出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/07/10 20:39:55」(JST)[Wiki en表示]
Monoamine oxidase inhibitors (MAOIs) are chemicals which inhibit the activity of the monoamine oxidase enzyme family. They have a long history of use as medications prescribed for the treatment of depression. They are particularly effective in treating atypical depression. They are also used in the treatment of Parkinson's disease and several other disorders.
Because of potentially lethal dietary and drug interactions, monoamine oxidase inhibitors have historically been reserved as a last line of treatment, used only when other classes of antidepressant drugs (for example selective serotonin reuptake inhibitors and tricyclic antidepressants) have failed. New research into MAOIs indicates that much of the concern over their dangerous dietary side effects stems from misconceptions and misinformation, and that despite proven effectiveness of this class of drugs, it is underutilized and misunderstood in the medical profession. New research also questions the validity of the perceived severity of dietary reactions, which has historically been based on outdated research.
- 1 Indications
- 2 Mechanism of action
- 2.1 Reversibility
- 2.2 Selectivity
- 3 Dangers
- 3.1 Diet and drug Interactions
- 3.2 Withdrawal
- 3.3 Listing of interactions
- 4 History
- 5 List of MAO inhibiting drugs
- 5.1 Marketed drugs
- 5.2 Drugs withdrawn from the market
- 6 Cultural references
- 7 See also
- 8 References
Newer MAOIs such as selegiline (typically used in the treatment of Parkinson's disease) and the reversible MAOI moclobemide provide a safer alternative and are now sometimes used as first-line therapy.
MAOIs have been found to be effective in the treatment of panic disorder with agoraphobia, social phobia, atypical depression or mixed anxiety and depression, bulimia, and post-traumatic stress disorder, as well as borderline personality disorder. MAOIs appear to be particularly effective in the management of bipolar depression according to a recent retrospective-analysis. There are reports of MAOI efficacy in obsessive-compulsive disorder (OCD), trichotillomania, dysmorphophobia, and avoidant personality disorder, but these reports are from uncontrolled case reports.
MAOIs can also be used in the treatment of Parkinson's disease by targeting MAO-B in particular (therefore affecting dopaminergic neurons), as well as providing an alternative for migraine prophylaxis. Inhibition of both MAO-A and MAO-B is used in the treatment of clinical depression and anxiety.
MAOIs appear to be particularly indicated for outpatients with "neurotic depression" complicated by panic disorder or hysteroid dysphoria, which involves repeated episodes of depressed mood in response to feeling rejected.
Mechanism of action
MAOIs act by inhibiting the activity of monoamine oxidase, thus preventing the breakdown of monoamine neurotransmitters and thereby increasing their availability. There are two isoforms of monoamine oxidase, MAO-A and MAO-B. MAO-A preferentially deaminates serotonin, melatonin, epinephrine, and norepinephrine. MAO-B preferentially deaminates phenethylamine and trace amines. Dopamine is equally deaminated by both types.
The early MAOIs covalently bound to the monoamine oxidase enzymes, thus inhibiting them irreversibly; the bound enzyme could not function and thus enzyme activity was blocked until the cell made new enzymes. The enzymes turn over approximately every two weeks. A few newer MAOIs, a notable one being moclobemide, are reversible, meaning that they are able to detach from the enzyme to facilitate usual catabolism of the substrate. The level of inhibition in this way is governed by the concentrations of the substrate and the MAOI.
Harmaline found in Peganum harmala, as well as the Ayahuasca vine, Banisteriopsis caapi, and Passiflora incarnata is a reversible inhibitor of MAO-A (RIMA).
In addition to reversibility, MAOIs differ by their selectivity of the MAO receptor. Some MAOIs inhibit both MAO-A and MAO-B equally, other MAOIs have been developed to target one over the other.
