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1
Dugan, Daniel J. "Antidepressants: Using Pharmacology to Individualize Therapy." Journal of Pharmacy Practice 14, no. 6 (December 2001): 458–66. http://dx.doi.org/10.1177/089719001129040955.
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The pharmacotherapy of depression has undergone significant change in the last two decades. A new generation of antidepressant agents has displaced older drugs as first-line therapies for depression. The clinician that seeks optimal outcomes for treatment of depression must be familiar with all of the available antidepressant agents. This article will discuss the pharmacologic profile of antidepressants currently marketed in the United States, identifying similarities and differences that have clinical relevance in the management of depression. Drug selection with an emphasis on antidepressant receptor affinity will be reviewed.
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Jackson, Cherry W. "Antidepressants in the Treatment of Chronic Pain." Journal of Pharmacy Practice 11, no. 5 (October 1998): 388–93. http://dx.doi.org/10.1177/089719009801100509.
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Antidepressants have been successfully used for chronic pain syndromes for approximately 30 years. One theory is that analgesic action is secondary to the antidepressant effects of the medications. Placebo-controlled trials have documented that antidepressants treat neuropathic pain, musculoskeletal pain, chronic pain, and cancer pain. The most frequently studied antidepressant for pain is amitriptyline. Other antidepressants that have shown analgesic activity include imipramine, citalopram, paroxetine, nortriptyline, desipramine, and mianserin. Fluoxetine and trazodone have not been shown to successfully treat pain syndromes. Venlafaxine, a new antidepressant, most recently was shown to have antidepressant activity in fibromyalgia. More studies need to be done with newer antidepressants to confirm their place in treating pain syndromes.
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Richelson, Elliott. "Pharmacology of antidepressants." Mayo Clinic Proceedings 76, no. 5 (May 2001): 511–27. http://dx.doi.org/10.4065/76.5.511.
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Frazer, Alan. "Pharmacology of Antidepressants." Journal of Clinical Psychopharmacology 17 (April 1997): 2S—18S. http://dx.doi.org/10.1097/00004714-199704001-00002.
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Richelson, Elliott. "Pharmacology of Antidepressants." Psychopathology 20, no. 1 (1987): 1–12. http://dx.doi.org/10.1159/000284517.
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Cohen, Lawrence J., and C. Lindsay DeVane. "Clinical Implications of Antidepressant Pharmacokinetics and Pharmacogenetics." Annals of Pharmacotherapy 30, no. 12 (December 1996): 1471–80. http://dx.doi.org/10.1177/106002809603001216.
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OBJECTIVE: To review available data on pharmacokinetic and pharmacogenetic influences on the response to antidepressant therapy, analyze the mechanisms for and clinical significance of pharmacokinetic and pharmacogenetic differences, and explain the implications of pharmacokinetics and pharmacogenetics for patient care. DATA SOURCES: A MEDLINE search of English-language clinical studies, abstracts, and review articles on antidepressant pharmacokinetics, pharmacogenetics, and drug interactions was used to identify pertinent literature. DATA SYNTHESIS: The pharmacokinetic profiles of selected antidepressants are reviewed and the impact of hepatic microsomal enzymes on antidepressant metabolism is considered. How phenotypic differences influence the metabolism of antidepressant drug therapy is addressed. To evaluate the clinical implications of these pharmacokinetic and pharmacogenetic considerations, the findings of studies designed to elucidate drug interactions involving antidepressant agents are discussed. CONCLUSIONS: Differences in antidepressant plasma concentrations, and possibly safety, are caused by polymorphism in the genes that encode some of the cytochrome P450 isoenzymes that metabolize antidepressants. The isoenzymes 1A2, 2C9/19, 2D6, and 3A4 are the major enzymes that catalyze antidepressant metabolic reactions. Antidepressants can be either substrates or inhibitors of these enzymes, which also metabolize many other pharmacologic agents. Although the cytochrome enzymes that metabolize antidepressants have not been fully characterized, interaction profiles of the newer antidepressants are becoming more clearly defined. Determining patient phenotypes is not practical in the clinical setting, but an awareness of the possibility of genetic polymorphism in antidepressant metabolism may help explain therapeutic failure or toxicity, help predict the likelihood of drug interactions, and help clinicians better manage antidepressant drug therapy.
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Saraghi, Mana, Leonard Golden, and Elliot V. Hersh. "Anesthetic Considerations for Patients on Antidepressant Therapy – Part II." Anesthesia Progress 65, no. 1 (March 1, 2018): 60–65. http://dx.doi.org/10.2344/anpr-65-01-10.
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Millions of patients take antidepressant medications in the United States for the treatment of depression or anxiety disorders. Some antidepressants are prescribed off-label to treat problems such as chronic pain, low energy, and menstrual symptoms. Antidepressants are a broad and expansive group of medications, but the more common drug classes include tricyclic antidepressants, selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, and monoamine oxidase inhibitors. A miscellaneous or “atypical” category covers other agents. Some herbal supplements that claim to have antidepressant activity will also be discussed. Part I of this series reviewed antidepressant pharmacology, adverse effects, and drug interactions with adrenergic agonists. In part II, drug–drug interactions with sedation and general anesthetics, bleeding effects, and serotonin syndrome will be discussed.
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Gers, Lynn, Mirko Petrovic, Stany Perkisas, and Maurits Vandewoude. "Antidepressant use in older inpatients: current situation and application of the revised STOPP criteria." Therapeutic Advances in Drug Safety 9, no. 8 (May 28, 2018): 373–84. http://dx.doi.org/10.1177/2042098618778974.
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Objectives: Antidepressant use increases as age rises. Moreover, older patients are more sensitive to side effects and drug interactions. This descriptive study aims to map antidepressant use among patients at the geriatrics department of a university hospital and to evaluate whether prescribing happens in an evidence-based manner. Methods: Patients aged 75 years and over, admitted to the geriatrics department of the Middelheim Hospital in Antwerp between February and July 2017 were included. We checked whether they took antidepressants, which types and doses were prescribed, who prescribed the antidepressants, and whether prescribing was in concordance with the revised STOPP (Screening Tool of Older People’s Prescriptions) criteria. Results: Out of the 239 included patients, 61 were found to use antidepressants, with depression being the most important indication. General practitioners appeared to be the most frequent prescribers. Trazodone was the most prescribed antidepressant and was often used for sleeping disorders. Antidepressants were taken longer than recommended in almost one out of five cases. Patients with diabetes and renal insufficiency were prescribed antidepressants less frequently. Only 2.8% of the study participants were prescribed antidepressants for anxiety disorders. Conclusion: We can conclude that prescription of antidepressants in older patients at the geriatrics department is often not evidence based. Clear guidelines may offer a solution; therefore more studies are needed on antidepressant use in older patients.
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Saraghi, Mana, Leonard R. Golden, and Elliot V. Hersh. "Anesthetic Considerations for Patients on Antidepressant Therapy—Part I." Anesthesia Progress 64, no. 4 (December 1, 2017): 253–61. http://dx.doi.org/10.2344/anpr-64-04-14.
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Millions of patients take antidepressant medications in the United States for the treatment of depression or anxiety disorders. Some antidepressants are prescribed off-label to treat problems such as chronic pain, low energy, and menstrual symptoms. Antidepressants are a broad and expansive group of medications, but the more common drug classes include tricyclic antidepressants, selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, and monoamine oxidase inhibitors. A miscellaneous or “atypical” category covers other agents. Some herbal supplements that claim to have antidepressant activity will also be discussed. In Part I of this review, antidepressant pharmacology, adverse effects, and drug interactions with adrenergic agonists will be discussed. In part II, drug interactions with sedation and general anesthetics will be reviewed. Bleeding effects and serotonin syndrome implications in anesthetic practice will also be highlighted.
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Cyr, Monica, and Candace S. Brown. "Nefazodone: Its Place among Antidepressants." Annals of Pharmacotherapy 30, no. 9 (September 1996): 1006–12. http://dx.doi.org/10.1177/106002809603000916.
