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Polymorphism of tryptophan hydroxylase, the rate-limiting enzyme in the synthesis of brain serotonin (5-HT), is associated with less synthesis of brain 5-HT in DBA/2J and BALB/c than in C57BL/6J and 129/Sv mice. We selected the forced swimming test, a mouse model used to assess the antidepressant potential of drugs, and neurochemical techniques to study strain differences in the response to citalopram, a selective 5-HT reuptake inhibitor. Citalopram reduced immobility time in C57BL/6J and 129/Sv mice but had no such effect in DBA/2J and BALB/c mice. The drug reduced accumulation of 5-hydroxytryptophan (5-HTP), an indicator of 5-HT synthesis, in C57BL/6J and 129/Sv mice but much less in DBA/2J and BALB/c mice. Pretreatment with tryptophan raised 5-HTP accumulation and reinstated the antidepressant-like effect of citalopram in DBA/2J and BALB/c mice, whereas pharmacological inhibition of 5-HT synthesis prevented the effect of citalopram in C57BL/6J and 129/Sv mice. Because there were no strain differences in catecholamine synthesis, locomotor activity, and brain levels of citalopram at the end of the behavioral test, the results suggest that the failure of citalopram to reduce immobility time in DBA/2J and BALB/c mice is attributable to genotype-dependent impairment of 5-HT synthesis. Interstrain comparisons could probably be a useful strategy for understanding the mechanisms underlying the response to selective serotonin reuptake inhibitors.
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To clarify the neuroendocrine response to 5HT across lifespan, we assessed ACTH, cortisol, DHEA, PRL, and GH responses to citalopram (CT) in young adults (YA) (no.=12, 29.2±1.7 yr mean±SEM), middle aged (MA) (no.=12, 54.3±0.9 yr), and elderly (ES) (no.=12, 69.3±0.9 yr) males. All the subjects received placebo (saline iv over 120 min) or CT (20 mg iv over 120 min). Blood samples were taken every 15 min up to 240 min.
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Many new mothers who need antidepressant or mood-stabilising drug treatment may wish to breastfeed their infants, but are hesitant to do so because of possible harmful effects of the medication on the infant. This article reviews current data on drug excretion into breast milk and the effects on the breast-fed child, and provides recommendations for the use of the different psychotropic drugs in lactating women. Relevant literature was identified through systematic searches of MEDLINE, EMBASE and the Science Citation Index Expanded (ISI) from 1966 to February 2005. The present knowledge is based on the accumulation of case studies. No randomised controlled trials in breast-fed infants have been performed and there is a lack of long-term follow-up studies. Use of SSRIs and TCAs (except doxepin) is compatible with breastfeeding. However, if treatment with an SSRI is started in the postpartum period, fluoxetine and citalopram may not be drugs of first choice. With regard to other antidepressants, such as venlafaxine, trazodone, mirtazapine, reboxetine, moclobemide and other MAOIs, very little knowledge exists. Breastfeeding should be avoided while using lithium. Carbamazepine and sodium valproate (valproic acid) are generally better tolerated by the breast-fed infant than lithium. Data on lamotrigine are still sparse. Knowledge is also scarce on the novel antipsychotics and thus recommendations in lactating women cannot be made for these agents. It is unwise to expose infants unnecessarily to drugs that may have severe adverse effects. As such, clozapine should probably be avoided because of the risk of agranulocytosis. Our knowledge of the impact of drug exposure through breast milk is still limited. Infant drug exposure is, however, generally higher during pregnancy through placental passage than through breast milk. Despite the low dosage transferred to the infant through breast milk, premature infants and infants with neonatal diseases or inherited disturbances in metabolism may be vulnerable to such exposure.
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Currently there are few studies directly comparing citalopram to other antidepressants for LLD. The small number of studies and methodological issues in many studies limit any conclusions about the relative efficacy and tolerability of citalopram compared to other antidepressants. Well-designed studies comparing citalopram to other antidepressants for LLD are required.
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Benefit from antidepressant treatment such as selective serotonin reuptake inhibitors (SSRIs) may depend on individual differences in acute effects on neural emotion processing. The short ('S') allele of the serotonin transporter (5-HTT)-linked polymorphic region (5-HTTLPR) is associated with both negative emotion processing biases and poorer treatment outcomes. Therefore, the aim of the present study was to explore the effects of 5-HTTLPR on the impact of the SSRI escitalopram during processing of positive and negative emotional images, as well as neutral stimuli.
