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甲基苯丙胺

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甲基苯丙胺
An image of the methamphetamine compound
Ball-and-stick model of the methamphetamine molecule
系统(IUPAC)命名名称
N-methyl-1-phenylpropan-2-amine
临床数据
商品名 Desoxyn
Drugs.com Monograph
医疗法规
妊娠分级
  • US: C (不排除有风险的可能)
依赖性 生理: 無
心理: 高
成瘾性
给药途径 Medical: oral
Recreational: oral, intravenous, insufflation, inhalation, suppository
合法狀態
合法状态
药代动力学数据
生物利用度 Oral: Varies widely[1]
Rectal: 99%
IV: 100%
蛋白结合度 Varies widely[1]
代谢 CYP2D6,[2] DBH[3]FMO3英语Flavin-containing monooxygenase,[4] XM-ligase英语butyrate-CoA ligase,[5] and ACGNAT英语glycine N-acyltransferase[6]
生物半衰期 9–12 hours[7]
排泄
识别信息
CAS注册号537-46-2 ✓
ATC代码 N06BA03
PubChem CID 1206
IUPHAR/BPS英语IUPHAR/BPS 4803
DrugBank DB01577 ✓
ChemSpider 1169 ✓
UNII 44RAL3456C ✓
KEGG D08187 ✓
ChEBI CHEBI:6809 ✓
ChEMBL英语ChEMBL CHEMBL1201201 ✓
其他名称 N-methylamphetamine, desoxyephedrine
化学信息
化学式 C10H15N
摩尔质量 149.2337 g/mol
物理性质
熔点 3 °C(37 °F) [8]
沸点 212 °C(414 °F) [9] at 760 MM HG
  (verify)
Methamphetamine-3d-CPK.png

甲基苯丙胺甲基安非他命(英語:Methamphetamine,全名是N-methylamphetamine英语methylamphetamine[note 1]))是強效的中樞神經系統刺激劑,主要被用於娛樂用途,較少被用於治療注意力不足過動症肥胖症,即便有也被當成第二線療法[15]。甲基苯丙胺是在1893年發現,有二種对映异构:分別是左旋甲基苯丙胺(levo-methamphetamine)及右旋甲基苯丙胺(dextro-methamphetamine)。「甲基苯丙胺」一般是指左旋甲基苯丙胺及右旋甲基苯丙胺各佔一半的外消旋混合物。甲基安非他命較少被醫師處方,因為可能會毒害神經英语neurotoxicity,以及有用作春藥欣快感促進劑等風險。而且已有療效相同,而對人體危害風險更低的替代藥物

在美國能直接在市面上購買主成分為左旋甲基苯丙胺的吸入型鼻塞緩解劑英语nasal decongestant因為它被視為非处方药[note 2]

甲基苯丙胺常因為它們的藥效動力學屬性而被非法交易,用於娛樂用途。非法使用甲基苯丙胺在亚洲部分地区、大洋洲和美国最为普遍。在美国,消旋以及左旋、右旋甲基苯丙胺均为第二类管制药品英语list of Schedule II drugs (US)

在國際間從事甲基安非他命的生產、散播、銷售和加工等活動都是被許多國家嚴格管制或禁止的,因為甲基安非他命名列精神药物公约中的第二級分類表(schedule II)。

低劑量服用甲基安非他命,會產生欣快感、提振警醒度、專注力和精神及降低食慾、減輕體重。高劑量服用甲基安非他命則會引起中樞神經刺激劑引起的精神病英语stimulant psychosis横纹肌溶解症全身癲癇英语Generalized seizures、和顱內出血

Dextromethamphetamine是一個比甲基苯丙胺更加強烈的藥物,但因為甲基苯丙胺的化学合成難度較低,因此有些非法製造生產甲基苯丙胺。

長期攝取高劑量的甲基安非他命可能加快那些不可預期且速度極快的副作用,例如:心情擺盪英语mood swing中樞神經刺激劑引起的精神病英语stimulant psychosis(譬如:偏執幻觉譫妄妄想等。)、及具有侵略性的行為

在娛樂用途,甲基安非他命提升能量英语wakefulness-promoting agent的能力主要體現於提振心情增加性慾到達使用者能連續從事性行為好幾天。[18]