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OBJECTIVE: To review the pharmacology, pharmacokinetics, efficacy, adverse effects, and drug interactions of nefazodone, as well as to determine its place among currently available antidepressants. DATA SOURCES: A search of European and American literature using EMBASE and MEDLINE was completed. Nefazodone was the search term. DATA SYNTHESIS: Nefazodone is an antidepressant that blocks serotonin type 2 (5-HT2) receptors in addition to inhibiting the reuptake of serotonin and norepinephrine. In double-blind, placebo-controlled studies, nefazodone demonstrates antidepressant activity at dosages ranging from 400 to 600 mg/d. Sedation, dry mouth, nausea, and dizziness are the more common adverse effects of nefazodone. Nefazodone, an analog of trazodone, has not been associated with priapism at this time, and may have fewer sexual adverse effects than other antidepressants. More studies are needed to determine the potential role of nefazodone in treating anxiety, pain, and premenstrual syndrome. STUDY SELECTION: Only double-blind, placebo-controlled studies designed to establish the efficacy of nefazodone as an antidepressant were reviewed. CONCLUSIONS: Based on placebo-controlled, double-blind, comparative trials, nefazodone demonstrates greater efficacy than placebo, and equivalent efficacy to imipramine. Somnolence, dry mouth, nausea, dizziness, and constipation are the most common adverse effects. Nefazodone appears to have a milder adverse effect profile than the tricyclic antidepressants, causes fewer sexual dysfunctions than the serotonin selective reuptake inhibitors, and may cause less dizziness than trazodone. Nefazodone at dosages of at least 300 mg/d provides another option for the treatment of depression.
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Pollock, Bruce G. "GERIATRIC PHARMACOLOGY OF ANTIDEPRESSANTS." American Journal of Geriatric Psychiatry 7 (September 1999): 14. http://dx.doi.org/10.1097/00019442-199911001-00043.
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Van Hoey, Nicole M. "Effect of Cyclobenzaprine on Tricyclic Antidepressant Assays." Annals of Pharmacotherapy 39, no. 7-8 (July 2005): 1314–17. http://dx.doi.org/10.1345/aph.1e632.
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OBJECTIVE To evaluate cyclobenzaprine interference on tricyclic antidepressant assays. DATA SOURCES Literature was identified through a MEDLINE search (1966–August 2004) using the search terms cyclobenzaprine, tricyclic antidepressant, toxicology, and assay. DATA SYNTHESIS Cyclobenzaprine is structurally similar to tricyclic antidepressants and is often identified as a tricyclic antidepressant on toxicology assays. Older chromatographic assays demonstrate retention time differences of only seconds and nearly identical color stains between cyclobenzaprine and individual tricyclic antidepressants. In comparison, ultraviolet absorption ratios of 4.18 for amitriptyline and 1.85 for cyclobenzaprine are easily distinguished. Spectroscopy also consistently identifies cyclobenzaprine's unique mass-to-charge ratio peaks of 275 and 215 compared with those of amitriptyline. Available bioanalytic techniques are reviewed for their ability to correctly identify cyclobenzaprine and differentiate the drug from tricyclic antidepressants. CONCLUSIONS When assays are positive for tricyclic antidepressants without a history of their use, an attempt should be made to identify confounders, such as cyclobenzaprine. Newer bioanalytic techniques, such as ultraviolet absorption and mass spectroscopy, accurately identify cyclobenzaprine in such instances.
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Hemels, Michiel EH, Adrienne Einarson, Gideon Koren, Krista L. Lanctôt, and Thomas R. Einarson. "Antidepressant Use during Pregnancy and the Rates of Spontaneous Abortions: A Meta-Analysis." Annals of Pharmacotherapy 39, no. 5 (May 2005): 803–9. http://dx.doi.org/10.1345/aph.1e547.
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BACKGROUND: Due to the high prevalence of depression in women of childbearing age and coupled with the fact that approximately 50% of the pregnancies are unplanned, there is a high chance that these women have been exposed to antidepressants in early pregnancy. OBJECTIVE: To determine baseline rates of spontaneous abortions (SAs) and whether antidepressants increase those rates. METHODS: Rates of SAs in women taking antidepressants compared with non-depressed women were combined into a relative risk using a random effects model. MEDLINE, EMBASE, Healthstar, Toxline, Psychlit, Cochrane database, and Reprotox were searched for studies published in any language from 1966 to 2003. Key words used to identify articles included pregnancy outcome, abortion, miscarriage, spontaneous, antidepressant, depression, and the generic names of each antidepressant and class. Bibliographies, review articles, and reference lists from studies were also used to identify potential articles expected to provide evidence of safety of antidepressants in pregnancy. RESULTS: Of 15 potential articles, 6 cohort studies of 3567 women (1534 exposed, 2033 nonexposed) provided extractable data. All matched on important confounders. Tests found no heterogeneity (χ 2 3.13; p = 0.98), and all quality scores were adequate (>50%). The baseline SA rate (95% CI) was 8.7% (7.5% to 9.9%; n = 2033). For antidepressants, the rate was 12.4% (10.8% to 14.1%; n = 1534), significantly increased by 3.9% (1.9% to 6.0%); RR was 1.45 (1.19 to 1.77; n = 3567). No differences were found among antidepressant classes. CONCLUSIONS: Maternal exposure to antidepressants may be associated with increased risk for SA; however, depression itself cannot be ruled out.
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Park, Susie H., Robin C. Wackernah, and Glen L. Stimmel. "Serotonin Syndrome." Journal of Pharmacy Practice 27, no. 1 (October 23, 2013): 71–78. http://dx.doi.org/10.1177/0897190013504957.
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Background: There is a warning associated with all serotonergic antidepressants and its concomitant use with tramadol due to the concern for a drug–drug interaction resulting in serotonin syndrome (SS). The prescribing of antidepressants with tramadol may be unnecessarily restricted due to fear of causing this syndrome. Objectives: There are 3 objectives of this review. To (1) review case reports of SS associated with the combination of tramadol and antidepressant drugs in recommended doses, (2) describe the mechanisms of the drug interaction, and (3) identify the potential risk factors for SS. Methods: Case reports of SS associated with tramadol and antidepressants were identified via Cochrane Library, PubMed, and Ovid (through October 2012) using search terms SS, tramadol, antidepressants, fluoxetine, sertraline, paroxetine, fluvoxamine, citalopram, escitalopram, venlafaxine, desvenlafaxine, duloxetine, mirtazapine, milnacipran, trazodone, vilazodone, and bupropion. Cases involving monoamine oxidase inhibitors (MAOIs) and tricyclic antidepressants were excluded. Results: Nine articles were identified describing 10 cases of suspected SS associated with therapeutic doses of tramadol combined with an antidepressant. Mechanisms of the drug–drug interactions involve pharmacodynamic, pharmacokinetic, and possible pharmacogenetic factors. Conclusions: Review of the available case reports of tramadol combined with antidepressant drugs in therapeutic doses indicates caution in regard to the potential for SS but does not constitute a contraindication to their use. Tramadol is only contraindicated in combination with MAOIs but not other antidepressants in common use today. These case reports do suggest several factors associated with a greater risk of SS, including increased age, higher dosages, and use of concomitant potent cytochrome P450 2D6 inhibitors. Tramadol can be safely combined with antidepressants; however, monitoring and counseling patients are prudent when starting a new serotonergic agent or when doses are increased.
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Scott, Allan I. F. "New classes of antidepressant drugs." Advances in Psychiatric Treatment 5, no. 2 (March 1999): 104–11. http://dx.doi.org/10.1192/apt.5.2.104.
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The January 1997 issue of this journal contained four reviews that compared tricyclic antidepressants with selective serotonin reuptake inhibitors (SSRIs) and other newer antidepressants in terms of their pharmacology (Palazidou, 1997), adverse effects, potential drug interactions and toxicity (Henry, 1997), efficacy in the prevention of relapse and recurrence (Edwards, 1997), and findings from meta-analyses (Anderson, 1997). In July 1997 reboxetine was promoted as the first selective noradrenaline reuptake inhibitor (NARI), and in October of the same year mirtazapine was promoted as the first noradrenergic and specific serotonergic antidepressant (NaSSA). Milnacipran is presently being registered by the manufacturers, after which it will be the second antidepressant drug promoted as a specific serotonin and noradrenaline reuptake inhibitor (SNRI).
