OBJECTIVES: The purpose of this study was to suggest recommendations of antidepressant efficacy compared with placebo, difference in efficacy of antidepressants, and appropriate time of efficacy judgment in antidepressant therapy. METHODS: Using recommendations from 12 international and domestic clinical practice guidelines for depression, drawing of recommendation drafts, and peer review, the executive committee developed the guideline. RESULTS: Tricyclic antidepressants (TCAs), monoamine oxidase inhibitors (MAOI), selective serotonin reuptake inhibitors (SSRI), serotonin and norepinephrine reuptake inhibitors (SNRIs), norepinephrine and specific serotonergic antidepressants (NaSSAs), norepinephrine and dopamine reuptake inhibitors (NDRIs), and serotonin antagonist and reuptake inhibitors (SARIs) were strongly recommended as having antidepressant efficacy compared with placebo. Difference in efficacy of antidepressants was as follows. TCAs, MAOI, SSRI, SNRIs, and NaSSAs were strongly recommended, however, NDRIs, SARIs were weakly recommended. If there was no or minimal improvement with treatment, appropriate time of efficacy judgment in antidepressant therapy was estimated to be after two to four weeks. CONCLUSION: We hope that the results of this study will be helpful in encouraging the optimal treatment by understanding antidepressant efficacy compared with placebo, difference in efficacy of antidepressants, and appropriate time of efficacy judgment in antidepressant therapy.
Antidepressive Agents* ; Antidepressive Agents, Tricyclic ; Depression* ; Depressive Disorder, Major ; Dopamine Uptake Inhibitors ; Judgment* ; Monoamine Oxidase Inhibitors ; Norepinephrine ; Peer Review ; Serotonin ; Serotonin Uptake Inhibitors

Escitalopram is one of the most popular selective serotonin reuptake inhibitors (SSRIs) in current use as a first-line treatment for depression. Escitalopram is well-tolerated and rarely associated with serious side effects. Endocrine and reproductive side effects of serotonergic antidepressants are uncommon and galactorrhea is very rarely mentioned among SSRI-related side effects. Serotonin-enhancing antidepressants may result in a rise in prolactin levels through suppression of dopamine neurotransmission. In the present study, we report a case of hyperprolactinemic galactorrhea associated with escitalopram. A 36-year-old woman developed galactorrhea after initiation of escitalopram for depression and was found to have an elevated prolactin level. Escitalopram was discontinued with resolution of the patient's galactorrhea and normalization of her prolactin level.
Adult ; Antidepressive Agents ; Citalopram ; Depression ; Dopamine ; Female ; Galactorrhea ; Humans ; Pregnancy ; Prolactin ; Serotonin Uptake Inhibitors ; Synaptic Transmission

Although selective serotonin reuptake inhibitors (SSRIs) have been widely used in both psychiatry and other medicine, few cases have been reported SSRI-related hyperprolactinemia and/or galactorrhea. We experienced one case which showed both galactorrhea and hyperprolactinemia following treatment with paroxetine. In the case, a 37-year-old multiparous woman reported galactorrhea after 8-weeks paroxetine treatment for her depression. After 1 month prescription of bromocriptine, dopamine agonist, as well as switching medication from paroxetine to venlafaxine, serotonin-norepinephrine reuptake inhibitor, both galactorrhea and hyperprolactinemia were disappeared. Both hyperprolactinemia and galactorrhea have not been observed even after the cessation of bromocriptine prescription.
Adult ; Bromocriptine ; Cyclohexanols ; Depression ; Dopamine Agonists ; Female ; Galactorrhea ; Humans ; Hyperprolactinemia ; Paroxetine ; Pregnancy ; Prescriptions ; Serotonin Uptake Inhibitors ; Venlafaxine Hydrochloride