用途[编辑]

医用[编辑]

d-甲基安非他命,药品商标Desoxyn®,医疗上用于治疗注意力不足過動症(ADHD)、嗜睡症以及极端的肥胖症等。它的右旋异构体(R+异构体)可以用于治疗注意力不足過動症,但不带甲基的安非他命更常用。它的右旋异构体药品商标为「Desoxyn」,可以用于治疗嗜睡症肥胖。当安非他命和甲基安非他命致使患者太多副作用时,Desoxyn作为次选药物。在精神方面的作用上,右旋的R(+)构型是左旋的S(-)构型的5倍[22]

禁忌症[编辑]

有以下症状的人不能使用甲基苯丙胺:曾有物質使用疾患心血管疾病或嚴重易怒或焦慮的人,若仍有动脉血管硬化青光眼甲状腺功能亢进症或嚴重高血壓,也不能使用甲基苯丙胺[23]

美国食品药品监督管理局(FDA)表示,若以往曾對其他的興奮劑有超敏反應,或是正在使用单胺氧化酶抑制剂,也不得使用甲基苯丙胺[23]。FDA也建議有躁鬱症重性抑郁障碍血壓偏高、有肝腎臟疾病、狂躁思覺失調雷诺氏综合征癲癇發作甲状腺問題、抽动综合症或是妥瑞症的病患,若要使用甲基苯丙胺需監控其症狀[23]。因為甲基苯丙胺有可能造成生長發育遲緩,FDA也建議若用甲基苯丙胺對兒童或青少年進行治療,需監控其身高及體重的資訊[23]

副作用[编辑]

生理[编辑]

甲基苯丙胺在生理上造成的副作用包括:食欲不振、過動、瞳孔放大散瞳)、過度流汗精神運動性激動英语Psychomotor agitation、口乾及磨牙(會造成甲基苯丙胺嘴英语meth mouth)、頭痛、心律不整(可能是心跳过速心跳过缓)、呼吸急促高血壓低血壓體溫過高、腹瀉或便秘、視線模糊英语blurred vision頭暈肌束震顫英语Fasciculation麻木顫抖、皮膚乾燥、痤疮皮膚蒼白英语pallor皮膚發紅英语Flushing (physiology)[24]。慢性高劑量使用的副作用有搔癢障礙英语excoriation disorder、身體異常的搔癢[25][不可靠的醫學來源]蟻走感英语formication(感覺有昆蟲在身上爬的感覺)[26][23]。可能會有腳抽筋英语charley horse之類的症狀,有時會格外嚴重,且時間會拉長,若長期使用下,因為飲食不當以及脱水造成的電解質不平衡,此症狀會格外危險[27]

過量時的症狀[编辑]

甲基苯丙胺過量時會出現許多的症狀[7][23]。甲基苯丙胺中等程度的過量會有以下的症狀:心律不整、意識不清、排尿疼痛、血壓偏高或是偏低、高熱过度活跃和/或过度反应的反射英语hyperreflexia肌肉痛、嚴重精神運動性激躁英语Psychomotor agitation呼吸急促顫抖、排尿猶豫以及無法排尿[7][27]。特別嚴重的過量會有肾上腺素风暴英语adrenergic storm甲基苯丙胺精神病英语methamphetamine psychosis无尿症、, 心源性休克英语cardiogenic shock顱內出血循環系統崩潰英语circulatory collapse、危險性的发热肺高壓腎功能衰竭横纹肌溶解症血清素症候群[sources 1]。甲基苯丙胺過量會因為多巴胺激活英语dopaminergic血清素激活英语serotonergic的神經毒性而造成輕微的腦損傷[19][21]。甲基苯丙胺中毒死亡一般會出現在驚厥昏迷之後[23]

精神病症[编辑]

濫用甲基苯丙胺會造成興奮劑精神病症英语Stimulant psychosis,有許多不同的症狀(例如偏執狂幻觉譫妄妄想等)[7][32]考科藍研究有針對因濫用苯丙胺,右旋苯丙胺和甲基苯丙胺等興奮劑造成精神病症治療,進行的回顧研究,指出其中約有5%至15%的濫用者無法完全復原[32][33]。同一份回顧研究也指出,根據至少一次的試驗,抗精神病药可以有效改善急性甲基苯丙胺精神疾病的症狀[32]