MAO-A inhibition reduces the breakdown of primarily serotonin, norepinephrine, and dopamine; selective inhibition of MAO-A allows for tyramine to be metabolised via MAO-B. Agents that act on serotonin if taken with another serotonin-enhancing agent may result in a potentially fatal interaction called serotonin syndrome or with irreversible and unselective inhibitors (such as older MAOIs), of MAO a hypertensive crisis as a result of tyramine food interactions is particularly problematic with older MAOIs. Tyramine is broken down by MAO-A and MAO-B, therefore inhibiting this action may result in its excessive build-up, so diet must be monitored for tyramine intake.
MAO-B inhibition reduces the breakdown mainly of dopamine and phenethylamine so there are no dietary restrictions associated with this. MAO-B would also metabolize tyramine, as the only differences between dopamine, phenethylamine, and tyramine are two phenylhydroxyl groups on carbons 3 and 4. The 4-OH would not be a steric hindrance to MAO-B on tyramine. Two MAO-Bi drugs, selegiline and rasagiline have been approved by the FDA without dietary restrictions, except in high-dosage treatment, wherein they lose their selectivity.
Diet and drug Interactions
When ingested orally, MAOIs inhibit the catabolism of dietary amines. When foods containing tyramine are consumed (so-called "cheese effect"), the individual may suffer from hypertensive crisis. The amount required to cause a reaction varies greatly from individual to individual, and depends on the degree of inhibition, which in turn depends on dosage and selectivity.
The exact mechanism by which tyramine causes a hypertensive reaction is not well-understood, but it is assumed that tyramine displaces norepinephrine from the storage vesicles. This may trigger a cascade in which excessive amounts of norepinephrine can lead to a hypertensive crisis. Another theory suggests that proliferation and accumulation of catecholamines causes hypertensive crisis
Tyrosine, not tyramine, is the precursor to catecholamines. Tyramine is a breakdown product of tyrosine. In the gut and during fermentation, tyrosine, an amino acid, is decarboxylated to tyramine. Under ordinary circumstances, tyramine is deaminated in the liver to an inactive metabolite, but, when the hepatic MAO (primarily MAO-A) is inhibited, the "first-pass" clearance of tyramine is blocked and circulating tyramine levels can climb. Elevated tyramine competes with tyrosine for transport across the blood–brain barrier (via aromatic amino acid transport) where it can then enter adrenergic nerve terminals. Once in the cytoplasmic space, tyramine will be transported via the vesicular monoamine transporter (VMAT) into synaptic vesicles, thereby displacing norepinephrine. The mass transfer of norepinephrine from its vesicular storage space into the extracellular space via mass action can precipitate the hypertensive crisis. Hypertensive crises can sometimes result in stroke or cardiac arrhythmia if not treated. In general, this risk is not present with RIMAs. Both kinds of intestinal MAO inhibition can cause hyperpyrexia, nausea, and psychosis if foods high in levodopa are consumed.
Examples of foods and drinks with potentially high levels of tyramine include liver and fermented substances, such as alcoholic beverages and aged cheeses. (See a List of foods containing tyramine). Examples of levodopa-containing foods include broad beans. These diet restrictions are not necessary for those taking selective MAO-B inhibitors, unless these are being taken in high dosages, as mentioned above.
It deserves separate mention that some meat extracts and yeast extracts (Bovril, Marmite, Vegemite) contain extremely high levels of tyramine, and should not be used with these medications.
When MAOIs were first introduced, these risks were not known, and, over the following four decades, fewer than 100 people have died from hypertensive crisis. Presumedly due to the sudden onset and violent appearance of the reaction, MAOIs gained a reputation for being so dangerous that, for a while, they were taken off the market in America entirely. However, it is now believed that, used as directed under the care of a qualified psychiatrist, this class of drugs is a viable alternative treatment for intermediate- to long-term use.
The most significant risk associated with the use of MAOIs is the potential for interactions with over-the-counter and prescription medicines, illicit drugs or medications, and some supplements (e.g., St. John's Wort, tryptophan). It is vital that a doctor supervise such combinations to avoid adverse reactions. For this reason, many users carry an MAOI-card, which lets emergency medical personnel know what drugs to avoid. (E.g., adrenaline dosage should be reduced by 75%, and duration is extended.)
