No Association between the Response to the Addition of an Atypical Antipsychotic Drug to an Selective Serotonin Reuptake Inhibitor or Serotonin Norepinephrine Reuptake Inhibitor and the Brain-Derived Neurotrophic Factor (Val66Met) Polymorphism in Refractory Major Depressive Disorder in Japanese Patients
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Objective: This study examined the association between the brain-derived neurotrophic factor (BDNF) (Val66Met) polymorphism and the response to the addition of an atypical antipsychotic drug to a selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor (SNRI) in treatment-refractory depression. Methods: The study enrolled 64 patients meeting the Diagnostic and Statistical Manual of Mental Disorders-IV criteria for major depressive disorder who were treated with at least two courses of a single antidepressant, but who had Hamilton Depression Rating Scale (HAMD-17) scores ≥15 points that were reduced less than 50% over at least a 4-week treatment period. There were 24 males and 40 females (age range 27-68 years; mean±SD, 48±13 years). The patients' clinical improvement was evaluated using the HAMD-17. Patients with at least a 50% decrease in the HAMD-17 score were defined as responders. Serum BDNF levels were assayed using enzyme-linked immunosorbent assays and the presence of the BDNF (Val66Met) polymorphism was determined using the TaqMan genotyping assay. Results: No correlation was found between the BDNF (Val66Met) polymorphism and a positive response to adding an atypical antipsychotic drug. No differences were observed in the changes in the serum BDNF levels and HAMD-17 scores between Val66Val and Met-carriers. In addition, in patients who experienced remission, the atypical antipsychotic drug was discontinued after at least 3 months of treatment and the patients were then followed for 1 year; 14 of 27 patients (52%) relapsed within 1 year. Conclusion: These results suggest that the BDNF (Val66Met) polymorphism is not associated with the response to the augmentation of a SSRI or SNRI with an atypical antipsychotic drug, and that the combination of an atypical antipsychotic drug and a SSRI or SNRI should be continued for 3 months or more in refractory depressed patients in the Japanese population.
Abstract
Objective: This study examined the association between the brain-derived neurotrophic factor (BDNF) (Val66Met) polymorphism and the response to the addition of an atypical antipsychotic drug to a selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor (SNRI) in treatment-refractory depression. Methods: The study enrolled 64 patients meeting the Diagnostic and Statistical Manual of Mental Disorders-IV criteria for major depressive disorder who were treated with at least two courses of a single antidepressant, but who had Hamilton Depression Rating Scale (HAMD-17) scores ≥15 points that were reduced less than 50% over at least a 4-week treatment period. There were 24 males and 40 females (age range 27-68 years; mean±SD, 48±13 years). The patients' clinical improvement was evaluated using the HAMD-17. Patients with at least a 50% decrease in the HAMD-17 score were defined as responders. Serum BDNF levels were assayed using enzyme-linked immunosorbent assays and the presence of the BDNF (Val66Met) polymorphism was determined using the TaqMan genotyping assay. Results: No correlation was found between the BDNF (Val66Met) polymorphism and a positive response to adding an atypical antipsychotic drug. No differences were observed in the changes in the serum BDNF levels and HAMD-17 scores between Val66Val and Met-carriers. In addition, in patients who experienced remission, the atypical antipsychotic drug was discontinued after at least 3 months of treatment and the patients were then followed for 1 year; 14 of 27 patients (52%) relapsed within 1 year. Conclusion: These results suggest that the BDNF (Val66Met) polymorphism is not associated with the response to the augmentation of a SSRI or SNRI with an atypical antipsychotic drug, and that the combination of an atypical antipsychotic drug and a SSRI or SNRI should be continued for 3 months or more in refractory depressed patients in the Japanese population.
참고문헌 (16)
- Rush AJ, "Acute and longer-term outcomes in depressed outpatients requiring one or several treatment steps: a STAR*D report", Am J Psychiatry, 163, pp.1905~1917 (2006)
- Kelsey JE, "Switching drug class after initial SSRI failure", J Clin Psychiatry, 58, pp.326~327 (1997)
- Crossley NA, "Acceleration and augmentation of antidepressants with lithium for depressive disorders: two meta-analyses of randomized, placebo-controlled trials", J Clin Psychiatry, 68, pp.935~940 (2007)
- Nelson JC, "Atypical antipsychotic augmentation in major depressive disorder: a meta-analysis of placebo-controlled randomized trials", Am J Psychiatry, 166, pp.980~991 (2009)
- Yoshimura R, "Adding a low dose atypical antipsychotic drug to an antidepressant induced a rapid increase of plasma brain-derived neurotrophic factor levels in patients with treatment-resistant depression", Prog Neuropsychopharmacol Biol Psychiatry, 34, pp.308~312 (2010)
- Mowla SJ, "Biosynthesis and post-translational processing of the precursor to brain-derived neurotrophic factor", J Biol Chem, 276, pp.12660~12666 (2001)
- Hamilton M, "A rating scale for depression", J Neurol Neurosurg Psychiatry, 23, pp.56~62 (1960)
- Yoshimura R, "Effects of paroxetine or milnacipran on serum brain-derived neurotrophic factor in depressed patients", Prog Neuropsychopharmacol Biol Psychiatry, 31, pp.1034~1037 (2007)
- Yoshimura R, "Effect of risperidone on plasma catecholamine metabolites and brain-derived neurotrophic factor in patients with bipolar disorders", Hum Psychopharmacol, 21, pp.433~438 (2006)
- Rizos EN, "Reduced serum BDNF levels in patients with chronic schizophrenic disorder in relapse, who were treated with typical or atypical antipsychotics", World J Biol Psychiatry, pp.1~5 (2008)
- Gonzá�lez-Pinto A, "Increase in brain-derived neurotrophic factor in first episode psychotic patients after treatment with atypical antipsychotics", Int Clin Psycho pharmacol, 25, pp.241~245 (2010)
- Hori H, "Effects of olanzapine on plasma levels of catecholamine metabolites, cytokines, and brain-derived neurotrophic factor in schizophrenic patients", Int Clin Psychopharmacol, 22, pp.21~27 (2007)
- Chlan-Fourney J, "Differential regulation of hippocampal BDNF mRNA by typical and atypical antipsychotic administration", Brain Res, 954, pp.11~20 (2002)
- Yoshimura R, "Aripiprazole altered plasma levels of brain-derived neurotrophic factor and catecholamine metabolites in first-episode untreated Japanese schizophrenia patients", Hum Psychopharmacol, 27, pp.33~38 (2012)
- Zou YF, "Meta-analysis of BDNF Val66Met polymorphism association with treatment response in patients with major depressive disorder", Eur Neuropsychopharmacol, 20, pp.535~544 (2010)
- Yoshimura R, "The brain-derived neurotrophic factor (BDNF) polymorphism Val66Met is associated with neither serum BDNF level nor response to selective serotonin reuptake inhibitors in depressed Japanese patients", Prog Neuropsychopharmacol Biol Psychiatry, 35, pp.1022~1025 (2011)