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Bingefors, Kerstin Al, Dag Gl Isacson, Lars Von Knorring, and Björn Smedby. "Prescription Drug and Healthcare Use Among Swedish Patients Treated with Antidepressants." Annals of Pharmacotherapy 29, no. 6 (June 1995): 566–72. http://dx.doi.org/10.1177/106002809502900602.
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Objective: To analyze healthcare and prescription drug use among patients taking and those not taking antidepressant drugs in a Swedish community. Design: Cross-sectional study. Setting: General population of the rural Swedish municipality Tierp of approximately 20 000 inhabitants. Participants: All residents of Tierp aged 25 years or older during 1988. Main Outcome Measures: Mean number of ambulatory care visits, hospital bed days, and prescriptions per person; proportion of those taking prescription drugs in different pharmacologic classes. Results: Patients treated with antidepressant drugs had a significantly (p < 0.05) greater use of ambulatory care, hospital care, and prescription drugs than those who did not take antidepressants in the study population. They also had an increased frequency of use of prescription drugs from virtually all pharmacologic classes. Furthermore, the risk for polypharmacy was high in patients treated with antidepressant medications. Conclusions: Those who took antidepressant drugs consumed more health services and prescription drugs than did those not taking an antidepressant. Patients receiving antidepressant treatment may be at serious risk for iatrogenic disease and should be evaluated carefully with respect to concomitant drug use.
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Obara, Keisuke, Mayumi Michino, Masataka Ito, Lin Ao, Ayano Sawada, Fumiko Yamaki, Kazuhiro Matsuo, Takashi Yoshio, and Yoshio Tanaka. "Evaluation of Antidepressant Effects on Recovery of Electrical Field Stimulation-Induced Contractions that have been Suppressed by Clonidine in Isolated Rat Vas Deferens." Pharmacology 103, no. 3-4 (2019): 189–201. http://dx.doi.org/10.1159/000495616.
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Background: A report examining whether clinically available antidepressants increase urethral smooth muscle contraction via antagonistic effects on the α2-adrenoceptor (α2-AR) is lacking. Objectives: The present study was performed to evaluate the potential of clinically available antidepressants to reverse α2-AR-mediated contractile inhibition in rat vas deferens, in order to predict whether they can induce voiding impairment. Method: The effects of 18 antidepressants of different classes on electrical field stimulation (EFS)-induced contractions suppressed by 10–8 mol/L clonidine (a selective α2-AR agonist) in isolated rat vas deferens were investigated and related to their respective clinical blood concentrations. Results: The EFS-induced contractions suppressed by clonidine were recovered by amitriptyline (a tricyclic antidepressant), mirtazapine (a noradrenergic and specific serotonergic antidepressant), and trazodone (a serotonin 5-HT2A receptor antagonist) at concentrations close to the clinical blood levels. EFS-induced contractions were also recovered by trimipramine, clomipramine (tricyclic antidepressants), mianserin (a tetracyclic antidepressant), sertraline (a selective serotonin reuptake inhibitor [SSRI]), and sulpiride (a dopamine D2-receptor antagonist), albeit at concentrations that substantially exceeded their clinically-achievable blood levels. EFS-induced contractions were not significantly affected by imipramine, nortriptyline, amoxapine (tricyclic antidepressants), maprotiline (a tetracyclic antidepressant), fluvoxamine, paroxetine, escitalopram (SSRIs), milnacipran, duloxetine (serotonin and noradrenaline reuptake inhibitors), and aripiprazole (a dopamine partial agonist). Conclusions: These findings suggest that amitriptyline, mirtazapine, and trazodone induce voiding impairment caused by increased urethral resistance by enhancing sympathetic nerve activities attributed to α2-AR antagonism.
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Taylor, Dale, Jason C. Walden, Ashley H. Robins, and Peter J. Smith. "Role of the Neurotransmitter Reuptake-Blocking Activity of Antidepressants in Reversing Chloroquine Resistance In Vitro in Plasmodium falciparum." Antimicrobial Agents and Chemotherapy 44, no. 10 (October 1, 2000): 2689–92. http://dx.doi.org/10.1128/aac.44.10.2689-2692.2000.
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ABSTRACT Since the discovery of the chloroquine (CQ) resistance reversal properties of several different, structurally unrelated classes of compounds, including antidepressants, the way is again open to employ the aminoquinoline drugs to combat malaria effectively. In this study, CQ sensitivity was restored to varying extents in vitro in the CQ-resistant Plasmodium falciparum strain RSA11 by using the antidepressants amitriptyline, citalopram, oxaprotiline, and nomifensine. The 50% inhibitory concentrations (IC50) of CQ were reduced from 360 to as low as 11 nM when antidepressants were present. These particular antidepressants are highly specific for blocking the ATP-binding cassette transport protein-mediated reuptake of different neurotransmitters at the synaptic level. This study was aimed at determining the extent to which the neurotransmitter reuptake-blocking properties of these antidepressants play a role in the reversal process. None of the compounds or CQ-antidepressant combinations tested had innate antimalarial activity. No chemosensitizer or combination showed an increased CQ accumulation or significant shift in the IC50 in the CQ-sensitive clone D10. Of the compounds tested, citalopram, a highly specific serotonin reuptake blocker, produced the largest shift observed in the IC50 for the resistant isolate RSA11. No particular class of antidepressant was found to be better than any other at restoring CQ sensitivity. We conclude that the resistance-reversing properties of these compounds do not correlate with their activities as reuptake blockers.
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Golan, Moran, Gabriel Schreiber, and Sofia Avissar. "Antidepressant-induced differential ubiquitination of β-arrestins 1 and 2 in mononuclear leucocytes of patients with depression." International Journal of Neuropsychopharmacology 16, no. 8 (September 1, 2013): 1745–54. http://dx.doi.org/10.1017/s1461145713000291.
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Abstract β-Arrestins 1 and 2, cytosolic proteins known to mediate receptor desensitization, endocytosis and G protein-independent signalling, are post-translationally modified by ubiquitination regulating their ability to serve as adaptors and scaffolds. β-Arrestins were suggested to play a role in the pathophysiology of depression and in antidepressant mechanism of action. To determine whether a depressive episode or antidepressant treatment induce significant selective differences in β-arrestin 1 and 2 levels or their ubiquitination patterns in leucocytes of patients with depression, 46 outpatients diagnosed with a depressive episode were examined before and after 4-wk antidepressant treatment compared with age- and gender-matched control subjects. β-Arrestin levels were measured by immunoblotting using anti-arrestin antibodies. Ubiquitination of β-arrestins was measured using anti-ubiquitin antibodies followed by an immunoprecipitation step and immunoblotting using anti-arrestin antibodies. Antidepressants induced selective alterations in leucocyte β-arrestin 1 and 2 levels and ubiquitination. The levels of β-arrestin 1 and 2 and their ubiquitinated forms in leucocytes of yet untreated patients with depression were significantly decreased in a symptom severity correlated manner compared to control subjects. Antidepressants normalized β-arrestin 1 and 2 levels and uncovered novel differences between the two isoforms: (a) while antidepressants normalized ubiquitination of β-arrestin 1, ubiquination of β-arrestin 2 was unaffected; (b) while under antidepressants ubiquitination extent of β-arrestin 1 positively correlated with its level, an inverse picture of negative correlation was found between ubiquitination extent of β-arrestin 2 and its level. We conclude that antidepressants may serve as a tool to detect functional differences between the two β-arrestin isoforms and that through these differential effects antidepressants can induce specific alterations in alternative cellular signalling.
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Amidfar, Meysam, and Yong-Ku Kim. "Recent Developments on Future Antidepressant-related Serotonin Receptors." Current Pharmaceutical Design 24, no. 22 (October 19, 2018): 2541–48. http://dx.doi.org/10.2174/1381612824666180803111240.
