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Section: Discussionsupporting

confidence: 93%

Section: Resultsmentioning

confidence: 89%

Section: Introductionmentioning

confidence: 88%

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Can Plasma Level of 3-methoxy-4-hydroxyphenylglycol Predict the Response for Selective Serotonin Reuptake Inhibitor and Serotonin Noradrenaline Reuptake Inhibitor in Major Depressive Disorder?

Yoshimura¹,

Katsuki²,

Atake³

et al. 2017

J Depress Anxiety

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“…Plasma levels of catecholamine metabolites may predict the response to fl uvoxamine in major depression [15] . A negative correlation has been observed between changes in plasma catecholamine metabolites and clinical response to paroxetine in depressed patients [16] . In a previous study, we described serotonin and fl uoxetine levels in plasma and platelets of 12 depressive patients after acute and chronic administration of fl uoxetine [17] ; in this paper, we describe plasma concentrations of norepinephrine, epinephrine and dopamine observed during the previous experience and not yet reported.…”

Section: Introductionmentioning

confidence: 98%

Plasma Catecholamine Levels after Fluoxetine Treatment in Depressive Patients

Blardi

Lalla²,

Auteri³

et al. 2005

Neuropsychobiology

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It is known that selective serotonin reuptake inhibitors, widely used as antidepressive drugs, act by inhibiting the cell reuptake of serotonin, but their effect on the catecholaminergic system is not yet completely understood. In this study, we investigated plasma concentrations of norepinephrine, epinephrine and dopamine after acute and chronic administration of fluoxetine in depressive patients. Twelve patients affected by major depression received a single oral dose of fluoxetine in the morning, 5 mg in the first 5 days, 10 mg from the 6th to the 10th day and 20 mg from the 11th to the 40th day. Twelve healthy subjects received a placebo under identical testing procedures. Blood samples were collected at baseline and 7, 10 and 24 h after drug administration on the 1st day of fluoxetine administration at a dose of 5 mg, and on the 1st and the 30th day of fluoxetine administration at a dose of 20 mg (days 11 and 40 of treatment, respectively). We found that plasma norepinephrine, epinephrine and dopamine levels significantly increased after acute and chronic treatment (p < 0.001), reaching the highest concentrations on the last day. No significant changes of these parameters were observed in control patients.

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“…In depressed patients, hyposensitivity of noradrenergic receptors, indicated by attenuated growth hormone responses to the ␣ 2 -adrenoreceptor agonist clonidine, might be accompanied by good response to electroconvulsive therapy, to desipramine treatment [26] and to amitriptyline treatment [27] . Lower serum levels of MHPG in depressed patients might be accompanied by response to the serotonin-noradrenaline reuptake inhibitor milnacipran and higher levels of MHPG might be accompanied by response to the serotonin reuptake inhibitor paroxetine [28] . It can be hypothesized that depressed patients with comparatively low BPV have a relatively low noradrenergic function.…”

Section: Discussionmentioning

confidence: 99%

Basal Prolactin Values Correlate with Response to Reboxetine Treatment in Major Depression, but Not with Response to Citalopram

Moeller¹,

Hetzel²,

Michael³

et al. 2005

Neuropsychobiology

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Little is known about variables that might predict outcome in major depression. Recently, basal prolactin values (BPV) have been suggested to predict response to treatment with tricyclic antidepressive drugs. In order to examine whether BPV predict response to selective mono-aminergic therapy, 24 in-patients with major depression were treated in a single-masked, randomised study using the most selective noradrenergic or serotonergic reuptake inhibitors available for antidepressant treatment, i.e. reboxetine and citalopram. A significant correlation between BPV and treatment response to reboxetine was found, but not between BPV and response to citalopram. As BPV are influenced by noradrenergic activity, it can be hypothesized that depressed patients with comparatively high BPV have a relatively high noradrenergic function. This might explain why in our study depressed patients with the highest BPV responded strongest to selective noradrenergic treatment with reboxetine. As measurement of BPV is simple, further studies are suggested to examine the possible clinical value of the link between prolactin, noradrenergic function in major depression and treatment response.

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Associations Between Baseline Plasma MHPG (3-methoxy-4-hydroxyphenylglycol) Levels and Clinical Responses With Respect to Milnacipran Versus Paroxetine Treatment

Cited by 42 publications

References 35 publications

Can Plasma Level of 3-methoxy-4-hydroxyphenylglycol Predict the Response for Selective Serotonin Reuptake Inhibitor and Serotonin Noradrenaline Reuptake Inhibitor in Major Depressive Disorder?

Can Plasma Level of 3-methoxy-4-hydroxyphenylglycol Predict the Response for Selective Serotonin Reuptake Inhibitor and Serotonin Noradrenaline Reuptake Inhibitor in Major Depressive Disorder?

Plasma Catecholamine Levels after Fluoxetine Treatment in Depressive Patients

Basal Prolactin Values Correlate with Response to Reboxetine Treatment in Major Depression, but Not with Response to Citalopram

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