Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obsessive-compulsive disorder (OCD) and serotonin reuptake inhibitors became inextricably joined with the discovery of their effectiveness for the treatment of OCD in 1969 and 1976. The specificity of response of OCD to serotonin reuptake inhibitors has provided an important platform for the exploration of the neurobiology of OCD. This knowledge has come from many different areas of investigation, including neuroimaging, neuroimmunology and pharmacologic challenge studies. As the research into the pharmacologic treatment of OCD has progressed, a number of serotonin reuptake inhibitors have been approved and marketed for the treatment of OCD. These agents include clomipramine, sertraline, paroxetine, fluoxetine, and fluvoxamine. Because these agents share the same mechanism of action (serotonin reuptake inhibition), choosing which agent to use must be based on other parameters. These include differences in efficacy, dosing, and side-effect profile. Citalopram, a newly marketed selective serotonin reuptake inhibitor could offer some advantages over those agents currently marketed. Theoretically, it should also be effective in the treatment of OCD. In treating depression, it has been shown to have minimal side-effects, low risk of withdrawal symptoms, and little possibility of interaction with other agents.
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PMID:Beyond depression: citalopram for obsessive-compulsive disorder. 1047 Nov 69

Patients suffering from anxiety and depression are often seen in clinical practice. In accordance with the diagnostic criteria of DSM-III/IV and ICD-10, respectively, there may be various combinations of symptoms and degrees of severity. The symptoms of these patients may range from subthreshold anxiety or depression to a combination of anxiety and depressive disorders. Besides giving an extensive survey of diagnostic problems and the epidemiological incidence of such combinations, pharmacotherapeutic approaches are critically reviewed. Metaanalyses have shown that various serotonin reuptake inhibitors (SSRI) are equivalent, if not superior, to tricyclic antidepressants (TCA) in their anti-anxiety effectiveness. Hence, SSRI may be considered a therapy of choice, not least on account of very few adverse effects and good tolerance. More recent antidepressants are under scrutiny for their anti-anxiety efficacy. Citalopram, venlafaxine and, because of its established sedative action, nefazodone seem to be particularly suited to fill a possible therapeutic gap and to provide agitated patients with an alternative to TCA.
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PMID:The importance of new antidepressants in the treatment of anxiety/depressive disorders. 1050 81

Selective serotonin reuptake inhibitors (SSRIs) are the treatment of choice for pathological crying after brain injury, independent of accompanying depression. In a series of 26 consecutive patients with acquired brain damage and episodes of involuntary crying, the efficacy and tolerability of paroxetine and citalopram were compared. The severity of pathological crying or laughing was rated based on clinical interviews with symptom provocation. The first 13 patients were treated with paroxetine and another 13 patients received citalopram in single daily doses of 10 to 40 mg. Rapid onset (within 1-3 days) and highly significant (p < 0.001) improvements of emotionalism were observed after both paroxetine and citalopram. There were no efficacy differences, despite the longer symptom duration in the citalopram group. The only adverse effect after paroxetine was nausea, which was reversible, in two patients, and nausea with vomiting in another two patients, who were switched to citalopram. Citalopram was tolerated without adverse effects.
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PMID:Paroxetine versus citalopram treatment of pathological crying after brain injury. 1057 64

