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P.2.b.021 Escitalopram in the treatment of depression
P.2.b. Affective disorders and antidepressants − Affective disorders (basic) encoding tyrosine hydroxylase, neuronal tryptophan hydroxylase, dopamine transporter 1, serotonin transporter, and downregulation of transcripts encoding brain-derived neurotrophic factor, cholecystokinin, neuropeptide Y, and many GABA, acetylcholine, and glutamate receptor genes). Several of the aforementioned genes were also differentially regulated after CVS, but not PCA, in the hippocampus and, to a lesser degree, in the frontal cortex, and these changes appeared to be reversed on the background of partial serotonergic denervation. These results suggest that chronic variable stress has a global effect on gene expression in the raphe and its projection areas, while partial serotonergic denervation and its combination with stress act to regulate gene expression in a more locally specific manner in the cell body region of the dorsal raphe serotonergic system. Furthermore, several changes observed after chronic stress may represent an adaptive shift that is dependent on intact serotonergic projections.
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conditioned the abandon of treatment: nausea 12%, dry mouth in 11%, somnolence 6%, and other 10%. Conclusions: We conclude that in this patients sample a quick and progressive response was observed, at the end of the follow up superior to 50% in the Hamilton Depression Rating Scale, with a good tolerance lets us suggest that Escitalopram, should be a first choice alternative in the treatment of Depression. Following oral administration escitalopram is rapidly absobed and reaches maximum plasma concentration in aproximatly 3−4 hours after either or multiple dose administration. The absortion of escitalopram is not afectted by food. The elimination half-life is about 27−33 hours and is consistent with once-dayly administration. This study confirms the interest of escitalopram in the treatment of depression and notably in the severe forms, with a particularly favourable efficacy/ tolerance. Likewise, the favourable pharmacokinetic profile of escitalopram suggests clinical utility in a broad range of patients.
References [1] Harro et al Brain Res 2001. [2] Kanarik et al Neurochem Int 2008. [3] Alttoa et al Eur Neuropsychopharmacol 2010.
P.2.b.021 Escitalopram in the treatment of depression I. Duran1 ° , R. Gomez1 , P. Sanchez1 , T. Alvarez1 , A. Chinchilla1 , M. Vega1 , A. Cebollada1 , R. Manzanero1 , A. Regidor1 , M. Serrano1 . 1 Ramon and Cajal Hospital, Psychiatry, Madrid, Spain Introduction: Although pharmacological and psychological interventions are both effective for major depression, antidepressant drugs remain the mainstay of treatment in primary and secondary care settings. During the last 20 years, antidepressant prescribing has risen dramatically in western countries, mainly because of the increasing consumption of selective serotonin reuptake inhibitors and newer antidepressants, which have progressively become the most commonly prescribed antidepressants. A very important problem with antidepressant response is the latency period, it is commonly accepted, that this latency period usually lasts for two or three weeks for antidepressant drugs. Escitalopram is the S-enantiomer of the racemic selective serotonin reuptake inhibitor antidepressant citalopram. It is considerated perhaps, the besttolerated selective reuptake inhibitors with the fewest CYP450mediated drug interationsThe objective of this study was to evaluate the evolution and response to escitalopram, with special interest in the measurement of the latency period. Material and Method: We have studied prospectively a group of 40 patients diagnosed of Depression (DSM-IV TR) and followed up during two months of treatment with a dose range of 20−40 mg/day of Escitalopram. 18 patients were previously treated with other antidepressant, that were suspended due to lack of response: 3 with eating disorders, 13 with SSRIs, and two SSNRIs. The other 22 were not actively treated. As evaluation method, for efficacy, the Hamilton Depression Rating Scale (17 items) was performed in basal conditions and then at day 7th, 30th and 60th during the 8 weeks of follow up. Escitalopram was the only antidepressant allowed, and in case of punctual anxiety or insomnia Benzodiazepines were permitted. Results: Mean basal punctuation for the Hamilton Depression Rating Scale was 21, and in the follow up: on day 7th, the mean punctuation was 18, at day 30th 11 points and at the end of the second month. It was reduced to 9. Secondary effects, were weak and did not
