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| Systematic (IUPAC) name | |
|---|---|
| (±)-2-methyl-1,2,3,4,10,14b-hexahydropyrazino[2,1-a]pyrido[2,3-c][2]benzazepine | |
| Clinical data | |
| Trade names | Remeron, Avanza, Zispin |
| AHFS/Drugs.com | monograph |
| MedlinePlus | a697009 |
| Pregnancy cat. | C |
| Legal status | ℞ Prescription only |
| Routes | Oral |
| Pharmacokinetic data | |
| Bioavailability | 50%[1] |
| Protein binding | 85%[1] |
| Metabolism | Liver (CYP1A2, CYP2D6, and CYP3A4)[2][1] |
| Half-life | 20–40 hours[1] |
| Excretion | Urine (75%)[1] Feces (15%)[1] |
| Identifiers | |
| CAS number | 61337-67-5 Y |
| ATC code | N06AX11 |
| PubChem | CID 4205 |
| DrugBank | DB00370 |
| ChemSpider | 4060 Y |
| UNII | A051Q2099Q N |
| KEGG | D00563 Y |
| ChEBI | CHEBI:6950 N |
| ChEMBL | CHEMBL654 Y |
| Synonyms | 6-Azamianserin, Org 3770 |
| Chemical data | |
| Formula | C17H19N3 |
| Mol. mass | 265.35 g/mol |
|
SMILES
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InChI
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| Physical data | |
| Density | 1.22 g/cm³ |
| Melt. point | 114–116 °C (237–241 °F) |
| Boiling point | 432 °C (810 °F) |
| Solubility in water | Soluble in methanol and chloroform mg/mL (20 °C) |
| N (what is this?) (verify) |
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Mirtazapine (Remeron, Avanza, Zispin) is a noradrenergic and specific serotonergic antidepressant (NaSSA) which was introduced by Organon International in the United States in 1990 and is used primarily in the treatment of depression. It is also commonly used as an anxiolytic, hypnotic, antiemetic, and appetite stimulant. Structurally, mirtazapine can also be classified as a tetracyclic antidepressant (TeCA).
Contents
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Medical uses
Approved and off-label
Mirtazapine's primary use is the treatment of major depressive disorder and other mood disorders.[3][4]
However, it has also been found useful in alleviating the following conditions and may be prescribed off-label for their treatment:
- Generalized anxiety disorder[2][5]
- Social anxiety disorder[6][7]
- Obsessive-compulsive disorder[6][8]
- Panic disorder[6][9][10]
- Post-traumatic stress disorder[6]
- Anorexia nervosa[11]
- Insomnia[12][13]
- Nausea/vomiting[14][15][16]
- Low appetite/underweightness[17][18][19]
- Itching[20][21]
- Headaches and migraine[22][23][15]
Investigational
Mirtazapine has had literature published on its efficacy in the experimental treatment of the following conditions:
- Sleep apnea/hypopnea[24][25]
- Inappropriate sexual behavior and other secondary symptoms of autistic spectrum conditions and other pervasive developmental disorders[26][27][28][29]
- Neuroleptic-induced akathisia[30][31]
- Drug withdrawal, dependence, and detoxification[32][33][34][35][36]
Efficacy and tolerability
In clinical studies, mirtazapine has been found to be an effective antidepressant with a generally tolerable side effect profile relative to other antidepressants.[37]
In a major systematic review published in 2009 which compared the efficacy and tolerability of 12 popular antidepressants, mirtazapine was found to be superior to all of the included selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs), and reboxetine, bupropion, and mianserin in terms of antidepressant efficacy, while it was average in regards to tolerability.[37] However, it is important to note that the efficacies of most of the antidepressants in this review differed only slightly. Hence, the apparent superiority of mirtazapine relative to most of the others included may not actually be all that prominent or significant in this case.