Tryptophan supplements should not be consumed with MAOIs as the potentially fatal serotonin syndrome may result.
MAOIs should not be combined with other psychoactive substances (antidepressants, painkillers, stimulants, both legal and illegal etc.) except under expert care. Certain combinations can cause lethal reactions, common examples including SSRIs, tricyclics, MDMA, meperidine, tramadol, and dextromethorphan. Agents with actions on epinephrine, norepinephrine, or dopamine must be administered at much lower doses due to potentiation and prolonged effect.
Nicotine, a substance frequently implicated in tobacco addiction, has been shown to have "relatively weak" addictive properties when administered alone. The addictive potential increases dramatically after co-administration of an MAOI, which specifically causes sensitization of the locomotor response in rats, a measure of addictive potential. This may be reflected in the difficulty of smoking cessation, as tobacco contains naturally-occurring MAOI compounds in addition to the nicotine.
Antidepressants including MAOIs have some dependence-producing effects, the most notable one being a withdrawal syndrome, which may be severe especially if MAOIs are discontinued abruptly or over-rapidly. However, the dependence-producing potential of MAOIs or antidepressants in general is not as significant as benzodiazepines. Withdrawal symptoms can be managed by a gradual reduction in dosage over a period of weeks, months or years to minimize or prevent withdrawal symptoms.
MAOIs, as with any antidepressant medications, do not alter the course of the disorder, so it is possible that discontinuation can return the patient to the pre-treatment state.
This consideration greatly complicates switching a patient between a MAOI and a SSRI, because it is necessary to clear the system completely of one drug before starting another. If one also tapers dosage gradually, the result is that for weeks a depressed patient will have to bear the depression without chemical help during the drug-free interval. This may be preferable to risking the effects of an interaction between the two drugs, but it is often not easy for the patient.
Listing of interactions
|This section needs more medical references for verification or relies too heavily on primary sources. Please review the contents of the section and add the appropriate references if you can. Unsourced or poorly sourced material may be removed. (November 2013)|
The MAOIs are infamous for their numerous drug interactions, including the following kinds of substances:
- Substances that are metabolized by monoamine oxidase, as they can be boosted by up to several-fold.
- Substances that increase serotonin, norepinephrine, or dopamine activity, as too much of any of these neurochemicals can result in severe acute consequences, including serotonin syndrome, hypertensive crisis, and psychosis, respectively.
Such substances that can react with MAOIs include:
- Phenethylamines: 2C-B, Mescaline, Phenethylamine (PEA), etc.
- Amphetamines: Amphetamine, MDMA, Dextroamphetamine, Methamphetamine, DOM, etc.
- Tryptamines: DMT, Psilocin/Psilocybin ("Magic Mushrooms"), etc.
- Lysergamides: Ergolines/LSA, LSD ("Acid"), etc.
- Serotonin, Norepinephrine, and/or Dopamine Reuptake Inhibitors:
- Selective Serotonin Reuptake Inhibitors (SSRIs): Citalopram, Dapoxetine, Escitalopram, Fluoxetine, Fluvoxamine, Paroxetine, Sertraline.
- Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs): Desvenlafaxine, Duloxetine, Milnacipran, Venlafaxine.
- Norepinephrine-Dopamine Reuptake Inhibitors (NDRIs): Amineptine, Bupropion, Methylphenidate, Nomifensine.
- Norepinephrine Reuptake Inhibitors (NRIs): Atomoxetine, Mazindol, Reboxetine.
- Tricyclic Antidepressants (TCAs): Amitriptyline, Butriptyline, Clomipramine, Desipramine, Dosulepin, Doxepin, Imipramine, Lofepramine, Nortriptyline, Protriptyline, Trimipramine.