P.2.b.022 Serum BDNF levels correlate with arousal status in women G. Bersani1 , A. Iannitelli1 , P. TIrassa2 , F. Cirulli3 ° , I. Branchi3 , L. Aloe2 , E. Alleva3 . 1 University of Rome Sapienza, Department of Psychiatric Sciences and Psychological Medicine, Rome, Italy; 3 Istituto Superiore di Sanit` a, Deptartment of Cell Biology and Neuroscience, Rome, Italy Compelling evidence from both animal and clinical studies indicate that neurotrophins, particularly Brain-derived neurotrophic factor (BDNF), may be implicated in the pathophysiology underlying mood disorders. Results from basic and clinical studies demonstrate that stress and depression decrease neurotrophins expression and neurogenesis in brain, and that antidepressant treatment blocks or reverses these effects, leading to a neurotrophic hypothesis of depression. Most studies point to a selective role of BDNF, in the etiopathogenesis of depression. In addition, recent findings indicate a role for BDNF in the modulation and mediation of the biological clock in response to light in animal models. The correlation between BDNF and cortisol circadian trend suggests that these two factors may be physiologically co-regulated in order to maintain the homeostasis of integrated cerebral activities. However, so far a correlation between BDNF ultradian changes and neuropsychological measures has not been performed. To further validate the use of BDNF as a biomarker for behavioural and mood disturbances, the aim of the present study was to investigate possible daily fluctuations of this neurotrophin in the serum of a sample of young healthy women in relation with their mood, personality and daily activity. Twenty women (age 25±1.6 years) recruited at the University of Rome “Sapienza” underwent psychiatric interview for rating the arousal status, including sleeping, restfulness, libido, etc, and for clinical assessment of anxiety and depression by State-Trait Anxiety Inventory (STAI) and Beck Depression Inventory (BDI) before blood sample collection. The study was approved by the intramural ethic committees and the participants accepted the experimental procedures. Serum was collected at the following time points: 8.00 a.m, 1.00 p.m. and 8.00 p.m. on the same day. Based on the clinical assessment, subjects did not present subclinical, pre-symptomatic or pathological signs of anxiety and depression. No mood or activity alterations were found and no sleeping disturbances reported. The analysis of serum BDNF levels showed a significant effect of time point (ANOVA for repeated measures p = 0.006), indicating that BDNF levels decrease in the
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conditioned the abandon of treatment: nausea 12%, dry mouth in 11%, somnolence 6%, and other 10%. Conclusions: We conclude that in this patients sample a quick and progressive response was observed, at the end of the follow up superior to 50% in the Hamilton Depression Rating Scale, with a good tolerance lets us suggest that Escitalopram, should be a first choice alternative in the treatment of Depression. Following oral administration escitalopram is rapidly absobed and reaches maximum plasma concentration in aproximatly 3−4 hours after either or multiple dose administration. The absortion of escitalopram is not afectted by food. The elimination half-life is about 27−33 hours and is consistent with once-dayly administration. This study confirms the interest of escitalopram in the treatment of depression and notably in the severe forms, with a particularly favourable efficacy/ tolerance. Likewise, the favourable pharmacokinetic profile of escitalopram suggests clinical utility in a broad range of patients.
References [1] Harro et al Brain Res 2001. [2] Kanarik et al Neurochem Int 2008. [3] Alttoa et al Eur Neuropsychopharmacol 2010.