The number of drugs used to treat affective disorders such as depression is rapidly increasing. Citalopram (CIT), an antidepressant, is a selective serotonin (5-hydroxytryptamine; 5-HT) reuptake inhibitor (SSRI). In the present study, rats were treated with 10 mg/kg/d racemic CIT for two weeks with use of osmotic pumps, and the following were monitored: open-field behavior, racemic and enantioselective concentrations of CIT and metabolites in blood, brain parenchyma, and extracellular space, and the brain extracellular monoamine levels. The racemic CIT concentration in serum was estimated about tenfold lower than in brain parenchyma but much higher than in brain extracellular fluid. The major CIT metabolites, demethylcitalopram (DCIT) and didemethylcitalopram (DDCIT) were 20% and 30%, respectively, of the amounts of CIT in serum and even lower in the brain parenchyma. The S-enantiomer/R-enantiomer ratios for CIT and DCIT were about 1.01 and 0.31, respectively, in blood and brain. There was a clear correlation between the different drug components within and between blood and brain compartments. Citalopram had no measured effect on open-field behavior, but it elevated extracellular 5-HT and decreased 5-HIAA levels. No correlations between any of the drug components and the brain monoamines were found. In summary, the drug components after chronic dosing correlated well between the periphery and the brain, but not with the brain monoamine concentrations. Further studies investigating the combined pharmacokinetic/dynamic effects could take advantage of blood drug monitoring for the commonly used novel antidepressant drugs.
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PMID:Pharmacokinetic and pharmacodynamic responses to chronic administration of the selective serotonin reuptake inhibitor citalopram in rats. 1062 92

More than 50% of the patients with Parkinson's disease (PD) may experience mood disturbances. Serotonin-selective reuptake inhibitors (SSRI) are very active in the management of depression. Citalopram is a new SSRI increasingly used in the treatment of depression. The question of a negative impact of SSRI on the motor function of patients with PD is an important clinical issue. A number of such observations have published with various SSRI, but none, up-to-now with citalopram. We report the case of a patient with PD who experienced a worsening in the motor status soon after the addition of citalopram to her antiparkinsonian drug regime. This single case report suggests that this potential adverse event is a class related side effect.
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PMID:Worsening of Parkinson's disease by citalopram. 1069 93

We investigated the effect of the selective serotonin reuptake inhibitor (SSRI) citalopram after 6-8 weeks and 6 months of treatment on clinical and peripheral indexes for central serotonergic function: platelet [14C]serotonin uptake and [3H]paroxetine- and [3H]LSD-binding to platelets membranes in 33 patients with panic disorder. Basal data from patients were compared with data from a control material consisting of 33 healthy volunteers. Bmax for platelet [3H]paroxetine binding was significantly lower in patients than in controls. There were no differences in serotonin uptake or [3H]LSD-binding between patients and controls. The degree of anxiety and depression was assessed using the Beck Anxiety Inventory (BAI) and Beck Depression Inventory self-assessment scales, and the Clinical Anxiety Scale and the Montgomery Asberg Depression Rating Scale for clinical evaluation. Complete remission was found in one third of the patients after 6-8 weeks and in two-thirds after 6 months of treatment. The reduction in assessment scores was parallelled with similar reductions in platelet 5-HT2-receptor density, [3H]LSD affinity variable (Kd) and Vmax for platelet [14C]5-HT uptake. Citalopram treatment did not alter Bmax and Kd for platelet [3H]paroxetine-binding. A positive correlation was found between Vmax for the platelet [14C]5-HT uptake and BAI after 6 months citalopram treatment. The present study shows that citalopram has a therapeutic effect in panic disorders. A prerequisite of responding to treatment might be plasticity in the serotonergic system.
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PMID:The effect of citalopram treatment on platelet serotonin function in panic disorders. 1075 39

The effect of citalopram, a selective serotonin reuptake inhibitor (SSRI) antidepressant, was studied on cardiac action potential configuration and compared with that of the tricyclic antidepressant (TCA) clomipramine. Conventional microelectrode techniques were used in right ventricular papillary muscle preparations of the guinea pig. Citalopram caused a concentration-dependent (10-100 microM) shortening of action potential duration (APD), depression of plateau and overshoot potential, and reduction of maximum velocity of depolarization (V(max)). No significant changes in resting membrane potential were observed. Similar results were obtained with clomipramine; however, reduction of V(max) and overshoot was more pronounced with clomipramine, whereas citalopram caused relatively greater shortening of APD. Effects of both drugs were partly reversible. The results indicate that the SSRI antidepressant citalopram, similarly to TCA compounds, alters cardiac action potential configuration in guinea pig ventricular muscle, probably owing to inhibition of cardiac Na(+) and Ca(2+) channels. Differences in cardiac side effects of the two drugs may be related to their different actions on cardiac action potential configuration.
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PMID:Cardiac electrophysiological effects of citalopram in guinea pig papillary muscle comparison with clomipramine. 1079 64