- Tetracyclic Antidepressants (TeCAs): Amoxapine, Maprotiline.
- Phenylpiperidine derivative Opioids: Meperidine/Pethidine, Tramadol, Methadone, Fentanyl, Dextropropoxyphene, Propoxyphene.
- Others: Brompheniramine, Chlorpheniramine, Cocaine, Cyclobenzaprine, Dextromethorphan (DXM), Ketamine, MDPV, Nefazodone, Phencyclidine (PCP), Pheniramine, Sibutramine, Trazodone.
- Serotonin, Norepinephrine, and/or Dopamine Releasers: 4-Methylaminorex (4-MAR), Amphetamine, Benzphetamine, Cathine, Cathinone, Diethylcathinone, Ephedrine, Levmetamfetamine, Lisdexamfetamine, MDMA ("Ecstasy"), Methamphetamine, Pemoline, Phendimetrazine, Phenethylamine (PEA), Phentermine, Propylhexedrine, Pseudoephedrine, Phenylephrine, Tyramine.
- Serotonin, Norepinephrine, and/or Dopamine Supplemental Precursors: 5-HTP, L-DOPA, L-Phenylalanine, L-Tryptophan, L-Tyrosine.
- Local and General anesthetic in surgery and dentistry in particular those containing Epinephrine. There is no universally taught or accepted practice regarding dentistry and use of MAOIs such as Phenelzine and it is, therefore, vital to inform all clinicians especially dentists of the potential effect of MAOIs and Local Anesthesia. In preparation for dental work, withdrawal from Phenelzine is specifically advised, however since this takes two weeks it is not always a desirable or practical option. Dentists using Local Anesthesia are advised to use a non-epinephrine anesthetic such as Carbocaine at a level of 3%. Specific attention should be paid to blood pressure during the procedure and the level of the anesthetic should be regularly and appropriately topped up since non-epinephrine anestetics take longer to come into effect and wear off faster. Patients taking Phenelzine are advised to notify their Psychiatrist prior to any dental treatment.
- Certain other supplements: Hypericum perforatum ("St John's Wort"), Inositol, Rhodiola rosea, S-Adenosyl-L-Methionine (SAMe), L-Theanine.
- Other Monoamine Oxidase Inhibitors.
MAOIs started off due to the serendipitous discovery that iproniazid was a weak MAO inhibitor (MAOI). Originally intended for the treatment of tuberculosis, in 1952, iproniazid antidepressant properties were discovered when researchers noted that the depressed patients given iproniazid experienced a relief of their depression. Subsequent in vitro work led to the discovery that it inhibited MAO and eventually to the monoamine theory of depression. MAOIs became widely used as antidepressants in the early 1950s. The discovery of the 2 isoenzymes of MAO has led to the development of selective MAOIs that may have a more favorable side-effect profile.
The older MAOIs' heyday was mostly between the years 1957 and 1970. The initial popularity of the 'classic' non-selective irreversible MAO inhibitors began to wane due to their serious interactions with sympathomimetic drugs and tyramine-containing foods that could lead to dangerous hypertensive emergencies. As a result, the use by medical practitioners of these older MAOIs declined. When scientists discovered that there are two different MAO enzymes (MAO-A and MAO-B), they developed selective compounds for MAO-B, (for example, selegiline, which is used for Parkinson's disease), to reduce the side-effects and serious interactions. Further improvement occurred with the development of compounds (moclobemide and toloxatone) that not only are selective but cause reversible MAO-A inhibition and a reduction in dietary and drug interactions. Moclobemide, was the first reversible inhibitor of MAO-A to enter widespread clinical practice.
A transdermal patch form of the MAOI selegiline, called Emsam, was approved for use in depression by the Food and Drug Administration in the United States on February 28, 2006.