P.2.b.021 Escitalopram in the treatment of depression I. Duran1 ° , R. Gomez1 , P. Sanchez1 , T. Alvarez1 , A. Chinchilla1 , M. Vega1 , A. Cebollada1 , R. Manzanero1 , A. Regidor1 , M. Serrano1 . 1 Ramon and Cajal Hospital, Psychiatry, Madrid, Spain Introduction: Although pharmacological and psychological interventions are both effective for major depression, antidepressant drugs remain the mainstay of treatment in primary and secondary care settings. During the last 20 years, antidepressant prescribing has risen dramatically in western countries, mainly because of the increasing consumption of selective serotonin reuptake inhibitors and newer antidepressants, which have progressively become the most commonly prescribed antidepressants. A very important problem with antidepressant response is the latency period, it is commonly accepted, that this latency period usually lasts for two or three weeks for antidepressant drugs. Escitalopram is the S-enantiomer of the racemic selective serotonin reuptake inhibitor antidepressant citalopram. It is considerated perhaps, the besttolerated selective reuptake inhibitors with the fewest CYP450mediated drug interationsThe objective of this study was to evaluate the evolution and response to escitalopram, with special interest in the measurement of the latency period. Material and Method: We have studied prospectively a group of 40 patients diagnosed of Depression (DSM-IV TR) and followed up during two months of treatment with a dose range of 20−40 mg/day of Escitalopram. 18 patients were previously treated with other antidepressant, that were suspended due to lack of response: 3 with eating disorders, 13 with SSRIs, and two SSNRIs. The other 22 were not actively treated. As evaluation method, for efficacy, the Hamilton Depression Rating Scale (17 items) was performed in basal conditions and then at day 7th, 30th and 60th during the 8 weeks of follow up. Escitalopram was the only antidepressant allowed, and in case of punctual anxiety or insomnia Benzodiazepines were permitted. Results: Mean basal punctuation for the Hamilton Depression Rating Scale was 21, and in the follow up: on day 7th, the mean punctuation was 18, at day 30th 11 points and at the end of the second month. It was reduced to 9. Secondary effects, were weak and did not
P.2.b.022 Serum BDNF levels correlate with arousal status in women G. Bersani1 , A. Iannitelli1 , P. TIrassa2 , F. Cirulli3 ° , I. Branchi3 , L. Aloe2 , E. Alleva3 . 1 University of Rome Sapienza, Department of Psychiatric Sciences and Psychological Medicine, Rome, Italy; 3 Istituto Superiore di Sanit` a, Deptartment of Cell Biology and Neuroscience, Rome, Italy Compelling evidence from both animal and clinical studies indicate that neurotrophins, particularly Brain-derived neurotrophic factor (BDNF), may be implicated in the pathophysiology underlying mood disorders. Results from basic and clinical studies demonstrate that stress and depression decrease neurotrophins expression and neurogenesis in brain, and that antidepressant treatment blocks or reverses these effects, leading to a neurotrophic hypothesis of depression. Most studies point to a selective role of BDNF, in the etiopathogenesis of depression. In addition, recent findings indicate a role for BDNF in the modulation and mediation of the biological clock in response to light in animal models. The correlation between BDNF and cortisol circadian trend suggests that these two factors may be physiologically co-regulated in order to maintain the homeostasis of integrated cerebral activities. However, so far a correlation between BDNF ultradian changes and neuropsychological measures has not been performed. To further validate the use of BDNF as a biomarker for behavioural and mood disturbances, the aim of the present study was to investigate possible daily fluctuations of this neurotrophin in the serum of a sample of young healthy women in relation with their mood, personality and daily activity. Twenty women (age 25±1.6 years) recruited at the University of Rome “Sapienza” underwent psychiatric interview for rating the arousal status, including sleeping, restfulness, libido, etc, and for clinical assessment of anxiety and depression by State-Trait Anxiety Inventory (STAI) and Beck Depression Inventory (BDI) before blood sample collection. The study was approved by the intramural ethic committees and the participants accepted the experimental procedures. Serum was collected at the following time points: 8.00 a.m, 1.00 p.m. and 8.00 p.m. on the same day. Based on the clinical assessment, subjects did not present subclinical, pre-symptomatic or pathological signs of anxiety and depression. No mood or activity alterations were found and no sleeping disturbances reported. The analysis of serum BDNF levels showed a significant effect of time point (ANOVA for repeated measures p = 0.006), indicating that BDNF levels decrease in the