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No Association between the Response to the Addition of an Atypical Antipsychotic Drug to an SSRI or SNRI and the BDNF (Val66Met) Polymorphism in Refractory Major Depressive Disorder in Japanese Patients.

Yoshimura R, Kishi T, Hori H, Ikenouchi-Sugita A, Umene-Nakano W, Katsuki A, Hayashi K, Iwata N, Nakamura J - Clin Psychopharmacol Neurosci (2012)

Bottom Line: Patients with at least a 50% decrease in the HAMD-17 score were defined as responders.No correlation was found between the BDNF (Val66Met) polymorphism and a positive response to adding an atypical antipsychotic drug.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychiatry, University of Occupational and Environmental Health, Kitakyushu, Japan.

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.

No MeSH data available.


Related in: MedlinePlus

Hamilton Depression Rating Scale (HAMD)-17 scores in each allele.
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Figure 2: Hamilton Depression Rating Scale (HAMD)-17 scores in each allele.

Mentions: Of the 64 patients, 27 (42%) responded to the addition of an antipsychotic drug to a SSRI or SNRI in refractory major depressive disorder. The Val66Met allele frequencies were in Hardy-Weinberg equilibrium (χ2=0.0693, p=0.727). The genotypes of the 64 patients were BDNF Val66Val, Val66Met, and Met66Met in 32.8, 53.1, and 14.09% of the subjects, respectively. There was no difference in the BDNF genotype (Val66Met) between responders and non-responders (χ2=0.01840, p=0.8319) (Table 1). No differences were also found in the changes in the plasma BDNF levels (p=0.138) (Fig. 1) and HAMD-17 scores (p=0.445) (Fig. 2) between patients with Val66Val and Met-carriers. Of the 27 responders, 19 (70%) achieved remission (HAMD-17≤7) within 8 weeks after atypical antipsychotic augmentation of the SSRI or SNRI. The atypical antipsychotic drug was discontinued at least 3 months (mean±SD, 11.8±1.4 weeks) after remission was achieved, and we followed the patients for up to 12 months. Thirteen of the 19 patients who achieved remission (68%) relapsed (Fig. 3).


No Association between the Response to the Addition of an Atypical Antipsychotic Drug to an SSRI or SNRI and the BDNF (Val66Met) Polymorphism in Refractory Major Depressive Disorder in Japanese Patients.

Yoshimura R, Kishi T, Hori H, Ikenouchi-Sugita A, Umene-Nakano W, Katsuki A, Hayashi K, Iwata N, Nakamura J - Clin Psychopharmacol Neurosci (2012)

Hamilton Depression Rating Scale (HAMD)-17 scores in each allele.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3569156&req=5

Figure 2: Hamilton Depression Rating Scale (HAMD)-17 scores in each allele.
Mentions: Of the 64 patients, 27 (42%) responded to the addition of an antipsychotic drug to a SSRI or SNRI in refractory major depressive disorder. The Val66Met allele frequencies were in Hardy-Weinberg equilibrium (χ2=0.0693, p=0.727). The genotypes of the 64 patients were BDNF Val66Val, Val66Met, and Met66Met in 32.8, 53.1, and 14.09% of the subjects, respectively. There was no difference in the BDNF genotype (Val66Met) between responders and non-responders (χ2=0.01840, p=0.8319) (Table 1). No differences were also found in the changes in the plasma BDNF levels (p=0.138) (Fig. 1) and HAMD-17 scores (p=0.445) (Fig. 2) between patients with Val66Val and Met-carriers. Of the 27 responders, 19 (70%) achieved remission (HAMD-17≤7) within 8 weeks after atypical antipsychotic augmentation of the SSRI or SNRI. The atypical antipsychotic drug was discontinued at least 3 months (mean±SD, 11.8±1.4 weeks) after remission was achieved, and we followed the patients for up to 12 months. Thirteen of the 19 patients who achieved remission (68%) relapsed (Fig. 3).

Bottom Line: Patients with at least a 50% decrease in the HAMD-17 score were defined as responders.No correlation was found between the BDNF (Val66Met) polymorphism and a positive response to adding an atypical antipsychotic drug.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychiatry, University of Occupational and Environmental Health, Kitakyushu, Japan.

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.

No MeSH data available.


Related in: MedlinePlus