List of MAO inhibiting drugs
- Nonselective MAO-A/MAO-B Inhibitors
- Isocarboxazid (Marplan)
- Nialamide (Niamid)
- Phenelzine (Nardil, Nardelzine)
- Tranylcypromine (Parnate, Jatrosom)
- Selective MAO-A Inhibitors
- Moclobemide (Aurorix, Manerix)
- Pirlindole (Pirazidol) (available in Russia)
- Toloxatone (Humoryl) (available in France)
- Selective MAO-B Inhibitors
- Rasagiline (Azilect)
- Selegiline (Deprenyl, Eldepryl, Emsam)
Linezolid is an antibiotic drug with weak MAO inhibiting activity.
Drugs withdrawn from the market
- Nonselective MAO-A/MAO-B Inhibitors
- Benmoxin (Nerusil, Neuralex)
- Iproclozide (Sursum)
- Iproniazid (Marsilid, Iprozid, Ipronid, Rivivol, Propilniazida) (discontinued worldwide except for France)
- Mebanazine (Actomol)
- Octamoxin (Ximaol, Nimaol)
- Pheniprazine (Catron)
- Phenoxypropazine (Drazine)
- Pivalylbenzhydrazine (Tersavid)
- Safrazine (Safra) (discontinued worldwide except for Japan)
- Caroxazone (Surodil, Timostenil)]
- Selective MAO-A inhibitors
- Minaprine (Cantor)
The pilot episode of Law and Order was similar to an actual event. Journalist Sidney Zion questioned the sudden death of his daughter Libby Zion in an emergency department in Manhattan on Oct 4, 1984. The cause of death was attributed to "mysterious infection". The father convinced authorities to launch a criminal investigation when it was discovered that several medications, including Demerol, were administered to his daughter, reacting with her Nardil medications. The DA sought charges of murder against a doctor who had approved use of restraints and narcotics when Zion became increasingly agitated. The case prompted many reforms in graduate medical education and limiting number of hours staff can work. Drug abuse was successfully argued as a major factor leading to her death.
- Reversible inhibitor of MAO-A (RIMA)
- Hydrazine (antidepressant)
- MAO, MAO-A, MAO-B
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At dosages above around 2 mg per day, rasagiline loses its selectivity for MAO type B and also inhibits MAO type A. An MAO-B selective regimen does not cause significant tyramine potentiation, the dreaded 'cheese effect' common to users of older unselective and irreversible MAOIs who eat tyramine-rich foods. This will be taken with and without food. Thus, low-dosage rasagiline demands no special dietary restrictions.
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- 1. 成人におけるうつ病治療としてのモノアミン酸化酵素阻害剤（MAOI） monoamine oxidase inhibitors maois for treating depressed adults
- 2. 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
- 3. Cardiovascular problems in the post-anesthesia care unit (PACU)
- 4. Serotonin syndrome (serotonin toxicity)
- 5. メチシリン耐性黄色ブドウ球菌およびバンコマイシン耐性腸球菌の治療のための抗菌薬の薬理学 pharmacology of antimicrobial agents for treatment of methicillin resistant staphylococcus aureus and vancomycin resistant enterococcus
- The evidence-based pharmacotherapy of social anxiety disorder.
- Blanco C, Bragdon LB, Schneier FR, Liebowitz MR.SourceDepartment of Psychiatry of Columbia College of Physicians and Surgeons and the New York State Psychiatric Institute, New York, NY, USA.
- The international journal of neuropsychopharmacology / official scientific journal of the Collegium Internationale Neuropsychopharmacologicum (CINP).Int J Neuropsychopharmacol.2013 Feb;16(1):235-49. doi: 10.1017/S1461145712000119. Epub 2012 Mar 21.
- Social anxiety disorder (SAD) is a highly prevalent and often disabling disorder. This paper reviews the pharmacological treatment of SAD based on published placebo-controlled studies and published meta-analyses. It addresses three specific questions: What is the first-line pharmacological treatment
- PMID 22436306
- Selective inhibition of monoamine oxidase A or B reduces striatal oxidative stress in rats with partial depletion of the nigro-striatal dopaminergic pathway.