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Conventional serotonin-enhancing antidepressants including selective serotonin reuptake inhibitors (SSRIs) and serotonin and norepinephrine reuptake inhibitors (SNRIs) have shown effectiveness in the treatment of major depression, but their significant limitations such as slowness of action have led to intensive research efforts to develop new antidepressants. Increased synaptic neurotransmission of serotonin (5-hdroxytryptamine; 5-HT) through orchestration of stimulation and blockade of various subtypes of 5-HT receptors is involved in the mechanisms of action of SSRIs. Agonists at the 5-HT1A, 5-HT1B, 5-HT2C, 5-HT4, and 5-HT6 receptors and antagonists at the 5-HT1A, 5-HT2A, 5-HT2C, 5-HT3, 5- HT6, and 5-HT7 receptors have shown antidepressant properties in clinical and preclinical studies. However, paradoxical antidepressant-like effects of both agonists and antagonists at particular 5-HT receptors suggest the need to consider the neurochemical mechanisms of each 5-HT receptor subtype. Therefore, better knowledge of the involvement of individual 5-HT receptors in the mechanisms of action of currently used antidepressants as well as antidepressant effects of selective ligands of 5- HT receptor subtypes will provide opportunities for the development of future antidepressants with more rapid onset of action, fewer side effects, and better efficacy than SSRIs.
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Maric, Nadja, Dragan Stojiljkovic, Zorana Pavlovic, and Miroslava Jasovic-Gasic. "Factors influencing the choice of antidepressants: A study of antidepressant prescribing practice at University psychiatric clinic in Belgrade." Vojnosanitetski pregled 69, no. 4 (2012): 308–13. http://dx.doi.org/10.2298/vsp1204308m.
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Background/Aim. Antidepressants are a widely used class of drugs. The aim of this study was to investigate different aspects of antidepressant prescribing practice at University Psychiatric Clinic in Belgrade. Methods. This cross-sectional study was carried out by retrospective analysis of the patient's medical charts. The study included all patients with antidepressant prescribed at discharge during 2009 (n = 296). The evaluation was focused on patient- related factors (socio-demographic and illness related), psychiatrist-related factors (sex and duration of working experience) and drug related factors (type of antidepressant, dose, polypharmacy and reimbursement by national health insurance). Results. Antidepressants were prescribed for unipolar depression (F32-34, ICD X) either without comorbidity (46.2%) or with comorbidity (24.7%), mostly as a monotherapy (91% had one antidepressant), to the patients who were 65% female, aged 50.1 ? 8.9, most of them with 12 years of education (52.6%), married (69.3%) and employed (55.9%). The majority of patients had a history of two hospitalizations (Med 2; 25th-75th perc. 1-4) during nine years (Med 9; 25th-75th perc. 2-15) after the first episode of depression. Among them, 19% were found to be suicidal in a lifetime. The single most prescribed antidepressant was sertraline (20.4%), followed by fluoxetine (13.3%) and maprotiline (11.7%). Utilization of antidepressants was positively correlated with the rate of reimbursement (p < 0.01). The most prescribed antidepressant group was selective serotonin reuptake inhibitors (SSRI) (47.8%), followed by tricyclic antidepresants (TCA) (25.3%) and new antidepressants - venlafaxine, tianeptine, mirtazapine, bupropion, trazodone (15.1%). Most of the drugs were prescribed in doses which are at the lower end of the recommended dose-range. Regarding severity of the actual depressive episode, TCA were prescribed for severe depression with psychotic features, while SSRI were choice for episodes with moderate symptom severity (p = 0.01). Psychiatrists with longer working age (20-30 years) hesitated to prescribe new antidepressants in comparison to younger colleagues (p = 0.01). Conclusion. Economic issues in Serbia as developing country influence the choice of antidepressants, as well as a psychiatrist?s working age and severity of depression. However, SSRI are the drugs of the first choice, as it was shown in most of the developed countries nowadays.
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Su, Jian-An, Chih-Cheng Chang, Yao-Hsu Yang, Ko-Jung Chen, Yueh-Ping Li, and Chung-Ying Lin. "Risk of incident dementia in late-life depression treated with antidepressants: A nationwide population cohort study." Journal of Psychopharmacology 34, no. 10 (August 27, 2020): 1134–42. http://dx.doi.org/10.1177/0269881120944152.
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Background: Antidepressants are frequently used to treat depression in patients with dementia. In addition, late-life depression is associated with the incidence of subsequent cognitive impairment or dementia. However, the association between exposure to antidepressants in late-life depression and the development of incident dementia remains understudied. Methods: Through a population-based retrospective cohort design, data were extracted from the Taiwan National Health Insurance Research Dataset of medical claims registered from 1998–2013. We collected data of individuals who had received a new diagnosis of depression between 2000 and 2007. We excluded those who received a diagnosis of depression and were given antidepressants before 2000 and those younger than 60 years. The primary outcome was the occurrence of incident dementia. The time from the prescription of antidepressants or the diagnosis of depression until the outcome or the end of 2013 was calculated as the time to event. A total of 563,918 cases were included and were divided into either antidepressant users or antidepressant nonusers. Cox proportional hazards models were used to calculate the hazard ratio and 95% confidence interval. Results: Exposure to antidepressants did not increase the risk of dementia in patients with late-life depression at either a low exposure dosage (hazard ratio: 1.06, 95% confidence interval: 0.91–1.23) or a high exposure dosage (hazard ratio: 1.07, 95% confidence interval: 0.95–1.20). To confirm the validity of our results, we performed a sensitivity analysis and subgroup analysis, and the post-hoc results were consistent with the main results. Conclusion: Antidepressants did not increase the risk of incident dementia in patients with late-life depression.
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Barton, Amy E., and Gary M. Levin. "Evaluating the Incidence of Antidepressant-Induced Sexual Dysfunction." Hospital Pharmacy 35, no. 6 (June 2000): 609–13. http://dx.doi.org/10.1177/001857870003500613.
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The incidence of sexual dysfunction (SD) associated with antidepressants may be higher than the rate reported in the product information. We conducted a study using a survey that included the Arizona Sexual Experiences (ASEX) scale to assess the incidence of SD before and with current antidepressant use. We also set out to determine if differences exist between antidepressant classes. Forty-four patients (12 males and 32 females) responded to the survey. Data was stratified into 3 groups, selective serotonin reuptake inhibitors (SSRIs; n = 36), tricyclic antidepressants (TCAs; n = 7), and novel agents (bupropion and nefazodone, or NA; n = 7). For the SSRI subgroup, there were significant increases in ASEX scores, indicative of SD after treatment. There were no differences in ASEX scores in the TCA or NA group. The incidence of SD was highest for the SSRIs (36%). Clinical implications of these findings include educating patients, improving clinical assessment, and enhancing awareness about options available to manage antidepressant-induced SD.
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Fedgchin, Maggie, Madhukar Trivedi, Ella J. Daly, Rama Melkote, Rosanne Lane, Pilar Lim, Dawn Vitagliano, et al. "Efficacy and Safety of Fixed-Dose Esketamine Nasal Spray Combined With a New Oral Antidepressant in Treatment-Resistant Depression: Results of a Randomized, Double-Blind, Active-Controlled Study (TRANSFORM-1)." International Journal of Neuropsychopharmacology 22, no. 10 (July 10, 2019): 616–30. http://dx.doi.org/10.1093/ijnp/pyz039.
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Abstract Background About one-third of patients with depression fail to achieve remission despite treatment with multiple antidepressants and are considered to have treatment-resistant depression. Methods This Phase 3, double-blind, multicenter study enrolled adults with moderate-to-severe depression and nonresponse to ≥2 antidepressants in the current depression episode. Eligible patients (N = 346) were randomized (1:1:1) to twice-weekly nasal spray treatment (esketamine [56 or 84 mg] or placebo) plus a newly initiated, open-label, oral antidepressant taken daily for 4 weeks. The primary efficacy endpoint was change from baseline to day 28 in the Montgomery-Asberg Depression Rating Scale total score, performed by blinded, remote raters. Based on the predefined statistical testing sequence, esketamine 84 mg/antidepressant had to be significant for esketamine 56 mg/antidepressant to be formally tested. Results Statistical significance was not achieved with esketamine 84 mg/antidepressant compared with antidepressant/placebo (least squares [LS] means difference [95% CI]: –3.2 [–6.88, 0.45]; 2-sided P value = .088). Although esketamine 56 mg/antidepressant could not be formally tested, the LS means difference was –4.1 [–7.67, –0.49] (nominal 2-sided P value = .027). The most common (>20%) adverse events reported for esketamine/antidepressant were nausea, dissociation, dizziness, vertigo, and headache. Conclusions Statistical significance was not achieved for the primary endpoint; nevertheless, the treatment effect (Montgomery-Asberg Depression Rating Scale) for both esketamine/antidepressant groups exceeded what has been considered clinically meaningful for approved antidepressants vs placebo. Safety was similar between esketamine/antidepressant groups and no new dose-related safety concerns were identified. This study provides supportive evidence for the safety and efficacy of esketamine nasal spray as a new, rapid-acting antidepressant for patients with treatment-resistant depression. Trial Registration ClinicalTrials.gov identifier: NCT02417064
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Vázquez, Gustavo H., Leonardo Tondo, Juan Undurraga, and Ross J. Baldessarini. "Overview of antidepressant treatment of bipolar depression." International Journal of Neuropsychopharmacology 16, no. 7 (August 1, 2013): 1673–85. http://dx.doi.org/10.1017/s1461145713000023.
