Determination of free 3-methoxy-4-hydroxyphenylglycol with several other monoamine metabolites in plasma by high-performance liquid chromatography with amperometric detection

Minegishi, Akemi; Ishizaki, Takashi

doi:10.1016/s0378-4347(00)84690-3

Cited by 60 publications

(27 citation statements)

References 22 publications

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“…In the present study, we reconfirmed our previous finding that SSRI-induced nausea is associated with higher p5-HIAA levels after drug administration, but is not related with the baseline serotonin activities [19], using other groups of subjects treated with paroxetine or fluvoxamine. In addition, we found the incidence of nausea to be higher in patients treated with fluvoxamine than in those treated with paroxetine.…”

Section: Discussionsupporting

confidence: 89%

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Higher Plasma 5-Hydroxyindoleacetic Acid Levels Are Associated with SSRI-Induced Nausea

et al. 2003

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We investigated the association between selective serotonin reuptake inhibitors (SSRIs; paroxetine or fluvoxamine) and nausea with regard to plasma 5-hydroxyindoleacetic acid (p5-HIAA) levels. Forty-eight patients meeting the DSM-IV criteria for major depressive disorder and treated with paroxetine or fluvoxamine participated in this study. p5-HIAA levels after SSRI administration were significantly higher in the nausea group than those in the nonnausea group (nausea group: 8.0 ± 4.6 ng/ml; nonnausea group: 3.6 ± 2.2 ng/ml; p < 0.01). On the other hand, no significant difference was found between the nausea and nonnausea group in terms of p5-HIAA levels before each drug administration. These results suggest that SSRI-induced nausea is associated with serotonergic hyperactivity in the gastrointestinal tract.

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Section: Discussionsupporting

confidence: 89%

“…p5-HIAA levels were analyzed by high-performance liquid chromatography according to the method of Minegishi and Ishizaki [19].…”

Section: Methodsmentioning

confidence: 99%

Higher Plasma 5-Hydroxyindoleacetic Acid Levels Are Associated with SSRI-Induced Nausea

et al. 2003

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“…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.…”

Section: Methodsmentioning

confidence: 99%

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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“…2223 Plasma concentrations of catecholamines were measured with the reported HPLC-ECD method 24 with alumina adsorption and subsequent elution with weak acids. 23 …”

Section: Methodsmentioning

confidence: 99%

Plasma 3-methoxy-4-hydroxyphenylethyleneglycol and homovanillic acid concentrations in patients with subarachnoid hemorrhage.

Minegishi¹,

Ishizaki²,

Yoshida³

et al. 1987

Stroke

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To ask if the determination of central-nervous-system-derived catecholamine metabolites in peripheral circulation could be a useful index of brain dysfunction after subarachnoid hemorrhage, 3-methoxy-4-hydroxyphenylethyleneglycol and homovanillic acid concentrations in plasma, together with those of free catecholamines (noradrenaline, adrenaline, and dopamine), were serially measured for up to 3 weeks after the initiation of symptoms in 23 patients with aneurysmal subarachnoid hemorrhage as compared to 17 healthy and 9 patient controls. Catecholamines and their metabolites were determined by using high-performance liquid chromatography with electrochemical detection. Plasma 3-methoxy-4-hydroxyphenylethylenegtycol concentrations were markedly elevated in subarachnoid hemorrhage patients with coma compared to those without, and the maximal concentrations observed in comatose patients never occurred in normal subjects or in patients with other neurological disorders. The mean maximal plasma concentrations of free catecholamines did not differ significantly between the comatose and noncomatose groups. Combining 3-methoxy-4-hydroxyphenylethyleneglycol with homovanillic acid level data more clearly discriminated between the comatose and noncomatose subarachnoid hemorrhage groups. The results suggest that plasma concentration of 3-methoxy-4-hydroxyphenylethyleneglycol, a major metabolite of brain noradrenaline, can be a prognostic discriminator for patients with subarachnoid hemorrhage and its discriminating power can be strengthened by combining it with homovanillic acid data. (Stroke 1987;18:223-228) D URING the past decade, convincing evidence I has accumulated indicating that free 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG), a major metabolite of brain noradrenaline, in the systemic circulation reflects a functional activity of noradrenergic neurons in the central nervous system (CNS).1 Free MHPG concentration in plasma is considered a reliable index of central noradrenergic turnover from the highly significant relation between plasma and brain levels in primates treated with drugs altering the central noradrenaline metabolism.2 In humans, a centrally acting a-adrenergic agonist, clonidine, is reported to reduce plasma MHPG level.3 Maas et al 4 have demonstrated that approximately 60% of total MHPG production in humans is derived from the brain, while others have indicated that the proportion may be lower because of the possible peripheral conversion of MHPG to vanillylmandelic acid.3 As well as of MHPG, plasma concentration of a major dopamine

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Determination of free 3-methoxy-4-hydroxyphenylglycol with several other monoamine metabolites in plasma by high-performance liquid chromatography with amperometric detection

Cited by 60 publications

References 22 publications

Higher Plasma 5-Hydroxyindoleacetic Acid Levels Are Associated with SSRI-Induced Nausea

Higher Plasma 5-Hydroxyindoleacetic Acid Levels Are Associated with SSRI-Induced Nausea

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 3-methoxy-4-hydroxyphenylethyleneglycol and homovanillic acid concentrations in patients with subarachnoid hemorrhage.

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