- Aluf Y, Vaya J, Khatib S, Loboda Y, Finberg JP.SourceDepartment of Molecular Pharmacology, Rappaport Medical Faculty, Technion, Haifa, Israel; Oxidative Stress Research Laboratory, Migal-Galilee Technology Center, Kiryat Shmona, and Tel Hai College, Israel.
- Neuropharmacology.Neuropharmacology.2013 Feb;65:48-57. doi: 10.1016/j.neuropharm.2012.08.023. Epub 2012 Sep 7.
- Partial lesion (50%) of the nigro-striatal dopaminergic pathway induces compensatory increase in dopamine release from the remaining neurons and increased extracellular oxidative stress (OS(-ec)) in the striatum. The present study was designed to explore the role of monoamine oxidase types A and B (
- PMID 22982254
- Anxiolytic-like effect of linezolid in experimental mouse models of anxiety.
- Jindal A, Mahesh R, Kumar B.SourceDepartment of Pharmacy, Birla Institute of Technology & Science, Pilani-333031, Rajasthan, India. Electronic address: email@example.com.
- Progress in neuro-psychopharmacology & biological psychiatry.Prog Neuropsychopharmacol Biol Psychiatry.2013 Jan 10;40:47-53. doi: 10.1016/j.pnpbp.2012.09.006. Epub 2012 Sep 25.
- Linezolid, an oxazolidinone class antibiotic is a reversible and nonselective inhibitor of monoamine oxidase (MAO) enzyme, mainly for MAO-A subtype. Its antidepressant-like effect has been previously demonstrated in the rodent models of depression. MAO-A enzyme has been shown to play a role in the p
- PMID 23021974
- Clorgyline Inhibits Orexin-A-Induced Arousal in Layer-Type Chicks
- Katayama Sachiko,Shigemi Kazutaka,Cline Mark A. [他],Furuse Mitsuhiro
- Journal of Veterinary Medical Science 73(4), 471-474, 2011
- … Because monoamine oxidase-A (MAO-A) is a potent degrading enzyme of these monoamines, we hypothesized that orexin-A may mediate its arousal-inducing effects through MAO-A. … Therefore, we simultaneously injected clorgyline, a specific inhibitor of MAO-A, with orexin-A and examined behavior of chicks. … For the monoamine turnover rate, enhancement of the turnover rate of serotonin by orexin-A was attenuated by clorgyline. …
- NAID 130000444419
- Rapid screening of monoamine oxidase B inhibitors in natural extracts by capillary electrophoresis after enzymatic reaction at capillary inlet
- HU Kun,ZHANG Lichun,LI Xiangtang,ZHAO Shulin
- Journal of chromatography. B, Analytical technologies in the biomedical and life sciences 878(30), 3156-3160, 2010-11-15
- NAID 10028043990
- Combined treatment with MAO-A inhibitor and MAO-B inhibitor increases extracellular noradrenaline levels more than MAO-A inhibitor alone through increases in β-phenylethylamine
- Kitaichi Yuji,Inoue Takeshi,Nakagawa Shin,Boku Shuken,Izumi Takeshi,Koyama Tsukasa
- European Journal of Pharmacology 637(1-3), 77-82, 2010-07-10
- … Monoamine oxidase inhibitors (MAO inhibitors) have been widely used as antidepressants. … Using in vivo microdialysis methods, we measured extracellular noradrenaline and serotonin levels following administration of Ro 41-1049, a reversible MAO-A inhibitor and/or lazabemide, a reversible MAO-B inhibitor in the medial prefrontal cortex (mPFC) of rats. …
- NAID 120002261718
|拡張検索||「monoamine oxidase inhibitors」|
- 起立性低血圧(once the body adapts to higher basal level of catecholamines, it is nolonger able to further vasoconstrict in response to stress), hepatotoxicity, and hypomania.
- bottle up, suppress
- See Biogenic amines