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Abstract Bipolar depression remains a major unresolved challenge for psychiatric therapeutics. It is associated with significant disability and mortality and represents the major proportion of the approximately half of follow-up time spent in morbid states despite use of available treatments. Evidence regarding effectiveness of standard treatments, particularly with antidepressants, remains limited and inconsistent. We reviewed available clinical and research literature concerning treatment with antidepressants in bipolar depression and its comparison with unipolar depression. Research evidence concerning efficacy and safety of commonly used antidepressant treatments for acute bipolar depression is very limited. Nevertheless, an updated meta-analysis indicated that overall efficacy was significantly greater with antidepressants than with placebo-treatment and not less than was found in trials for unipolar major depression. Moreover, risks of non-spontaneous mood-switching specifically associated with antidepressant treatment are less than appears to be widely believed. The findings encourage additional efforts to test antidepressants adequately in bipolar depression, and to consider options for depression in types I vs. II bipolar disorder, depression with subsyndromal hypomania and optimal treatment of mixed agitated-dysphoric states – both short- and long-term. Many therapeutic trials considered were small, varied in design, often involved co-treatments, or lacked adequate controls.
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Warren, Matthew B., Philip J. Cowen, and Catherine J. Harmer. "Subchronic treatment with St John’s wort produces a positive shift in emotional processing in healthy volunteers." Journal of Psychopharmacology 33, no. 2 (November 28, 2018): 194–201. http://dx.doi.org/10.1177/0269881118812101.
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Background: The neurocognitive model of antidepressant treatment in depression states that antidepressants work by producing relatively immediate positive shifts in emotional processing, which translate into clinical improvement with time. St John’s Wort has shown antidepressant potential in randomised controlled trials; however, its pharmacological actions are broad and it is unknown whether treatment also produces changes in emotional processing. Aims: We investigated whether short-term treatment with St John’s wort has similar effects on emotional processing to those reported with other antidepressants such as selective serotonergic reuptake inhibitors. Methods: Forty-eight healthy participants were given St John’s wort or placebo treatment for seven days. On day 7 they completed a battery of tasks to measure emotional processing and other elements of cognition. Results: St John’s wort treatment produced similar changes to other antidepressants, for example reducing recognition of disgusted faces and attention to fearful faces, while increasing memory for positive words. We failed to find evidence for an effect of St John’s wort on other aspects of cognition including working memory. Conclusions: These findings lend support to the theory that the production of early positive biases in emotional processing may be a common feature of all clinically effective antidepressants with diverse pharmacological mechanisms.
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Sindrup, S. H., K. Brøsen, and L. F. Gram. "ANTIDEPRESSANTS IN PAIN TREATMENT: ANTIDEPRESSANT OR ANALGESIC EFFECT?" Clinical Neuropharmacology 15 (1992): 636A—637A. http://dx.doi.org/10.1097/00002826-199201001-00329.
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Hsu, Chih-Wei, Sheng-Yu Lee, Yao-Hsu Yang, and Liang-Jen Wang. "Brand-Name Antidepressants Outperform Their Generic Counterparts in Preventing Hospitalization for Depression: The Real-World Evidence from Taiwan." International Journal of Neuropsychopharmacology 23, no. 10 (June 29, 2020): 653–61. http://dx.doi.org/10.1093/ijnp/pyaa041.
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Abstract Background Generic antidepressants are approved on the market based on evidence of bioequivalence to their brand-name versions. We aimed to assess whether generic antidepressants exert equal effectiveness as their brand-name counterparts for treating patients with depressive disorders. Methods In a nationwide, population-based cohort in Taiwan from 1997 through 2013, patients with a diagnosis of a depressive disorder aged between 18 and 65 years who were new users of antidepressant drugs were classified into either the brand-name group or the generic group. All patients were followed up until medication discontinuation or the end of the study period. We assessed the risk for hospitalization as a primary outcome and augmentation therapy, daily dose, medication discontinuation, or switching to another antidepressant as secondary outcomes. Results A total of 277 651 brand-name users (35.8% male; mean age: 41.2 years) and 270 583 generic users (35.8% male; mean age: 41.0 years) were divided into 10 different antidepressant groups (fluoxetine, sertraline, paroxetine, escitalopram, citalopram, venlafaxine, mirtazapine, moclobemide, imipramine, and bupropion). We found that patients treated with the generic form of sertraline, paroxetine, escitalopram, venlafaxine, mirtazapine, and bupropion demonstrated significantly higher risks of psychiatric hospitalization (adjusted hazard ratios ranged from 1.20–2.34), compared to their brand-name counterparts. The differences between brand-name antidepressants and their generic counterparts in secondary outcomes varied across different drugs. Conclusions Compared to most generic antidepressants, brand-name drugs exhibited more protective effects on psychiatric hospitalization for depressive patients. These findings could serve as an important reference for clinicians when encountering patients with depressive disorder.
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Mathys, Monica, and Brian G. Mitchell. "Targeting Treatment-Resistant Depression." Journal of Pharmacy Practice 24, no. 6 (November 17, 2011): 520–33. http://dx.doi.org/10.1177/0897190011426972.
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Only 50% of depressed patients achieve remission of symptoms after 2 trials of antidepressants. Therefore one half of patients are considered treatment resistant. Studies have shown that with each failed antidepressant, chances of remission continue to decline. Untreated depressive symptoms lead to impaired social and occupational function, decline of physical health, suicidal thoughts, and increased health care utilization. Clinicians recognize there is an urgent need to find an efficacious treatment, but it becomes more difficult to decide on an appropriate therapy once a patient has failed 2 to 3 trials of antidepressants. An evidence-based review was performed to assess the efficacy and safety of several different antidepressant strategies to help the clinician decide which may be beneficial for specific patients.
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Witkin, Jeffrey M., Daniel E. Knutson, Gabriel J. Rodriguez, and Samuel Shi. "Rapid-Acting Antidepressants." Current Pharmaceutical Design 24, no. 22 (October 19, 2018): 2556–63. http://dx.doi.org/10.2174/1381612824666180730104707.
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Background: Conventional antidepressants are thought to produce their impact on clinical symptoms by increasing the central availability of biogenic amine neurotransmitters (the monoamine hypothesis of depression). These drugs continue to be the primary medicines used in major depressive disorder. Although they have biological effects after acute dosing, full antidepressant response generally takes weeks of daily administration. Lack of rapid onset is a large limitation in antidepressant therapy (e.g., suicide, lack of medication compliance, difficulty switching medications). Methods: The present review of the literature discusses the preclinical and clinical findings on compounds that can produce immediate symptom relief. Results: These compounds include ketamine, scopolamine, and mechanistically-related drugs. Newer additions to the list of potential rapid-acting agents include antagonists of metabotropic (mGlu) 2/3 receptors, negative allosteric modulators of α5-containing GABAA receptors, and psychedelic compounds. An additional benefit of these compounds is that they have demonstrated large effect sizes and, importantly, demonstrated efficacy in patient’s refractory to other treatments. A drawback of some of these compounds, to date, is finding ways to expand the duration of clinical efficacy. In addition, for some compounds, the side-effect profile requires management. A primary mechanism by which rapid effects might be produced is through the amplification of excitatory neurotransmission through activation of AMPA receptors. The extracellular efflux of glutamate induced by these drugs has been documented and provides the hypothesized triggering mechanism for AMPA receptor amplification. Conclusion: The preclinical and clinical literature strongly suggests that rapid-acting antidepressants are the current focus of antidepressant drug discovery. Promising clinical findings exist for several compounds including ketamine and other NMDA receptor antagonists, scopolamine, and psilocybin. Two compounds are in late stage clinical development: GLYX-13 (Rapastinel) and eskekamine.