Compared to earlier antidepressants, mirtazapine has been found to be significantly superior to trazodone,[38] while it has been shown to be approximately equivalent in efficacy to several of the tricyclic antidepressants (TCAs) including amitriptyline, doxepin, and clomipramine, though with a much improved tolerability profile.[2][39] However, two other studies found mirtazapine to be significantly inferior to imipramine, another TCA.[40][41] One study compared the combination of venlafaxine and mirtazapine to the monoamine oxidase inhibitor (MAOI) tranylcypromine alone and found them to be similarly effective, though tranylcypromine was much less tolerable in regards to side effects and drug interactions.[42]
All antidepressants, including mirtazapine, generally require a few weeks for their therapeutic benefits on depressive and anxious symptoms to become apparent.[43] Unlike most antidepressants, however, mirtazapine has demonstrated itself to have a faster onset of antidepressant action with an initial reduction in affective symptoms being seen within the first week of treatment and the maximal change in improvement occurring over the course of the first two weeks.[43][44] Hence, it may be a better choice for patients in whom hastened relief is dire, such as those who are considered to be a suicide risk.
Adverse reactions
Side effects
Common side effects of mirtazapine include dizziness, blurred vision, sedation, somnolence, malaise, increased appetite, weight gain, dry mouth, constipation, and joint and muscle pain. Less common side effects that tend to occur more often at higher doses include restlessness, irritability, aggression, apathy, anhedonia, difficulty swallowing, shallow breathing, decreased body temperature, pupil constriction, nocturnal emissions, spontaneous orgasms, impaired balance, restless legs syndrome, and vivid dreams.[2][45][46][47] Rare and potentially serious adverse reactions of mirtazapine include allergic reaction, edema, fainting, seizures, bone marrow suppression, myelodysplasia, and agranulocytosis.[12]
Mirtazapine is not considered to have a risk of many of the side effects often associated with other antidepressants like the SSRIs, and may actually improve certain ones when taken in conjunction with them.[2][39] These adverse effects include decreased appetite, weight loss, insomnia, nausea and vomiting, diarrhea, urinary retention, increased body temperature, excessive sweating, pupil dilation, and sexual dysfunction.[2][39]
In general, some antidepressants, especially SSRIs, can paradoxically exacerbate some patients' depression or anxiety or cause suicidal ideation.[48] Mirtazapine is also believed to be capable of this, and for this reason in the United States and certain other countries it carries a black box label warning of these potential effects.
Discontinuation
Mirtazapine and other antidepressants may cause a withdrawal syndrome upon discontinuation.[2][49][50][51] A gradual and slow reduction in dose is recommended in order to minimize withdrawal symptoms.[52] Effects of sudden cessation of treatment with mirtazapine may include depression, anxiety, panic attacks, vertigo, restlessness, irritability, decreased appetite, insomnia, diarrhea, nausea, vomiting, flu-like symptoms such as allergies and pruritus, headaches, and sometimes hypomania or mania.[49][50][53][54][55]
Overdose
Mirtazapine is considered to be relatively safe in the event of an overdose.[56] Unlike the TCAs, mirtazapine showed no significant cardiovascular adverse effects at 7 to 22 times the maximum recommended dose.[39] Case reports of overdose with as much as 30 to 50 times the standard dose described the drug as relatively nontoxic, compared to TCAs.[57][58]
Only 12 fatalities have been attributed to mirtazapine overdose in literature.[59][60] However, the fatal toxicity index (deaths per million prescriptions) for mirtazapine is only 3.1 (95% CI: 0.1 to 17.2). This is similar to that observed with SSRIs.[61]
Pharmacology
Binding profile
Mirtazapine is an antagonist/inverse agonist at the following receptors:[62][63]
- 5-HT1A receptor (Ki=18nM; IC50=1,000nM) [64]
- 5-HT2A receptor (Ki = 69 nM)
- 5-HT2B receptor (Ki = ? (~20-fold lower than for 5-HT2A/2C))[65]
- 5-HT2C receptor (Ki = 39 nM)
- 5-HT3 receptor (Ki = ? (similar to 5-HT2A/2C (mouse neuroblastoma cell)))[66]
- 5-HT7 receptor (Ki = 265 nM)
- α1-adrenergic receptor (Ki = 608 nM (rat))
- α2A-adrenergic receptor (Ki = 20 nM)
- α2B-adrenergic receptor (Ki = ? nM (likely similar to α2A/α2B-adrenergic))[citation needed]