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Herein we report the analysis of 27 selected psychoactive compounds found in the wastewater of the largest suburb in the eastern part of Central Europe Bratislava—Petržalka, Slovakia. Thirteen of them (MDMA, methamphetamine, amphetamine, THC-COOH, benzoylecgonine, codeine, tramadol, venlafaxine, oxazepam, citalopram, methadone, EDDP, cocaine) were found in concentrations above 30 ng/L. These compoundswere selected for further monitoring. The possibility of complete degradation of these 13 substances by zerovalent iron and iron(VI) was studied in thewastewater from the Petržalka treatment plant. During the week the concentration of themajority of the studied compounds inwastewaterwas stable. Concentrations of MDMA, cocaine, tramadol, and oxazepam reached significantly higher levels during the weekend.Only about 10% removal efficiency for tramadol, venlafaxine, oxazepam, MDMA, citalopram, methadone, and EDDP was observed at the treatment plant. In contrast, methamphetamine, amphetamine, and codeine were removed with 68%, 83%, and 53% efficiency, respectively. The degradation of synthetic drugs (methamphetamine, cocaine, MDMA) in wastewater is limited, while cannabis (of natural biological origin) is degradedwith efficiency greater than 90%. After utilization of the Fenton reaction, its modification, and use of ferrate(VI), a high efficiency of eliminating all of these substances to values below the limit of detection was achieved.
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Citalopram and sertraline can be used during pregnancy, while some controversy remains over in utero exposure to paroxetine and fluoxetine, which might be associated with an increased risk of foetal cardiovascular malformation. Less data is available concerning fluvoxamine and escitalopram use but current data does not indicate a specific risk. Citalopram, paroxetine and sertraline can be used during breast-feeding, while fluoxetine probably should be avoided. Nortriptyline, amitriptyline and clomipramine can be used during pregnancy and lactation, although data are more abundant for SSRI treatment. Venlafaxine can be used during pregnancy, while caution is advised during breast-feeding. Other antidepressants should be avoided because of lack of data on their effect. A strongly indicated lithium therapy should be continued. Close monitoring of lithium levels throughout pregnancy is mandatory, as is detailed foetal echocardiography in weeks 18-22 of gestation. Lithium should not be used during breast-feeding. Electroconvulsive therapy (ECT) is a valid option if indicated, both during pregnancy and breast-feeding.
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Employing a two-lever discrimination procedure, rats were trained to discriminate reboxetine (2.5 mg/kg, IP) from saline. In parallel, the influence of reboxetine (2.5 mg/kg) upon dialysate levels of monoamines in frontal cortex and dorsal hippocampus of freely moving rats was determined.
These results support the utility of antidepressants for dysthymic disorder. In fact, the margin of efficacy of antidepressants for dysthymic disorder was larger than for MDD. Future studies providing longer-term data on the treatment of dysthymic disorder with antidepressants are essential.
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This was an open, randomised pilot study. A total of 34 male volunteers with no existing urinary symptoms were randomised: 17 to escitalopram 10 mg once daily and 17 to duloxetine 60 mg once daily for 16 days. Doses were then tapered to 5 mg and 30 mg, respectively for 14 days. Subjects measured their urinary flow at home using a Urospec device for 48 hours pre-dose, immediately after the first dose, at 2 weeks and 5 days after stopping treatment.
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Hyperbilirubinemia is a pathological condition of excessive accumulation of conjugated or unconjugated bilirubin in blood. It has been associated with neurotoxicity and non-neural organ dysfunctions, while it can also be a warning of liver side effects. Hyperbilirubinemia can either be a result of overproduction of bilirubin due to hemolysis or dyserythropoiesis, or the outcome of impaired bilirubin elimination due to liver transporter malfunction or inhibition. There are several reports in literature that inhibition of organic anion transporting polypeptides 1B1 and 1B3 (OATP1B1 and OATP1B3) might lead to hyperbilirubinemia. In this study we created a set of classification models for hyperbilirubinemia, which, besides physicochemical descriptors, also include the output of classification models of human OATP1B1 and 1B3 inhibition. Models were based on either human data derived from public toxicity reports or animal data extracted from the eTOX database VITIC. The generated models showed satisfactory accuracy (68%) and area under the curve (AUC) for human data and 71% accuracy and 70% AUC for animal data. However, our results did not indicate strong association between OATP inhibition and hyperbilirubinemia, neither for humans nor for animals.