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Gregorian, Razmic S., Katharine A. Golden, Asena Bahce, Clifford Goodman, W. Jacqueline Kwong, and Zeba M. Khan. "Antidepressant-Induced Sexual Dysfunction." Annals of Pharmacotherapy 36, no. 10 (October 2002): 1577–89. http://dx.doi.org/10.1345/aph.1a195.
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OBJECTIVE: To review the evidence regarding antidepressant-induced sexual dysfunction and address implications for treatment strategy and health plan coverage policies for antidepressant medications. DATA SOURCES: Primary articles were identified by a MEDLINE and HealthSTAR search to identify English-language studies published between January 1986 and July 2000. Search terms included sexual dysfunction or sexual function and antidepressants, fluoxetine, sertraline, paroxetine, fluvoxamine, citalopram, venlafaxine, nefazodone, bupropion, and mirtazapine. A cross-check of references cited in 10 published reviews yielded additional in-scope articles. STUDY SELECTION AND DATA EXTRACTION: Approximately 200 articles were identified, including 8 randomized controlled trials and numerous open-label studies, case series, and case reports. Of the randomized controlled trials, only 5 were designed to evaluate the incidence of sexual dysfunction associated with antidepressant treatment. Three additional randomized controlled trials included a structured assessment of sexual dysfunction within an efficacy trial. Data extraction excluded case reports, letters, and other limited study designs. A panel survey augmented published reports. DATA SYNTHESIS: Sexual dysfunction is a relatively common adverse effect of many of the antidepressants in common use today. Rates of sexual dysfunction observed in clinical practice may be higher than those reported in the product information for several agents. Selective serotonin-reuptake inhibitors (SSRIs) appear to be the class of antidepressants most likely to cause sexual dysfunction. Published studies suggest that between 30% and 60% of SSRI-treated patients may experience some form of treatment-induced sexual dysfunction. Bupropion and nefazodone appear to be much less likely to cause sexual dysfunction (≤10% of patients). Mirtazapine also appears to be associated with a low rate of sexual adverse effects. Panel results largely reflect the consensus of the literature. CONCLUSIONS: Sexual dysfunction is a common adverse effect of antidepressant treatment. Physicians should monitor their patients for antidepressant-induced sexual adverse effects, as these may affect compliance with therapy and ultimate treatment success. In addition to the consequences for patient health and well-being, managed-care organizations should be concerned with sexually related adverse effects of antidepressants, insofar as additional healthcare resources may be required to treat depressed patients in whom these adverse effects arise.
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Marcy, Todd R., and Mark L. Britton. "Antidepressant-Induced Sweating." Annals of Pharmacotherapy 39, no. 4 (April 2005): 748–52. http://dx.doi.org/10.1345/aph.1e564.
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OBJECTIVE: To report a case of excessive sweating probably caused by paroxetine, review the literature on antidepressant-induced sweating, and provide recommendations for the management of antidepressant-induced sweating. CASE SUMMARY: A 59-year-old white female presented to a pharmacist-staffed pharmacotherapy clinic with episodes of excessive sweating. The episodes occurred primarily on her head and back of the neck. Other etiologies were ruled out and paroxetine was discontinued. Paroxetine had been initiated at least 7 months prior to the reporting of symptoms. Sweating symptoms gradually improved until resolution 5 weeks following discontinuation of paroxetine. The Naranjo probability scale indicated a causal relationship is probable. DISCUSSION: Excessive sweating has been associated with antidepressants including tricyclic antidepressants, selective serotonin-reuptake inhibitors, and venlafaxine. In some patients, these symptoms require therapeutic intervention such as dose reduction, antidepressant substitution, antidepressant discontinuation, or addition of an agent to control sweating. Agents that have been reported successful in controlling the sweating include benztropine and cyproheptadine. CONCLUSIONS: We recommend a patient-specific approach for the management of antidepressant-induced sweating. First, consider dose reduction or a trial off antidepressant medication. In patients in whom this is inappropriate or ineffective, substitution of another antidepressant should be considered. If episodes of excessive sweating persist, consider treatment of sweating symptoms with benztropine or cyproheptadine in the absence of contraindications.
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Mars, Becky, Jon Heron, David Gunnell, Richard M. Martin, Kyla H. Thomas, and David Kessler. "Prevalence and patterns of antidepressant switching amongst primary care patients in the UK." Journal of Psychopharmacology 31, no. 5 (February 1, 2017): 553–60. http://dx.doi.org/10.1177/0269881117693748.
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Objective: Non-response to antidepressant treatment is a substantial problem in primary care, and many patients with depression require additional second-line treatments. This study aimed to examine the prevalence and patterns of antidepressant switching in the UK, and identify associated demographic and clinical factors. Method: Cohort analysis of antidepressant prescribing data from the Clinical Practice Research Datalink, a large, anonymised UK primary care database. The sample included 262,844 patients who initiated antidepressant therapy between 1 January 2005 and 31 June 2011. Results: 9.3% of patients switched to a different antidepressant product, with most switches (60%) occurring within 8 weeks of the index date. The proportion switching was similar for selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants and other antidepressants (9.3%, 9.8% and 9.2%, respectively). Most switches were to an SSRI (64.5%), and this was the preferred option regardless of initial antidepressant class. Factors predictive of switching included male gender, age, and history of self-harm and psychiatric illness. Conclusion: Over one in every 11 patients who initiates antidepressant therapy will switch medication, suggesting that initial antidepressant treatment has been unsatisfactory. Evidence to guide choice of second-line treatment for individual patients is currently limited. Additional research comparing different pharmacological and psychological second-line treatment strategies is required in order to inform guidelines and improve patient outcomes.
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Markovic, Marija, Alyssa Gallipani, Krina H. Patel, and Megan Maroney. "Brexpiprazole." Annals of Pharmacotherapy 51, no. 4 (December 15, 2016): 315–22. http://dx.doi.org/10.1177/1060028016678262.
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Objective: To review the pharmacology and clinical data for brexpiprazole in schizophrenia and major depressive disorder (MDD). Data Sources: An English-language literature search using PubMed and MEDLINE was performed using the term brexpiprazole. All articles containing human clinical trial data published up to September 2016 were evaluated for inclusion as well as information from the manufacturer’s product labeling. Study Selection/Data Extraction: Phase 3 trials for brexpiprazole were evaluated. Key in vitro and animal data were incorporated into the pharmacology and pharmacokinetic sections where appropriate. Data Synthesis: Four phase 3 trials have evaluated the use of brexpiprazole as a primary therapy for schizophrenia or as an antidepressant adjunct for MDD. For its schizophrenia indication, brexpiprazole was studied in 2 placebo-controlled trials of approximately 1300 patients, with 4 mg of brexpiprazole consistently showing superiority over placebo. For MDD, brexpiprazole was compared with placebo as an adjunct to antidepressants in approximately 1000 patients who had failed trials of 1 to 3 prior antidepressants. The 2-mg and 3-mg dosages of brexpiprazole showed consistent superiority over placebo in the MDD trials. Common treatment emergent adverse effects included akathisia and weight gain. Conclusions: Brexpiprazole showed efficacy for the treatment of schizophrenia in the range of 2 to 4 mg/d and as an adjunct to antidepressant therapy in MDD when dosed at 2 to 3 mg/d. Advantages of this drug include once-daily dosing, good tolerability, and lack of effect on sexual function. Disadvantages include the lack of long-term safety data and potentially high cost.
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&NA;. "Antidepressants." Drugs & Therapy Perspectives 10, no. 7 (September 1997): 14–16. http://dx.doi.org/10.2165/00042310-199710070-00005.
