SOURCE: DocGuide
May 21, 2015 | Louise Gagnon
May 21, 2015 | Louise Gagnon
Patients who possess a specific allele of the brain-derived neurotrophic factor (BDNF) gene may be better early responders to the antidepressant escitalopram, according to a study presented here at the 168th Annual Meeting of the American Psychiatric Association (APA).
“We tried to find the effects of this BDNF polymorphism on the response to escitalopram 3 weeks and 6 weeks after starting treatment,” said Wissam El-Hage, MD, PhD, Centre Hospitalier Régional and Universitaire de Tours, Tours, France, on May 17.
Several studies support the concept that antidepressant medications elevate BDNF concentrations in several areas of the brain, and investigators are aiming to identify biomarkers to predict responses to antidepressant therapy.
This study included 187 patients with depression who were prospectively followed, of whom 153 completed the 6-week study. Investigators, blinded to the genotype of the patients, used the Montgomery and Asberg depression rating scale to assess the severity of depression before treatment, after 3 weeks, and after 6 weeks.
Patients had other comorbidities and were concomitantly treated with other therapies, including benzodiazepines, hypnotic medications, mood stabilisers, and antipsychotic agents, in addition to the selective serotonin reuptake inhibitor. These treatments were included in the statistical analysis that looked at the link between treatment response and polymorphisms so that no treatments could be considered a confounding variable, said Dr. El-Hage.
After 3 weeks of therapy, significantly better responses to escitalopram treatment were seen in patients who were Met allele (Val66Met) carriers than in patients carrying the BDNF Val/Val genotype (77.94% vs 59.78%; P = .015). After 6 weeks, the same pattern of response was observed, but the difference in improvement did not reach statistical significance.
Dr. El-Hage postulated that the dropout rate of patients was the reason for the lack of a statistically significant difference between the 2 groups of patients after 6 weeks of therapy.
“We lost subjects, and lost statistical power, but we observed the same trend in results,” said Dr. El-Hage.
The study had a few limitations. It was uncontrolled and allowed for use of other medications, and the study population was white. Dr. El-Hage recommended that the study be replicated in nonwhite populations to see whether the polymorphism plays a role in response to the specific antidepressant therapy.
"We would like to see if the response we observed is confirmed in different populations," said Dr. El-Hage, adding that the findings cannot be generalised to other selective serotonin reuptake inhibitors.
Funding for this study was provided by a hospital clinical research program at CHRU de Tours, Tours, France, and an unrestricted educational grant from H. Lundbeck A/S.
[Presentation Title: BDNF Gene Polymorphism (VAL66 MET) Is Associated With Response to Escitalopram in Severe Depression. Abstract P3-052]
“We tried to find the effects of this BDNF polymorphism on the response to escitalopram 3 weeks and 6 weeks after starting treatment,” said Wissam El-Hage, MD, PhD, Centre Hospitalier Régional and Universitaire de Tours, Tours, France, on May 17.
Several studies support the concept that antidepressant medications elevate BDNF concentrations in several areas of the brain, and investigators are aiming to identify biomarkers to predict responses to antidepressant therapy.
This study included 187 patients with depression who were prospectively followed, of whom 153 completed the 6-week study. Investigators, blinded to the genotype of the patients, used the Montgomery and Asberg depression rating scale to assess the severity of depression before treatment, after 3 weeks, and after 6 weeks.
Patients had other comorbidities and were concomitantly treated with other therapies, including benzodiazepines, hypnotic medications, mood stabilisers, and antipsychotic agents, in addition to the selective serotonin reuptake inhibitor. These treatments were included in the statistical analysis that looked at the link between treatment response and polymorphisms so that no treatments could be considered a confounding variable, said Dr. El-Hage.
After 3 weeks of therapy, significantly better responses to escitalopram treatment were seen in patients who were Met allele (Val66Met) carriers than in patients carrying the BDNF Val/Val genotype (77.94% vs 59.78%; P = .015). After 6 weeks, the same pattern of response was observed, but the difference in improvement did not reach statistical significance.
Dr. El-Hage postulated that the dropout rate of patients was the reason for the lack of a statistically significant difference between the 2 groups of patients after 6 weeks of therapy.
“We lost subjects, and lost statistical power, but we observed the same trend in results,” said Dr. El-Hage.
The study had a few limitations. It was uncontrolled and allowed for use of other medications, and the study population was white. Dr. El-Hage recommended that the study be replicated in nonwhite populations to see whether the polymorphism plays a role in response to the specific antidepressant therapy.
"We would like to see if the response we observed is confirmed in different populations," said Dr. El-Hage, adding that the findings cannot be generalised to other selective serotonin reuptake inhibitors.
Funding for this study was provided by a hospital clinical research program at CHRU de Tours, Tours, France, and an unrestricted educational grant from H. Lundbeck A/S.
[Presentation Title: BDNF Gene Polymorphism (VAL66 MET) Is Associated With Response to Escitalopram in Severe Depression. Abstract P3-052]