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Hippocampal neurogenesis is potentially implicated in etiology of depression and as the final common mechanism underlying antidepressant treatments. However, decreased neurogenesis has not been demonstrated in depressed patients and, in animals, reduced cytogenesis was shown in healthy rats exposed to stressors, but, so far, not in models of depression. Here we report that the number of BrdU positive cells in hippocampus was (1) significantly higher in a rat model of depression, the Flinders Sensitive Line (FSL) compared to control FRL, (2) increased in both FSL and FRL following maternal separation, (3) reduced by escitalopram treatment in maternally separated animals to the level found in non-separated animals. These results argue against the prevailing hypothesis that adult cytogenesis is reduced in depression and that the common mechanism underlying antidepressant treatments is to increase adult cytogenesis. The results also point to the importance of using a disease model and not healthy animals for testing effects of potential treatments for human depression and suggest other cellular mechanisms of action than those that had previously been proposed for escitalopram.
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Pinoline (6-methoxy-1,2,3,4-tetrahydro-beta-carboline) is a naturally occurring compound in the mammalian body which inhibits 5-hydroxytryptamine (5-HT) uptake and exerts antidepressant-like behavioural effects in rats. The present study investigates the effects of pinoline on [3H]citalopram binding to the 5-HT transporter on rat brain. Our experiments revealed that pinoline inhibits [3H]citalopram binding with IC50 1255 +/- 167 nM and Ki 572 +/- 76 nM; Hill coefficient for inhibition was close to 1. In saturation experiments, pinoline co-incubated with [3H]citalopram, increased dose-dependently the Kd value but had no effect on the Bmax value of [3H]citalopram binding. Micromolar concentrations of pinoline did not have influence on the dissociation rate of specifically bound [3H]citalopram. Binding parameters of [3H]citalopram did not differ significantly in cerebral cortex and hippocampus of rats treated for 10 days with pinoline or vehicle. These results indicate that pinoline did not have any modulative influence on the activity of 5-HT transporter and it interacts competitively with citalopram on the substrate recognition site of the 5-HT transporter.
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Citalopram appears to be a safe and effective treatment for compulsive shopping disorder. Further trials of citalopram and other selective serotonin reuptake inhibitors are warranted.
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Untreated major depressive disorder (MDD) is a major risk factor for suicide, but some data suggest antidepressants may be associated with increased suicidal ideation (SI) in some depressed patients. The purpose of this study was to determine whether, and in whom, treatment of MDD is associated with increased or emergent SI.
Melancholic features are associated with a significantly reduced remission rate with an SSRI. This effect appears to be accounted for by demographic and clinical features associated with melancholic features.
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There is limited documentation of the importance of heterozygous cytochrome P450 (CYP) mutations on drug exposure. This study was designed to evaluate the influence of heterozygous mutations in CYP2C19 on the serum concentration of racemic citalopram and escitalopram (S-citalopram). Eighty-three samples from subjects with determined CYP2C19 and CYP2D6 genotype receiving racemic citalopram or S-citalopram as part of their clinical treatment were collected from a routine therapeutic drug monitoring database. Concentration/dose (C/D) ratios, parent drug/metabolite ratios, and serum concentrations in CYP2C19 homozygous extensive metabolizers (EMs) and heterozygous extensive metabolizers (HEMs) were compared. The median C/D ratio was significantly higher in the HEM group compared with the EM group, both for racemic citalopram (8.0 vs. 4.9, P < 0.01) and S-citalopram (5.3 vs. 2.6, P < 0.01). The median parent drug/metabolite ratio was significantly higher in the HEM group compared with the EM group, both for racemic citalopram (2.9 vs. 1.6, P < 0.01) and for S-citalopram (2.4 vs. 1.2, P < 0.01). A higher median non-dose-corrected serum concentration also was observed in HEMs compared with EMs both for S-citalopram (P < 0.01) and racemic citalopram (P = 0.066). This study shows that the metabolism of racemic citalopram and S-citalopram is significantly impaired in CYP2C19 HEMs. Higher absolute serum concentrations indicate that this is not compensated for by dose reductions in clinical practice.