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Rudorfer, Matthew V., and William Z. Potter. "Antidepressants." Drugs 37, no. 5 (May 1989): 713–38. http://dx.doi.org/10.2165/00003495-198937050-00006.
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Snead, Tarolyn J., and Cherry W. Jackson. "St. John's Wort: A Review of an Herbal Antidepressant." Journal of Pharmacy Practice 12, no. 3 (June 1999): 210–16. http://dx.doi.org/10.1177/089719009901200308.
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Hypericum perforatum, more commonly known as St. John's wort, is an herbal product that has been utilized as an antidepressant in Europe for many years. This product has become popular in the United States as an alternative to traditional antidepressants. Due to the fact that St. John's wort is not regulated by the Food and Drug Administration (FDA), many questions exist about the safety and efficacy of this product. This article will provide a review of the history, pharmacology, and safety profile of St. John' wort, as well as its efficacy in the treatment of major depressive disorder.
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Yan, Kuo, Yi-Bing Chen, Jia-Rong Wu, Kuang-Dai Li, and Yuan-Lu Cui. "Current Rapid-Onset Antidepressants and Related Animal Models." Current Pharmaceutical Design 24, no. 22 (October 19, 2018): 2564–72. http://dx.doi.org/10.2174/1381612824666180727115222.
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Depression is a common mental disease, and it is one of the most crippling diseases in the world. Although current pharmacotherapies contribute to the treatment of depression, the high incidence of a partial responses or no responses, and delayed onset of the antidepressants, make many patients to experience unsatisfactory results from treatment. In view of the high suicide rate during the period of drug onset, it is critical to find antidepressant drugs with rapid onset for the treatment of depression. This paper mainly reviews some drugs that have rapid antidepressant effect and their mechanisms, including monoaminergic receptor drugs, glutamate receptor drugs, mammalian target of rapamycin (mTOR) signaling agonist, gamma-aminobutyric acid energy (GABAergic) agonist and drug combinations. In addition, we introduce several rodent models currently used to assess antidepressant onset in this review: chronic unpredictable mild stress (CUMS), forced swimming test (FST) and tail suspension test (TST), olfactory bulbectomy (OBX) and other models, which provide a methodological approach for assessing the rapid onset of antidepressant drugs.
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Alén, Francisco, Laura Orio, Miguel Á. Gorriti, Raquel Gómez de Heras, María Teresa Ramírez-López, Miguel Ángel Pozo, and Fernando Rodríguez de Fonseca. "Increased alcohol consumption in rats after subchronic antidepressant treatment." International Journal of Neuropsychopharmacology 16, no. 8 (September 1, 2013): 1809–18. http://dx.doi.org/10.1017/s1461145713000217.
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AbstractThe use of antidepressants for alcoholism in humans has been a matter of controversy in recent years. Despite the existence of an important co-morbidity for depression and alcoholism, some studies suggest that the use of antidepressants could worsen the prognosis of alcoholism. However, there is a lack of studies in animal models exploring this phenomenon. In the present study, we show how the 15-d treatment with fluoxetine (10 mg/kg) or venlafaxine (50 mg/kg) affected alcohol deprivation effect (ADE) and subsequent alcohol consumption. Initially, fluoxetine reduced ADE and venlafaxine did not affect it. However, in the following days, both antidepressants increased alcohol consumption, an effect that was found to last at least 5 wk. Fluoxetine treatment was shown to cause a locomotor sensitized response to a challenge dose of amphetamine (0.5 mg/kg), indicating the presence of a supersensitive dopaminergic transmission. In summary, antidepressant treatment may increase alcohol consumption in rats after a period of alcohol deprivation and this could be related to alterations in the reward circuitry. This finding confirms in an animal model previous reports in humans that may limit the use of antidepressants for alcoholism.
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Undurraga, Juan, Kang Sim, Leonardo Tondo, Ariel Gorodischer, Emilio Azua, Kai Hong Tay, David Tan, and Ross J. Baldessarini. "Lithium treatment for unipolar major depressive disorder: Systematic review." Journal of Psychopharmacology 33, no. 2 (January 30, 2019): 167–76. http://dx.doi.org/10.1177/0269881118822161.
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Background: The potential value of lithium treatment in particular aspects of unipolar major depressive disorder remains uncertain. Methods: With reports of controlled trials identified by systematic searching of Medline, Cochrane Library, and PsycINFO literature databases, we summarized responses with lithium and controls followed by selective random-effects meta-analyses. Results: We identified 36 reports with 39 randomized controlled trials: six for monotherapy and 12 for adding lithium to antidepressants for acute major depression, and 21 for long-term treatment. Data for monotherapy of acute depression were few and inconclusive. As an adjunct to antidepressants, lithium was much more effective than placebo ( p<0.0001). For long-term maintenance treatment, lithium was more effective than placebo in monotherapy ( p=0.011) and to supplement antidepressants ( p=0.038), and indistinguishable from antidepressant monotherapy. Conclusions: The findings indicate efficacy of lithium as a treatment for some aspects of major depressive disorder, especially as an add-on to antidepressants and for long-term prophylaxis. It remains uncertain whether some benefits of lithium treatment occur with many major depressive disorder patients, or if efficacy is particular to a subgroup with bipolar disorder-like characteristics or mixed-features.
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Lotrich, Francis E., and Bruce G. Pollock. "Aging and Clinical Pharmacology: Implications for Antidepressants." Journal of Clinical Pharmacology 45, no. 10 (October 2005): 1106–22. http://dx.doi.org/10.1177/0091270005280297.
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Vázquez, Gustavo H., Anees Bahji, Juan Undurraga, Leonardo Tondo, and Ross J. Baldessarini. "Efficacy and Tolerability of Combination Treatments for Major Depression: Antidepressants plus Second-Generation Antipsychotics vs. Esketamine vs. Lithium." Journal of Psychopharmacology 35, no. 8 (July 9, 2021): 890–900. http://dx.doi.org/10.1177/02698811211013579.
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Background: Successful treatment of major depressive disorder (MDD) can be challenging, and failures ("treatment-resistant depression" [TRD]) are frequent. Steps to address TRD include increasing antidepressant dose, combining antidepressants, adding adjunctive agents, or using nonpharmacological treatments. Their relative efficacy and tolerability remain inadequately tested. In particular, the value and safety of increasingly employed second-generation antipsychotics (SGAs) and new esketamine, compared to lithium as antidepressant adjuncts remain unclear. Methods: We reviewed randomized, placebo-controlled trials and used random-effects meta-analysis to compare odds ratio (OR) versus placebo, as well as numbers-needed-to-treat (NNT) and to-harm (NNH), for adding SGAs, esketamine, or lithium to antidepressants for major depressive episodes. Results: Analyses involved 49 drug-placebo pairs. By NNT, SGAs were more effective than placebo (NNT = 11 [CI: 9–15]); esketamine (7 [5–10]) and lithium (5 [4–10]) were even more effective. Individually, aripiprazole, olanzapine+fluoxetine, risperidone, and ziprasidone all were more effective (all NNT < 10) than quetiapine (NNT = 13), brexpiprazole (16), or cariprazine (16), with overlapping NNT CIs. Risk of adverse effects, as NNH for most-frequently reported effects, among SGAs versus placebo was 5 [4–6] overall, and highest with quetiapine (NNH = 3), lowest with brexpiprazole (19), 5 (4–6) for esketamine, and 9 (5–106) with lithium. The risk/benefit ratio (NNH/NNT) was 1.80 (1.25–10.60) for lithium and much less favorable for esketamine (0.71 [0.60–0.80]) or SGAs (0.45 [0.17–0.77]). Conclusions: Several modern antipsychotics and esketamine appeared to be useful adjuncts to antidepressants for acute major depressive episodes, but lithium was somewhat more effective and better tolerated. Limitations: Most trials of adding lithium involved older, mainly tricyclic, antidepressants, and the dosing of adjunctive treatments were not optimized.
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Hafferty, Jonathan D., Eleanor M. Wigmore, David M. Howard, Mark J. Adams, Toni-Kim Clarke, Archie I. Campbell, Donald J. MacIntyre, et al. "Pharmaco-epidemiology of antidepressant exposure in a UK cohort record-linkage study." Journal of Psychopharmacology 33, no. 4 (February 27, 2019): 482–93. http://dx.doi.org/10.1177/0269881119827888.