- α2C-adrenergic receptor (Ki = 18 nM)
- H1 receptor (Ki = 1.6 nM)
- mACh receptors (Ki = 794 nM (rat))
- Dopamine D1 receptor (Ki=4,167nM) [67]
- Dopamine D2 receptor (Ki=1,460nM) [68]
- Dopamine D3 receptor (Ki=5,723nM) [69]
- Dopamine D4 receptor (Ki=25nM) [70]
Mirtazapine has also shown affinity towards the norepinephrine transporter and perhaps also (results of test unspecified) the serotonin and dopamine transporter:
- Norepinephrine transporter (IC50=260nM) [71]
- Serotonin transporter (IC50=100nM) [72]
- Dopamine transporter (IC50=1,000nM) [73]
All affinities listed were assayed using human materials except those for α1-adrenergic and mACh which are for rat tissues, due to human values being unavailable.[62][63]
Though not known to have ever been screened at this site, it is possible that mirtazapine may act on the 5-HT6 receptor as well. Supporting this speculation is the fact that its analogue mianserin (which, structurally, can also be called 6-desazamirtazapine) has been shown to have high affinity for 5-HT6 and does not produce cAMP accumulation (indicating it is an antagonist).[74]
Correspondence to clinical effects
Antagonization of the α2-adrenergic receptors which function largely as autoreceptors and heteroreceptors enhances adrenergic and serotonergic neurotransmission, notably central 5-HT1A receptor-mediated transmission in the dorsal raphe nucleus and hippocampus; hence mirtazapine's classification as a NaSSA. Indirect α1-adrenoceptor-mediated enhancement of 5-HT cell firing and direct blockade of inhibitory α2-heteroreceptors located on 5-HT terminals are held responsible for the increase in extracellular 5-HT.[3][2][75][76][77] Because of this, mirtazapine has been said to be a functional "indirect agonist" of the 5-HT1A receptor.[76] Increased activation of the central 5-HT1A receptor is thought to be a major mediator of efficacy of most antidepressant drugs.[78] Unlike most conventional antidepressants, however, at clinically used doses mirtazapine has no appreciable affinity for the serotonin, norepinephrine, or dopamine transporters and thus lacks any significant effects as a reuptake inhibitor of these neurotransmitters,[79] nor does it have any significant inhibitory effects on monoamine oxidase.[80]
Antagonism of the 5-HT2 subfamily of receptors, especially the 5-HT2C receptor, appears to be in part responsible for mirtazapine's efficacy in the treatment of depressive states.[81][82] The 5-HT2C receptor is known to inhibit the release of the neurotransmitters dopamine and norepinephrine in various parts of the brains of rodents, notably in reward pathways such as the ventral tegmental area.[83][84] Accordingly, it was shown that by blocking the α2-adrenergic receptors and 5-HT2C receptors mirtazapine disinhibited dopamine and norepinephrine activity in these areas in rats.[85] In addition, mirtazapine's antagonism of the 5-HT2A and 5-HT2C receptors has beneficial effects on anxiety, sleep and appetite, as well as sexual function regarding the latter receptor.[2][39]
Antagonism of the 5-HT3 receptor, an action mirtazapine shares with the approved antiemetic ondansetron, significantly improves pre-existing symptoms of nausea, vomiting, diarrhea, and irritable bowel syndrome in afflicted individuals.[86] Mirtazapine may be used as an inexpensive antiemetic alternative to ondansetron.[16] Blockade of the 5-HT3 receptors has also shown to improve anxiety and to be effective in the treatment of drug addiction in several studies.[87] Accordingly, in conjunction with substance abuse counseling, mirtazapine has been investigated for the purpose of reducing methamphetamine use in dependent individuals with success.[36] In contrast to mirtazapine, the SSRIs, SNRIs, MAOIs, and some TCAs increase the general activity of the 5-HT2A, 5-HT2C, and 5-HT3 receptors leading to a host of negative changes and side effects, the most prominent of which include anorexia, insomnia, sexual dysfunction (loss of libido and anorgasmia), nausea, and diarrhea, among others. As a result, mirtazapine is often combined with these drugs to reduce their side effect profile and to produce a stronger antidepressant effect.[39][42][88][89][90][91]