OBJECTIVES: The aim of this study was to demonstrate the recommendations for antidepressant treatment strategy of dose increment, switching, combination, and augmentation therapy derived from Evidence-Based Korean Pharmacological Treatment Guideline for Depression, Revised Edition. METHODS: The guideline was developed through adaptation of 12 domestic and foreign clinical guidelines for depression, with key questions concerning pharmacotherapy of depression, and drawing of recommendations. RESULTS: The guideline strongly recommended dose increment, switching, and combination and augmentation therapy of antidepressant when patients with depression showed inadequate treatment outcomes from initial antidepressant treatment. The dose increment was strongly recommended when the patients had insufficient response from treatment with tricyclic antidepressants (TCAs), monoamine oxidase inhibitors, selective serotonin reuptake inhibitors (SSRIs), and serotonin and norepinephrine reuptake inhibitors (SNRIs). Switching from SSRI to non-SSRI was also strongly recommended. The combination of initial medication and other classes of antidepressants could benefit from treatment with TCAs, SSRIs, SNRIs, and noradrenergic and specific serotonergic antidepressants. Combination with norepinephrine and dopamine reuptake inhibitors or serotonin-2 antagonist/reuptake inhibitors was weakly recommended. The guideline strongly recommended use of the augmentation strategy of adding lithium or benzodiazepine to initial antidepressants. Augmentation of lamotrigine, T3, methylphenidate, and modafinil was weakly recommended. CONCLUSION: If the initial outcomes of antidepressant therapy are unsatisfactory to the patients the next-step strategies of dose increment, switching, combination and augmentation of antidepressants should be considered after rechecking the patients' drug compliance, dose, and diagnosis.
Antidepressive Agents ; Antidepressive Agents, Tricyclic ; Benzhydryl Compounds ; Benzodiazepines ; Compliance ; Depression* ; Depressive Disorder, Major ; Dopamine Uptake Inhibitors ; Drug Therapy ; Humans ; Lithium ; Methylphenidate ; Monoamine Oxidase Inhibitors ; Norepinephrine ; Serotonin ; Serotonin Uptake Inhibitors ; Triazines

Bupropion is a selective norepinephrine and dopamine reuptake inhibitor with no serotonergic activity, and is therefore an antidepressant with unique pharmacological properties. There are some reports that selective serotonin reuptake inhibitors (SSRIs) or mirtazapine can induce adverse effects including restless legs syndrome (RLS) and that bupropion can reverse these adverse effects. Here, we report about a patient with a major depressive disorder who exhibited RLS after being treated with pregabalin and mirtazapine. This adverse effect disappeared after having switched from mirtazapine to bupropion. Bupropion inhibits the reuptake of dopamine and increases dopamine neurotransmission in both the nucleus accumbens and the prefrontal cortex. This pharmacological profile can be effective in patients with RLS related to dopamine hypoactivity. However, the limitations of this single case report mean that further investigations with larger samples are needed.
Bupropion ; Depressive Disorder, Major ; Dopamine ; gamma-Aminobutyric Acid ; Humans ; Mianserin ; Norepinephrine ; Nucleus Accumbens ; Prefrontal Cortex ; Restless Legs Syndrome ; Serotonin Uptake Inhibitors ; Synaptic Transmission ; Pregabalin

Bupropion is a selective norepinephrine and dopamine reuptake inhibitor with no serotonergic activity, and is therefore an antidepressant with unique pharmacological properties. There are some reports that selective serotonin reuptake inhibitors (SSRIs) or mirtazapine can induce adverse effects including restless legs syndrome (RLS) and that bupropion can reverse these adverse effects. Here, we report about a patient with a major depressive disorder who exhibited RLS after being treated with pregabalin and mirtazapine. This adverse effect disappeared after having switched from mirtazapine to bupropion. Bupropion inhibits the reuptake of dopamine and increases dopamine neurotransmission in both the nucleus accumbens and the prefrontal cortex. This pharmacological profile can be effective in patients with RLS related to dopamine hypoactivity. However, the limitations of this single case report mean that further investigations with larger samples are needed.
Bupropion ; Depressive Disorder, Major ; Dopamine ; gamma-Aminobutyric Acid ; Humans ; Mianserin ; Norepinephrine ; Nucleus Accumbens ; Prefrontal Cortex ; Restless Legs Syndrome ; Serotonin Uptake Inhibitors ; Synaptic Transmission ; Pregabalin