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Objectives: Antidepressants are the most commonly prescribed psychiatric medication but concern has been raised about significant increases in their usage in high income countries. We aimed to quantify antidepressant prevalence, incidence, adherence and predictors of use in the adult population. Methods: The study record-linked administrative prescribing and morbidity data to the Generation Scotland cohort ( N = 11,052), between 2009 and 2016. Prevalence and incidence of any antidepressant use was determined. Antidepressant adherence was measured using Proportion of Days Covered and Medication Possession Ratio. Time-to-event analysis for incident antidepressant use within 5 years of Generation Scotland: Scottish Family Health Study (GS:SFHS) recruitment was performed to reveal patient-level predictors of use. Results: Almost one-third (28.0%, 95%CI 26.9–29.1) of the adults in our sample were prescribed at least one antidepressant in the 5-year period 2012–2016. There was a 36.2% increase in annual prevalence between 2010 and 2016. Incidence was 2.4(2.1–2.7)% per year. The majority of antidepressant episodes (57.6%) were greater than 9 months duration and adherence was generally high (69.0% with Proportion of Days Covered >80%). Predictors of new antidepressant use included history of affective disorder, being female, physical comorbidities, higher neuroticism scores, and lower cognitive function scores. Conclusions: Antidepressant prevalence is greater than previously reported but incidence remains relatively stable. We found the majority of antidepressant episodes to be of relatively long duration with good estimated adherence. Our study supports the hypothesis that increased long-term use among existing (and returning) users, along with wider ranges of indications for antidepressants, has significantly increased the prevalence of these medications.
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Hunter, Tracy S. "L-methylfolate in the Therapeutic Management of Major Depressive Disorder." Journal of Pharmacy Practice 21, no. 4 (July 22, 2008): 278–86. http://dx.doi.org/10.1177/0897190008318132.
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Optimal levels of the bioactive folate are necessary for maintaining proper brain and body functioning. Folate deprivation and impaired folate metabolism are clinically associated with defects in the developing nervous system. Numerous studies implicate a deficiency of bioactive folate with an increased risk of major depressive disorder and other neuropsychiatric disorders. Bioactive forms of folate, particularly L-methylfolate, have been found to augment the therapeutic efficacy of antidepressants in patients with major depressive disorder, who fail to adequately respond to standard therapies. The antidepressant action of L-methylfolate appears to improve treatment outcomes most effectively when administered as an adjuvant to traditional antidepressants. This new understanding of the role of folates in major depressive disorder and other mood disorders offers opportunities to improve treatment outcomes.
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Du, Dan, Qiong Tang, Qiong Han, Jin Zhang, Xuemei Liang, Youguo Tan, Kezhi Liu, and Bo Xiang. "Association between genetic polymorphism and antidepressants in major depression: a network meta-analysis." Pharmacogenomics 21, no. 13 (August 2020): 963–74. http://dx.doi.org/10.2217/pgs-2020-0037.
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This network meta-analysis was conducted to compare the predictive value of eight SNPs on the efficacy of antidepressants in major depressive disorder (MDD), including 5-HTTLPR, 5HTR2A (rs6311, rs6314, rs7997012 and rs6313), 5HTR2A (rs6295), BDNF (rs6265) and 5HTTSTin2. Databases were searched for related studies published up to December 2019. A total of 16 studies were included in this study. The predictive value were evaluated by the use of the odd ratios (OR) and drawing surface under the cumulative ranking curves (SUCRA). The pairwise meta-analysis indicated that in terms of overall response ratio, the SNPs were not associated with the efficacy of antidepressants in MDD. The result of this network meta-analysis suggested that there was no significant difference in predictive value of eight SNPs on the efficacy of antidepressants in MDD. More research is needed to explore the relationship between SNPs and antidepressant response.
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Cohen, Henry, Robert S. Hoffman, and Mary Ann Howland. "Cyclic Antidepressant Poisoning: A Review and Case Report." Journal of Pharmacy Practice 6, no. 2 (April 1993): 89–102. http://dx.doi.org/10.1177/089719009300600208.
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Although newer cyclic antidepressants have been introduced over the past several years, the tricyclic antidepressants (TCAs) continue to be the leading cause of morbidity from drug overdose in the United States. Overdose features depend on the particular cyclic antidepressant ingested and its pharmacological properties, and can include CNS depression, cardiac arrhythmias, hypotension, seizures, and anticholinergic symptomatology. Life-threatening symptomatology almost always begins within 2 hours, and certainly within 6 hours, after arrival to the emergency department. Plasma TCA levels are unreliable predictors of TCA toxicity and are not recommended. An ECG with a prolonged QRS complex more than 100 msec seems to be the best indicator of serious sequelae with TCAs. Management consists of stabilization of vital signs, gastrointestinal decontamination, intravenous sodium bicarbonate, and supportive care. Agents once thought to be useful for the treatment of cardiac dysrhythmias and seizures such as phenytoin and physostigmine should be avoided. The future of TCA antibody fragments in the treatment of TCA overdose seems promising. Newer and, to some degree, safer antidepressants in overdose have recently been introduced, and they include fluoxetine, trazodone, and sertraline. Amoxapine, bupropion, and maprotiline seem to be as toxic as the TCAs. A significant interaction between cyclic antidepressants and monoamine-oxidase inhibitors exists. Management includes supportive care and basic poison management. Prevention of poisoning seems to be the most logical and effective method of maintaining patient safety. TCAs should be avoided in children younger than 6 years old. All adults with suicidal ideations should receive no more than a 1-week supply (about 1 g) of drug. Finally consideration should be given to using one of the newer, safer antidepressants in all patients with suicidal ideations.
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Maneeton, Benchalak, Narong Maneeton, Pakapan Woottiluk, and Surinporn Likhitsathian. "Repetitive Transcranial Magnetic Stimulation Combined with Antidepressants for the First Episode of Major Depressive Disorder." Current Neuropharmacology 18, no. 9 (October 6, 2020): 852–60. http://dx.doi.org/10.2174/1570159x18666200221113134.
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Objectives: The aims of this study were to systematically review the efficacy, acceptability, and tolerability of repetitive transcranial magnetic stimulation (rTMS) combined with antidepressants in the treatment of the first major depressive disorder (MDD) episode. Materials and Methods: The primary efficacious outcome was the pooled mean-endpoint scores of the Hamilton Depression Rating Scale (HAMD). Rates of response, remission rate, overall discontinuation and discontinuation due to adverse events were also evaluated. Search in the Scopus, PubMed, CINAHL, and Cochrane Controlled Trials Register databases for interesting outcomes was carried out in March 2018. Results: A total of 108 randomized patients of two randomized controlled trials were included in this study. The pooled mean- endpoint scores of the HAMD in one, two, and four weeks for rTMS plus antidepressants (citalopram or paroxetine) were greater than that of sham plus the antidepressants. The pooled rates of overall discontinuation and discontinuation rates due to adverse events were not different between the two groups. Conclusion: According to a piece of limited evidence, the high-frequency repetitive transcranial magnetic stimulation (HF-rTMS) could accelerate the antidepressant effect of SSRIs in young patients with a first-episode major depressive disorder. However, the acceptability and tolerability of HF-rTMS in the treatment of such patients are no better than an antidepressant alone. However, further well-defined and large sample-size studies of HF-rTMS combined with an antidepressant in MDD should be carried out to warrant these results.
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Schweitzer, Isaac, and Kay Maguire. "Stopping antidepressants." Australian Prescriber 24, no. 1 (February 1, 2001): 13–15. http://dx.doi.org/10.18773/austprescr.2001.008.
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Hollister, L. E., and J. L. Claghorn. "New Antidepressants." Annual Review of Pharmacology and Toxicology 33, no. 1 (April 1993): 165–77. http://dx.doi.org/10.1146/annurev.pa.33.040193.001121.
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Hollister, L. E. "Current Antidepressants." Annual Review of Pharmacology and Toxicology 26, no. 1 (April 1986): 23–37. http://dx.doi.org/10.1146/annurev.pa.26.040186.000323.
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