Mirtazapine is a very strong H1 receptor inverse agonist and as a result, it can cause powerful sedative and hypnotic effects.[2] After a short period of chronic treatment, however, the H1 receptor tends to sensitize and the antihistamine effects become more tolerable. Many patients may also dose at night to avoid the effects and this appears to be an effective strategy for combating them. Blockade of the H1 receptor may improve pre-existing allergies, pruritus, nausea, and insomnia in afflicted individuals. It may also contribute to weight gain, however.[92] In contrast to the H1 receptor, mirtazapine has very low affinity for the mACh receptors, and thus is virtually devoid of any anticholinergic properties at clinically used doses.[93]
Similarly to many other antidepressants, mirtazapine has been found to have antinociceptive properties in mice.[94] However, unlike most other antidepressants, though similarly to venlafaxine, these effects are mostly mediated through downstream modulation of the endogenous opioid system, of which in the case of mirtazapine the μ-opioid and κ3-opioid receptors are mainly involved.[94] Interestingly, while virtually all antidepressants differ little in their maximal effectiveness in the treatment of major depression, mirtazapine and venlafaxine have demonstrated superior efficacy in treating severe types of depression such as psychotic depression and treatment-resistant depression.[94] It has been suggested that this may be due to their unique influence on the opioid system, which is a property that has been hypothesized to somehow give them an advantage over other antidepressants in cases of severe depressive symptomatology.[94]
Pharmacokinetics
Dosage
Mirtazapine is typically prescribed in doses ranging from 15 mg to 45 mg. However, clinical doses as high as 120 mg have been reported in the medical literature.[95]
Interactions
Concurrent use with inhibitors or inducers of the cytochrome (CYP) P450 isoenzymes CYP1A2, CYP2D6, and/or CYP3A4 can result in altered concentrations of mirtazapine, as these are the main enzymes responsible for its metabolism.[2][1] As examples, fluoxetine and paroxetine, inhibitors of these enzymes, are known to modestly increase mirtazapine levels, while carbamazepine, an inducer, considerably decreases them.[1]
According to information from the manufacturers, mirtazapine should not be started within two weeks of any MAOI usage; similarly, MAOIs should not be administered within two weeks of discontinuing mirtazapine.[96] Contradictorily, however, a single study regarding the combination reported that it does not result in any incidence of serotonin-related toxicity.[97] In addition, a case report claimed that mirtazapine can actually be used to treat serotonin syndrome.[98] Mirtazapine in combination with an SSRI, SNRI, or TCA as an augmentation strategy is considered to be relatively safe and is often employed therapeutically,[39][42][88][89][90] with a combination of venlafaxine and mirtazapine sometimes referred to as "California rocket fuel".[99]
A case report described mirtazapine as inducing hypertension in a clonidine-treated patient, likely due to occupancy of α2 autoreceptors by mirtazapine limiting the efficacy of concurrent clonidine therapy.[100]
Liver and moderate renal impairment has been reported to decrease the oral clearance of mirtazapine by approximately 30%; severe renal impairment decreases it by 50%.[1]
Chemistry
Mirtazapine is a racemic mixture of enantiomers. The (S)-(+)-enantiomer is known as esmirtazapine.
A four-step chemical synthesis of mirtazapine has been published.[101][102]
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- ^ Unspecified as to whether it was active or inactive in this assay neither was its actions towards 5-HT1A specified; PMID=14640559 (IC50) and PMID=12109911 (Ki)
- ^ De Boer, T (1996). "The pharmacologic profile of mirtazapine". The Journal of clinical psychiatry 57 Suppl 4: 19–25. PMID 8636062.
- ^ Kooyman AR, Zwart R, Vanderheijden PM, Van Hooft JA, Vijverberg HP (1994). "Interaction between enantiomers of mianserin and ORG3770 at 5-HT3 receptors in cultured mouse neuroblastoma cells". Neuropharmacology 33 (3-4): 501–7. doi:10.1016/0028-3908(94)90081-7. PMID 7984289.
- ^ Unknown whether this is agonist or antagonist activity see - PMID=15771415
- ^ As above, PMID=12109911
- ^ As above, PMID=15771415
- ^ As above, PMID=12109911
- ^ As above, PMID=12109911
- ^ As above, plus whether the mirtazapine was active or inactive in the assay was unspecified, PMID=12109911
- ^ As above, PMID=14640559
- ^ Boess FG, Monsma FJ, Carolo C, Meyer V, Rudler A, Zwingelstein C, Sleight AJ (1997). "Functional and radioligand binding characterization of rat 5-HT6 receptors stably expressed in HEK293 cells". Neuropharmacology 36 (4-5): 713–20. doi:10.1016/S0028-3908(97)00019-1. PMID 9225298.
