Search

Introduction To investigate whether early improvement can predict 8-week treatment outcome in generalized anxiety disorder (GAD) patients. Methods For 8 weeks, 226 GAD patients were randomly treated with escitalopram or venlafaxine. Early improvement was defined as a ...20% reduction from baseline in Hamilton anxiety rating scale at week 1 or 2. The positive and negative predictive values were calculated. Results The positive and negative predictive values of early improvement in escitalopram or venlafaxine group at week 1 were (85.19%, 67.53%) vs (84.62%, 65.33%) Discussion The early improvement achieved within the first week treatment can predict a good 8-week treatment outcome in GAD patients. [ABSTRACT FROM AUTHOR]

The catechol-O-methyltransferase ( COMT ) Val158Met polymorphism has been reported to be implicated in generalized anxiety disorder (GAD) as well as the treatment response to antidepressants in patients with GAD, but the findings are inconsistent. In this study, we explore the association among COMT , GAD, and the antidepressant response in the Chinese Han population. One hundred and two patients with GAD and 120 healthy controls (HC) were recruited. All the patients were treated with escitalopram or venlafaxine for 8 weeks. The Hamilton Rating Scale for Anxiety (HAMA) was used to assess the treatment response. All the participants were genotyped for the COMT Val158Met polymorphism using the polymerase chain reaction method. No significant differences in the frequency of the COMT rs4680 polymorphism were found between the GAD and HC groups, or between patients with different genders. Further, we found no significant correlation between the COMT rs4680 polymorphism, gender, and the antidepressant treatment outcomes after eight weeks in the GAD patients. This study indicated that the COMT rs4680 genotype might not be related to GAD or to the genders of the GAD patients, nor did it have any effect on the antidepressant therapeutic response in the GAD patients. Even so, our research will be helpful by providing guidance and direction for future, more in depth, research., Competing Interests: None., (IJCEP Copyright © 2020.)

Objective: To assess the association of BDNF gene Val66Met polymorphism with efficacy of antidepressant treatment and plasma BDNF level., Methods: Two hundred and forty-nine ethnic Han Chinese patients with depression(study group), who have met the diagnostic criteria of DSM-IV, were prescribed with venlafaxine or paroxetine. Two hundred and two healthy individuals were recruited as the control group. General demographic information such as gender, age, educational status, occupation, and marriage status were collected. HAMD-17 was adopted as the primary rating tool to evaluate the severity of depression on the baseline and at the end of 1st, 2nd, 4th, 6th week of treatment. PCR-restriction fragment length polymorphism was applied to determine the Val66Met polymorphism of the BDNF gene in the two groups. Plasma BDNF concentration was measured with ELISA before and after 6 weeks of treatment., Results: No significant differences have been found in HAMD scores and reduction of HAMD scores on the baseline and at the end of 1 st, 2nd, 4th, 6th weeks of treatment for each genotype. Nor were significant differences found in the Val66Met genotypes and allelic frequency between patients who achieved remission or not after 6 weeks' treatment as well as the healthy volunteers. The plasma BDNF level in depression patients was lower than that in healthy controls. The BDNF level has increased significantly after 6 weeks' treatment with both venlafaxine and paroxetine, but was still lower than the healthy controls. The BDNF level in the patients achieved remission who were treated with venlafaxine was similar to the normal controls, while those treated with paroxetine was still lower than normal controls. The BDNF level in patients who have not achieved remission was lower than normal controls. The BDNF level was not associated with the Val66Met polymorphism on the baseline and the end of 6th week., Conclusion: No association has been found between the efficacy of venlafaxine or paroxetine and the BDNF Val66Met polymorphism. The BDNF level of patients with depression is significantly lower than healthy controls on the baseline, and can be enhanced with the treatment. Particularly, the BDNF level in patients who achieved remission after the treatment of venlafaxine can rise to normal. The level of BDNF has certain value in the forecasting of efficacy in the anti-depression therapy. BDNF level is not associated with the Val66Met polymorphism of the BDNF gene.

Background: Previous candidate gene studies of major depressive disorder (MDD) have provided inconclusive evidence of association for genes with strong biological rationale for MDD. In this study, we aimed to investigate the association of tryptophan hydroxylase 2 gene with MDD and its treatment response in the Chinese Han population., Methods: Three hundred and sixty eight depressed patients who met DSM-IV criteria for major depressive disorder were recruited for the study. 371 normal controls were recruited from local community. Patients and normal controls were genotyped for TPH2 (rs4290270 and rs7305115) variants by polymerase chain reaction. Male and female subjects were analyzed separately., Results: No differences were found in the frequencies of the single alleles and genotypes of the tested polymorphisms between MDD patients and normal group. The frequency of the A-A haplotype was significantly higher in female MDD compared to healthy female controls (P<0.05). No significant association with treatment response was discovered in haplotype and single-marker analysis., Limitations: This study lacks a placebo control and we cannot definitively exclude the possibility that some patients in the responder group responded to the placebo effect alone., Conclusion: The result suggests that TPH2 gene may have a gender dependent effect on susceptibility to MDD but not with its treatment response in Chinese Han population. Further studies are needed to replicate the association that we observed., (Copyright © 2011 Elsevier B.V. All rights reserved.)