Pharmacokinetic and pharmacodynamic parameters of the selective serotonin reuptake inhibitor 1-(3-dimethylaminopropyl)-1-(4-fluorophenyl)-5-phtalancarbonitril (citalopram) were determined in order to find optimal conditions for augmentation of its effect on extracellular serotonin [5-hydroxytryptamine (5-HT)] through blockade of 5-HT(1A) and 5-HT(1B) autoreceptors. Citalopram dose-dependently (0.3-10 micromol/kg s.c.) increased serotonin levels in ventral hippocampus of conscious rats. At plasma levels above approximately 0.15 microM, the effect of citalopram on extracellular 5-HT was augmented by both a 5-HT(1A) [N-[2-[4-(2-mehoxyphenyl)-1-piperazinyl]ethyl]-N-(2-pyridil) cyclohexa necarboxamide trihydrochloride (Way 100635), 1 micromol/kg s.c.] and a 5-HT(1B) receptor antagonist (2'-methyl-4'-(5-methyl-[1,2, 4]oxadiazol-3-yl)biphenyl-4-carboxylic acid [4-methoxy]-3-(4-methylpiperazin-1-yl)phenyl]amide (GR 127935), 1 micromol/kg s.c.). However, at plasma levels of the selective serotonin reuptake inhibitor below 0.15 microM, the effects of the antagonists diverged viz. the 5-HT(1B) receptor antagonist was still able to potentiate citalopram's effect on extracellular 5-HT, while the 5-HT(1A) receptor antagonist was no longer effective. These results suggest that in contrast to 5-HT(1B) autoreceptors, indirect activation of 5-HT(1A) autoreceptors by citalopram is critically related to the dose of selective serotonin reuptake inhibitor administered. The latter may have consequences for selective serotonin reuptake inhibitor augmentation strategies with 5-HT(1A) receptor antagonists in the therapy of depression and anxiety disorders.
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PMID:Augmentation with a 5-HT(1A), but not a 5-HT(1B) receptor antagonist critically depends on the dose of citalopram. 1084

Citalopram at a dose of 20 mg was used as monotherapy in the treatment of 91 outpatients with depression mostly of moderate intensity. The duration of treatment was 2 months. Patients were assessed by Clinical Global Impression Scale (CGI) before, after 1st and 2nd months of therapy. Twenty three patients were additionally rated after 2 weeks. Observed and spontaneously adverse events were also recorded. A large proportion of treated patients (75%) showed full or almost full remission (1 or 2 on CGI) at the end of study. There were only few mainly mild adverse events during treatment. Nausea (7.7%) and headache (3.3%) occurred most often. The author conclude that citalopram is a well-tolerated and efficacious antidepressant drug for outpatients.
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PMID:[Citalopram (Cipramil) in monotherapy of depressed outpatients]. 1105 87

Although antidepressant medications are effective in approximately 70% of patients with major depressive disorder, they have a delayed onset of therapeutic effect. This latency is problematic in that it prolongs the impairments associated with depression, leaves patients vulnerable to an increased risk of suicide, increases the likelihood that a patient will prematurely discontinue therapy, and increases medical costs associated with severe depression. No adequately designed prospective trials have been conducted to evaluate comparative time to onset of antidepressant effect. However, evidence suggests that some antidepressant agents may begin to work faster than others. Citalopram, venlafaxine, and mirtazapine each have exhibited statistically significant differences in some measures of antidepressant action within the first 2 weeks of treatment, both in placebo-controlled trials and in head-to-head comparisons with other antidepressants. This article reviews the data that hint at these drug-specific differences in time to onset of action. Given the potential benefits of early-acting antidepressant treatments, the possibility of superior speed of onset of citalopram, venlafaxine, and mirtazapine presented here merits further study in adequately designed, prospective clinical trials.
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PMID:Evidence of early onset of antidepressant effect in randomized controlled trials. 1122 83


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