- ^ De Boer T, Nefkens F, Van Helvoirt A (February 1994). "The alpha 2-adrenoceptor antagonist Org 3770 enhances serotonin transmission in vivo". Eur. J. Pharmacol. 253 (1-2): R5–6. doi:10.1016/0014-2999(94)90778-1. PMID 7912194. [unreliable medical source?]
- ^ a b Berendsen HH, Broekkamp CL (October 1997). "Indirect in vivo 5-HT1A-agonistic effects of the new antidepressant mirtazapine". Psychopharmacology (Berl.) 133 (3): 275–82. doi:10.1007/s002130050402. PMID 9361334.
- ^ Nakayama K, Sakurai T, Katsu H (April 2004). "Mirtazapine increases dopamine release in prefrontal cortex by 5-HT1A receptor activation". Brain Res. Bull. 63 (3): 237–41. doi:10.1016/j.brainresbull.2004.02.007. PMID 15145142. [unreliable medical source?]
- ^ Blier P, Abbott FV (January 2001). "Putative mechanisms of action of antidepressant drugs in affective and anxiety disorders and pain". J Psychiatry Neurosci 26 (1): 37–43. PMC 1408043. PMID 11212592. http://www.cma.ca/multimedia/staticContent/HTML/N0/l2/jpn/vol-26/issue-1/pdf/pg37.pdf.
- ^ Tatsumi M, Groshan K, Blakely RD, Richelson E (December 1997). "Pharmacological profile of antidepressants and related compounds at human monoamine transporters". European Journal of Pharmacology 340 (2-3): 249–58. doi:10.1016/S0014-2999(97)01393-9. PMID 9537821. http://linkinghub.elsevier.com/retrieve/pii/S0014-2999(97)01393-9.
- ^ Fisar Z, Hroudová J, Raboch J (2010). "Inhibition of monoamine oxidase activity by antidepressants and mood stabilizers". Neuro Endocrinology Letters 31 (5): 645–56. PMID 21200377.
- ^ Millan MJ (2005). "Serotonin 5-HT2C receptors as a target for the treatment of depressive and anxious states: focus on novel therapeutic strategies". Therapie 60 (5): 441–60. doi:10.2515/therapie:2005065. PMID 16433010.
- ^ Dekeyne A, Millan MJ (April 2009). "Discriminative stimulus properties of the atypical antidepressant, mirtazapine, in rats: a pharmacological characterization". Psychopharmacology (Berl.) 203 (2): 329–41. doi:10.1007/s00213-008-1259-8. PMID 18709360.
- ^ De Deurwaerdère P, Navailles S, Berg KA, Clarke WP, Spampinato U (March 2004). "Constitutive activity of the serotonin2C receptor inhibits in vivo dopamine release in the rat striatum and nucleus accumbens". J. Neurosci. 24 (13): 3235–41. doi:10.1523/JNEUROSCI.0112-04.2004. PMID 15056702. [unreliable medical source?]
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- ^ Millan MJ, Gobert A, Rivet JM, Adhumeau-Auclair A, Cussac D, Newman-Tancredi A, Dekeyne A, Nicolas JP, Lejeune F (March 2000). "Mirtazapine enhances frontocortical dopaminergic and corticolimbic adrenergic, but not serotonergic, transmission by blockade of α2-adrenergic and serotonin2C receptors: a comparison with citalopram". Eur. J. Neurosci. 12 (3): 1079–95. doi:10.1046/j.1460-9568.2000.00982.x. PMID 10762339.
- ^ Kast RE (September 2001). "Mirtazapine may be useful in treating nausea and insomnia of cancer chemotherapy". Support Care Cancer 9 (6): 469–70. doi:10.1007/s005200000215. PMID 11585276.
- ^ Costall B, Naylor RJ, Tyers MB (1990). "The psychopharmacology of 5-HT3 receptors". Pharmacology & Therapeutics 47 (2): 181. doi:10.1016/0163-7258(90)90086-H.
- ^ a b Sennef C, Timmer CJ, Sitsen JM (March 2003). "Mirtazapine in combination with amitriptyline: a drug-drug interaction study in healthy subjects". Hum Psychopharmacol 18 (2): 91–101. doi:10.1002/hup.441. PMID 12590402. [unreliable medical source?]
