title: Bcl1 polymorphism of the glucocorticoid receptor gene and treatment response to milnacipran and fluvoxamine in Japanese patients with depression.
abstract: BACKGROUND
  Polymorphisms in the glucocorticoid receptors (GRs) have been widely studied with rather less emphasis on relating their differences with possible pharmacological treatment outcomes. The purpose of this study was to investigate whether Bcl1 polymorphisms of GRs are associated with the antidepressant effect of milnacipran, a serotonin noradrenaline reuptake inhibitor (SNRI), and fluvoxamine, a selective serotonin reuptake inhibitor (SSRI), in Japanese patients with depression.
  
  
  METHODS
  Patients were prescribed either milnacipran (n = 98) or fluvoxamine (n = 95). The severity of depression was assessed with the Montgomery-Åsberg Depression Rating Scale (MADRS) at 0, 1, 2, 4 and 6 weeks of treatment.
  
  
  RESULTS
  Both agents were similarly effective in reducing MADRS scores in 6 weeks. In all subjects receiving milnacipran or fluvoxamine, our data showed no significant interaction between Bcl1 polymorphisms and therapeutic effects. However, when milnacipran- and fluvoxamine-treated subjects were analyzed independently, patients with G allele in Bcl1 polymorphism had a significantly better response to fluvoxamine than those with C/C genotype. On the other hand, no significant relationship was found between treatment response to milnacipran and Bcl1 polymorphism.
  
  
  CONCLUSIONS
  Bcl1 polymorphism may be one of the genetic factors in predicting treatment response to SSRI but not SNRI in Japanese patients with depression.
authors.affiliation: Department of Psychiatry, Tokyo Women's Medical University, Tokyo, Japan.
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Takahashi
authors.forename: Keizo
authors.initials: K
authors.lastname: Yoshida
authors.forename: Hisashi
authors.initials: H
authors.lastname: Higuchi
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Kamata
authors.forename: Kazuyuki
authors.initials: K
authors.lastname: Inoue
authors.forename: Toshio
authors.initials: T
authors.lastname: Suzuki
authors.forename: Jun
authors.initials: J
authors.lastname: Ishigooka
mesh_terms: D000928:Antidepressive Agents / Q000097:blood / Q000627:therapeutic use*; D044466:Asian People; D019938:Cyclin D1 / Q000235:genetics*; D003521:Cyclopropanes / Q000097:blood / Q000627:therapeutic use*; D003865:Major Depressive Disorder / Q000097:blood / Q000188:drug therapy* / Q000235:genetics; D005260:Female; D016666:Fluvoxamine / Q000097:blood / Q000627:therapeutic use*; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D000078764:Milnacipran; D020641:Polymorphism, Single Nucleotide; D011965:Receptors, Glucocorticoid / Q000235:genetics*; D017367:Selective Serotonin Reuptake Inhibitors / Q000097:blood / Q000627:therapeutic use; D012720:Severity of Illness Index; D016896:Treatment Outcome
chemical_list: D000928:Antidepressive Agents; D019938:Cyclin D1; D003521:Cyclopropanes; D016666:Fluvoxamine; D000078764:Milnacipran; D011965:Receptors, Glucocorticoid; D017367:Selective Serotonin Reuptake Inhibitors; C530104:CCND1 protein, human