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We used the Hamilton Depression Rating Scale (HDRS), with a minimum follow-up of 24 months if no evidence of disease, or until recurrence or death from disease.
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Participants with chronic MDD were at greater socioeconomic disadvantage and had greater medical and psychiatric disease burden. The chronic and nonchronic groups did not differ in rates of remission at 12 weeks (35.9% vs 42.0%, respectively; odds ratio [OR] = 0.778, P = .1500; adjusted OR [AOR] = 0.956, P = .8130) or at 28 weeks (41.0% vs 49.8%, respectively; OR = 0.706, P = .0416; AOR = 0.837, P = .3448). Participants with chronic MDD had higher final QIDS-SR(16) scores and smaller overall percent changes in QIDS-SR(16) from baseline to exit, but these differences did not remain after adjusting for covariates. There were no significant differences in adverse events or side effect burden. No significant interactions were found between chronicity and type of treatment at 12 or 28 weeks.
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Among all women, median composite baseline Female Sexual Function Index score was 18.1 (interquartile range 2.4-26.5, n=200) and among sexually active women was 22.8 (interquartile range 17.4-27.0, n=75) in the escitalopram group and 23.6 (interquartile range 14.9-31.0, n=70) in the placebo group. Treatment with escitalopram did not affect composite Female Sexual Function Index score at follow-up compared with placebo (P=.18 all women; P=.47 sexually active at baseline). Composite mean Female Sexual Function Index change from baseline to week 8 was 0.1 (95% confidence interval [CI] -1.5 to 1.7) for escitalopram and 2.0 (95% CI 0.2-3.8) for placebo. The Female Sexual Distress Scale results did not differ between groups (P=.73) nor did adverse reports of sexual function. At week 8, among those women sexually active at baseline, there was a small difference between groups in Female Sexual Function Index domain mean score change in lubrication (P=.02) and a marginal nonsignificant difference in orgasm (P=.07).
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Results from pilot studies of several SSRIs and SNRIs suggest that they may improve menopausal mood and sleep symptoms, but few studies have demonstrated significant improvement compared with placebo. One SNRI (venlafaxine) improved menopausal mood symptoms and two SSRIs (citalopram and paroxetine) improved sleep, each in a single placebo-controlled trial of women with VMS. Additional placebo-controlled trials are needed to determine whether SSRIs or SNRIs are effective treatment options for women who cannot or choose not to use hormone therapy.
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It may be possible to identify patients treated with specific serotonin reuptake inhibitors who will not achieve sustained remission by 8 weeks. If supplementation were implemented accordingly, the number of overtreated patients would be small. However, a substantial number of patients who should be supplemented would be missed, indicating a need for greater sensitivity of the prediction model. Further studies are needed.
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Second-generation antipsychotics (SGAs) are prescribed for psychosis, aggression, and agitation in Alzheimer disease (AD).
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We used data available through the Sequenced Treatment Alternatives to Relieve Depression database. We created three boosted Classification and Regression Trees to identify 16 subgroups of patients, among whom anticipation of positive or negative response to citalopram was significantly different from 0.5 (P≤0.1).
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The analytical measuring range for all analytes spanned from 5 to 1000ng/mL. Intra- and inter-assay precision across four quality control levels were ≤9.2% and ≤14.8%, respectively. A comparison to other LC-MS/MS methods resulted in a strong correlation with correlation coefficients ranging from 0.9929 to 0.9971. Carryover, stability, recovery, matrix effects, extraction and processing efficiency were also deemed acceptable in accordance with FDA recommendations.
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The functional polymorphism rs10245483 differentially affects remission and side effect outcomes depending on the antidepressant. The predictive power of the SNP for response or side effects was not lessened by the presence of cognitive impairment.
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Medication dosing regimens may have contributed to the failure of several RPCTs to show drug efficacy in the treatment of pediatric MDD. In addition, the doses of medication used in these RPCTs may also have contributed to the safety and tolerability concerns that have been raised with these drugs. PK and dose-ranging studies should be performed prior to the initiation of definitive efficacy trials so that empirically supported dosing strategies can be incorporated into the design of RPCTs of antidepressants in children and adolescents suffering from MDD.