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- ^ a b Ravindran LN, Eisfeld BS, Kennedy SH (February 2008). "Combining mirtazapine and duloxetine in treatment-resistant depression improves outcomes and sexual function". J Clin Psychopharmacol 28 (1): 107–8. doi:10.1097/JCP.0b013e318160d609. PMID 18204355. [unreliable medical source?]
- ^ Caldis EV, Gair RD (October 2004). "Mirtazapine for treatment of nausea induced by selective serotonin reuptake inhibitors". Can J Psychiatry 49 (10): 707. PMID 15560319.
- ^ Chiu HW, Li TC (2011). "Rapid weight gain during mirtazapine treatment". The Journal of Neuropsychiatry and Clinical Neurosciences 23 (1): E7. doi:10.1176/appi.neuropsych.23.1.E7. PMID 21304130. http://neuro.psychiatryonline.org/article.aspx?volume=23&page=E7.
- ^ Burrows GD, Kremer CM (April 1997). "Mirtazapine: clinical advantages in the treatment of depression". Journal of Clinical Psychopharmacology 17 Suppl 1: 34S–39S. PMID 9090576. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0271-0749&volume=17&issue=&spage=34S.
- ^ a b c d Schreiber S, Bleich A, Pick CG (2002). "Venlafaxine and mirtazapine: different mechanisms of antidepressant action, common opioid-mediated antinociceptive effects--a possible opioid involvement in severe depression?". J. Mol. Neurosci. 18 (1-2): 143–9. doi:10.1385/JMN:18:1-2:143. PMID 11931344.
- ^ Kristensen JH, Ilett KF, Rampono J, Kohan R, Hackett LP (March 2007). "Transfer of the antidepressant mirtazapine into breast milk". British Journal of Clinical Pharmacology 63 (3): 322–7. doi:10.1111/j.1365-2125.2006.02773.x. PMC 2000733. PMID 16970569. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2000733/.
- ^ Mirtazapine monograph
- ^ Gillman PK (June 2006). "A review of serotonin toxicity data: implications for the mechanisms of antidepressant drug action". Biol. Psychiatry 59 (11): 1046–51. doi:10.1016/j.biopsych.2005.11.016. PMID 16460699.
- ^ Hoes MJ, Zeijpveld JH (March 1996). "Mirtazapine as treatment for serotonin syndrome". Pharmacopsychiatry 29 (2): 81. doi:10.1055/s-2007-979550. PMID 8741027. [unreliable medical source?]
- ^ Stahl, Stephen M. (2008). Stahl's Essential Psychopharmacology Online: Print and Online. Cambridge, UK: Cambridge University Press. ISBN 0-521-74609-4. http://stahlonline.cambridge.org/prescribers_drug.jsf?page=0521683505c57_p325-330.html.therapeutics&name=Mirtazapine&title=Therapeutics.
- ^ Abo-Zena RA, Bobek MB, Dweik RA (April 2000). "Hypertensive urgency induced by an interaction of mirtazapine and clonidine". Pharmacotherapy 20 (4): 476–8. doi:10.1592/phco.20.5.476.35061. PMID 10772378. [unreliable medical source?]
- ^ Rao, Divvela V. N. Srinivasa; Dandala, Ramesh; Bharathi, Chalamakuri; Handa, Vijay Kumar; Sivakumaran, Meenakshisunderam; Naidub, Andra (2006). "Synthesis of potential related substances of mirtazapine". Arkivoc 2006 (15): 127–32. http://www.arkat-usa.org/get-file/22868/.
- ^ US patent 4062848, Van der Burg WJ, "Tetracyclic compounds", published 1977-12-13, issued 1977-12-13
Further reading
- Stimmel GL, Dopheide JA, Stahl SM (1997). "Mirtazapine: an antidepressant with noradrenergic and specific serotonergic effects". Pharmacotherapy 17 (1): 10–21. PMID 9017762.
- Anttila SA, Leinonen EV (2001). "A review of the pharmacological and clinical profile of mirtazapine". CNS Drug Rev 7 (3): 249–64. doi:10.1111/j.1527-3458.2001.tb00198.x. PMID 11607047.