This article reviews the characteristics and major pharmacological treatment modalities of bipolar depression, which is distinguished from unipolar depression by etiologic differences, symptomatic features, clinical courses, and treatment responses. Bipolar depression is often disabling and very challenging to treat. In acute and prophylactic phases, mood stabilizers such as lithium, divalproex, and lamotrigine are used as first-line treatment, unless the patient is psychotic or markedly dysfunctional. Carbamazepine and oxcarbazepine can be used as a second-line treatment or in a combination regimen. Depressive episodes that do not respond to mood stabilizers, as well as relapsing episodes despite prophylactic therapy, justify treatment with antidepressants. Many clinicians also advocate the early use of antidepressants and antipsychotics when depressive episodes are severe or psychotic. Selective serotonin reuptake inhibitors and bupropion are considered the first choices for use in combination with a mood stabilizer. Bupropion in particular yields stability against manic switches or cycle acceleration. Traditionally, clinicians have used antipsychotics as a combination option when treating patients with bipolar depression who exhibit psychotic features. However, extensive and well controlled recent studies have shown that atypical antipsychotics such as quetiapine, olanzapine, and an olanzapine/fluoxetine combination can yield therapeutic efficacy and good tolerability for treating bipolar depression with or without psychotic features. In particular, a randomized controlled trial (RCT) using quetiapine monotherapy to treat patients with bipolar depression yielded significantly reduced depressive symptomatology. Other atypical antipsychotics such as amisulpride, aripirazole, risperidone, and ziprasidone have yielded antidepressive efficacy, but no RCT trials have been conducted on patients with bipolar depression. Some preliminary studies have shown that newly developed agents such as dopamine agonist, agomelatine, riluzole, mefepristone, and uridine effectively improve mood symptoms among patients with bipolar depression. More extensive clinical trials are needed.
Acceleration ; Acetamides ; Antidepressive Agents ; Antipsychotic Agents ; Benzodiazepines ; Bipolar Disorder ; Bupropion ; Carbamazepine ; Depressive Disorder ; Dibenzothiazepines ; Dopamine Agonists ; Humans ; Lithium ; Piperazines ; Riluzole ; Risperidone ; Serotonin Uptake Inhibitors ; Sulpiride ; Thiazoles ; Triazines ; Uridine ; Valproic Acid ; Quetiapine Fumarate

This article reviews the characteristics and major pharmacological treatment modalities of bipolar depression, which is distinguished from unipolar depression by etiologic differences, symptomatic features, clinical courses, and treatment responses. Bipolar depression is often disabling and very challenging to treat. In acute and prophylactic phases, mood stabilizers such as lithium, divalproex, and lamotrigine are used as first-line treatment, unless the patient is psychotic or markedly dysfunctional. Carbamazepine and oxcarbazepine can be used as a second-line treatment or in a combination regimen. Depressive episodes that do not respond to mood stabilizers, as well as relapsing episodes despite prophylactic therapy, justify treatment with antidepressants. Many clinicians also advocate the early use of antidepressants and antipsychotics when depressive episodes are severe or psychotic. Selective serotonin reuptake inhibitors and bupropion are considered the first choices for use in combination with a mood stabilizer. Bupropion in particular yields stability against manic switches or cycle acceleration. Traditionally, clinicians have used antipsychotics as a combination option when treating patients with bipolar depression who exhibit psychotic features. However, extensive and well controlled recent studies have shown that atypical antipsychotics such as quetiapine, olanzapine, and an olanzapine/fluoxetine combination can yield therapeutic efficacy and good tolerability for treating bipolar depression with or without psychotic features. In particular, a randomized controlled trial (RCT) using quetiapine monotherapy to treat patients with bipolar depression yielded significantly reduced depressive symptomatology. Other atypical antipsychotics such as amisulpride, aripirazole, risperidone, and ziprasidone have yielded antidepressive efficacy, but no RCT trials have been conducted on patients with bipolar depression. Some preliminary studies have shown that newly developed agents such as dopamine agonist, agomelatine, riluzole, mefepristone, and uridine effectively improve mood symptoms among patients with bipolar depression. More extensive clinical trials are needed.
Acceleration ; Acetamides ; Antidepressive Agents ; Antipsychotic Agents ; Benzodiazepines ; Bipolar Disorder ; Bupropion ; Carbamazepine ; Depressive Disorder ; Dibenzothiazepines ; Dopamine Agonists ; Humans ; Lithium ; Piperazines ; Riluzole ; Risperidone ; Serotonin Uptake Inhibitors ; Sulpiride ; Thiazoles ; Triazines ; Uridine ; Valproic Acid ; Quetiapine Fumarate