External links
- Mirtazapine - Drugs.com
- Remeron - Rxlist.com
- Mirtazapine - MedicineNet.com
- Mirtazapine - MedlinePlus
- Mirtazapine - About.com
- U.S. National Library of Medicine: Drug Information Portal - Mirtazapine
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UpToDate Contents
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- 1. 非定型抗うつ薬：薬理学、投与方法、および副作用 atypical antidepressants pharmacology administration and side effects
- 2. 成人における双極性障害：薬物治療の催奇形性および出生後のリスク bipolar disorder in adults teratogenic and postnatal risks of pharmacotherapy
- 3. フェチシズム fetishism
- 4. 成人における抗うつ剤：薬剤の変更および投与中止 antidepressant medication in adults switching and discontinuing medication
- 5. 癌における食欲不振および悪液質の薬理学的マネージメント pharmacologic management of cancer anorexia cachexia
English Journal
- Predictors and mediators of add-on mirtazapine-induced cognitive enhancement in schizophrenia--a path model investigation.
- Stenberg JH, Terevnikov V, Joffe M, Tiihonen J, Chukhin E, Burkin M, Joffe G.SourceHelsinki University Central Hospital (HUCH), Helsinki, PO Box 750, FI-00029 HUCH, Finland. jan-henry.stenberg@hus.fi
- Neuropharmacology.Neuropharmacology.2013 Jan;64:248-53. doi: 10.1016/j.neuropharm.2012.06.028. Epub 2012 Jun 26.
- We aimed to evaluate predictors and mediators of enhancing effect of adjunctive mirtazapine on cognition in schizophrenia. Patients with difficult-to-treat schizophrenia received either mirtazapine (n = 19) or placebo (n = 18) in a double-blind fashion for six weeks. Mirtazapine outperformed placebo
- PMID 22750079
- The relevance of oxidative stress status in first episode and recurrent depression.
- Stefanescu C, Ciobica A.Source(")Gr. T. Popa" University of Medicine and Pharmacy, 16 Universitatii Street, 700115, Iasi, Romania.
- Journal of affective disorders.J Affect Disord.2012 Dec 20;143(1-3):34-8. doi: 10.1016/j.jad.2012.05.022. Epub 2012 Jul 25.
- Oxidative and nitrosative stress (O&NS) could play an important role in the pathophysiology of major depression (MDD). The aim of the present work was to evaluate the specific activity of the main peripheral antioxidant defences (superoxide dismutase-SOD and glutathione peroxidase-GPX) and the l
- PMID 22840610
Japanese Journal
- 症例 Mirtazapineの併用療法が奏功した超高齢者うつ病の2例 : 抗うつ効果における食欲増進の意義について
- 堀 正士
- 精神科 21(4), 490-494, 2012-10
- NAID 40019452757
- 疼痛コントロールが困難であった術後神経障害性疼痛にミルタザピンが有効であった1症例
- 増澤 宗洋,田口 仁士,杉本 達哉 [他]
- 麻酔 61(9), 1003-1005, 2012-09
- NAID 40019423054
Related Links
- ミルタザピン（Mirtazapine）は、オランダのオルガノン社（前シェリング・プラウ社、現 メルク社）が創製した四環系抗うつ薬。ノルアドレナリン作動性・特異的セロトニン作動性 抗うつ薬 (NaSSA) というカテゴリに分類される。SSRIやSNRIとは異なる作用機序で あり、 ...
- Mirtazapine (Remeron, Avanza, Zispin) is a noradrenergic and specific serotonergic antidepressant (NaSSA) which was introduced by Organon International in the United States in 1990 and is used primarily in the treatment of depression.
Related Pictures
★リンクテーブル★
| リンク元 | 「ミルタザピン」 |
「ミルタザピン」
特徴
- ノルアドレナリン作動性・特異的セロトニン作動性抗うつ薬
- シナプス前部の自己受容体のα2受容体を阻害し、セロトニン・ノルアドレナリン放出を促進。立ち上がりが早く、胃腸症状や性機能障害が少ない。
適応
- うつ病、うつ状態
禁忌
- 1. 本剤の成分に対して過敏症の既往歴のある患者
- 2. MAO阻害剤を投与中あるいは投与中止後２週間以内の患者
副作用
- うつ病・うつ状態の患者を対象とした国内臨床試験において、総症例330例中273例（82.7％）、914件に臨床検査値を含む副作用が報告された。その主なものは傾眠165例（50.0％）、口渇68例（20.6％）、倦怠感50例（15.2％）、便秘42例（12.7％）、アラニン・アミノトランスフェラーゼ増加41例（12.4％）であった（承認時）。
添付文書
- レメロン錠
- リフレックス錠15mg