Tobacco use is the single most preventable cause of death, disability and disease in the world and is projected to be the leading cause of death and disability across all developed and developing countries by 2020. Nicotine, the primary active ingredient of cigarettes that contributes to physical dependence, acts on nicotine receptors in the central nervous system and leads to the release of neurotransmitters (such as dopamine). Like other drugs of abuse, nicotine is thought to produce reinforcing effect by activating the mesocorticolimbic dopamine system. A wide variety of cessation treatments of nicotine dependence is commercially available, yet only 2 general approaches have received empirical validation: behavioral intervention (including 5 As brief intervention) and pharmacotherapy. The evidences show that 5 As brief intervention is one of the most cost-effective treatments in clinical work for busy physicians. Three types of medications have been available in market for smoking cessation treatment: nicotine replacement treatment (NRT, i.e., transdermal patch, gum, inhaler, nasal spray, and lozenge), sustained release bupropion and varenicline. Varenicline, a novel alpha4beta2 nicotinic receptor partial agonist, is effective for tobacco dependence. Phase III trials suggest that it is more effective than NRT and bupropion SR. The safety profile of varenicline is excellent, with the most commonly occurring adverse events, nausea, typically mild and well tolerated. However, new safety warnings are added to the varenicline label because of post-marketing report including agitation, depression and suicidality. A causal connection between varenicline use and these symptoms has not been established.
Benzazepines ; adverse effects ; therapeutic use ; Bupropion ; therapeutic use ; Dopamine Uptake Inhibitors ; therapeutic use ; Humans ; Nicotinic Agonists ; adverse effects ; therapeutic use ; Quinoxalines ; adverse effects ; therapeutic use ; Smoking Cessation ; methods ; psychology ; Tobacco Use Disorder ; therapy ; Varenicline

OBJECTIVETo investigate the associations between the drug responses to obsessive -pulsive disorder (OCD) and six functional genes related with serotonin and dopamine.

METHODSOne hundred and thirteen OCD nuclear families were collected. The OCD patients were treated with serotonin reuptake inhibitors (SRIs) for 8 weeks and the drug responses were assessed using the Yale-Brown obsessive-compulsive scale (Y-BOCS). The patients were divided into drug responders group and non-responders group according to the reducing rate of Y-BOCS score. The genotypes of six genes were determined with the Amp-FLP and Amp-RFLP techniques and analyzed by transmission disequilibrium test (TDT). The six genes are serotonin 2A receptor (5-HT2A), serotonin transporter (5-HTT), dopamine D2 receptor ( DRD2), dopamine D4 receptor (DRD4), catechol-O- methyltransferase (COMT) and monoamine oxidase A (MAOA).

RESULTSNo association was found between the six genes and different drug responses groups. However, there was significant difference between the drug responders and non-responders in homozygosity at the 5-HT2A -1438G/A locus (chi(2)=4.69, P=0.03).

CONCLUSIONThe results suggested that the 5-HT2A may play some roles in the effects of drug treatment on OCD.

Adolescent ; Adult ; Catechol O-Methyltransferase ; genetics ; Female ; Humans ; Male ; Monoamine Oxidase ; genetics ; Obsessive-Compulsive Disorder ; drug therapy ; genetics ; Pharmacogenetics ; methods ; Receptor, Serotonin, 5-HT2A ; genetics ; Receptors, Dopamine D2 ; genetics ; Receptors, Dopamine D4 ; genetics ; Serotonin Plasma Membrane Transport Proteins ; genetics ; Serotonin Uptake Inhibitors ; therapeutic use ; Treatment Outcome ; Young Adult