緊急治療[编辑]

急性甲基苯丙胺中毒的治療主要是在治療其症狀,治療過程一開始可能會包括活性炭鎮靜劑[7],有關血液透析腹膜透析應用在甲基苯丙胺解毒上的效果,目前還沒有足夠證據來確認其是否有效[23]強制性利尿英语Forced acid diuresis(例如透過维生素C)會增加甲基苯丙胺的排泄量,不過會增加重度酸中毒、引發癲癇或橫紋肌溶解的風險,因此不建議使用[7]。高血壓會有顱內出血的風險,若是嚴重的話,可以用注射苄胺唑啉英语phentolamine硝普钠來治療[7],若提供足量苯二氮䓬类鎮靜劑以及提供安靜的環境,血壓會漸漸下降[7]

在治療甲基苯丙胺過量造成的躁動和精神病時,可以用氟哌啶醇等抗精神病藥[34][35]。具有親脂性及中樞神經系統滲透性的β阻断药(例如美托洛尔拉贝洛尔)可以治療中樞神經系統及心血管的毒性[36]。混合的α-英语alpha blockerβ-阻断药拉貝洛爾在治療甲基苯丙胺引起的心動過速和高血壓上格外有效[34],在使用β阻断药來治療甲基苯丙胺中毒的過程,目前還沒有unopposed alpha stimulation的紀錄[34]

成瘾的治療與管理[编辑]

认知行为疗法是目前最有效治療精神興奮劑成瘾的療法[37]。截至2014年 (2014-Missing required parameter 1=month!),還沒有有效治療甲基苯丙胺成瘾的藥物療法[38][39][40]。甲基苯丙胺成瘾主要會透過多巴胺受體英语dopamine receptor的增強活化及伏核中共定位N-甲基-D-天門冬胺酸受體(NMDA受體)來調整[note 3][42][43]離子可以阻断受体钙通道,因此可以抑制NMDA受体[41][44]

依賴及戒斷症狀[编辑]

若固定的使用甲基苯丙胺,會出現藥物耐受性,若是因為非醫療的原因而使用,其耐受性會快速增強[45][46]。若是有依賴性的使用者,其戒斷症狀和藥物耐受性的程度呈正相關[47]。甲基苯丙胺戒斷產生的抑郁會持續的比可卡因戒斷症狀要長,其情形也較可卡因戒斷症狀要嚴重[48]

依目前考科藍文獻回顧有關甲基苯丙胺非醫療使用者的物質依賴藥物戒斷資料來看,「若慢性重度使用者突然停用[甲基苯丙胺],許多人會有時間限制的戒斷症狀,會在最後一次用藥後24小時內出現。」[47]。慢性重度使用者的戒斷症狀相當常見,慢性重度使用者中有87.6%會有戒斷症狀,會持續三週到四週,第一週會有明顯的「崩潰期」[47]。甲基苯丙胺的戒斷症狀包括焦慮、藥物渴望英语Craving (withdrawal)煩躁疲勞胃口變好運動增加英语Psychomotor agitation運動減少英语psychomotor retardation失去動力失眠或是嗜睡症以及清醒夢[47]

若孕婦使用甲基苯丙胺,其體內循環系統會有甲基苯丙胺,而且會透過胎盤傳遞給胎兒,嬰兒也會在母乳中攝取到甲基苯丙胺[49]。甲基苯丙胺濫用的婦女所生的嬰兒,考慮妊娠年齡英语gestational調整後的頭圍數據顯著較小,而且其出生重量也會較輕[49]。新生兒暴露在甲基苯丙胺下,也和其新生兒戒斷英语neonatal withdrawal症候群有關,其症狀有激動,嘔吐和呼吸加快[49]。不過此戒斷症狀相對較輕微,只有4%需要藥物干預[48]

化學[编辑]

甲基苯丙胺爲人工合成,結構與苯丙胺MDMA(摇头丸)近似,比起其他毒品,結構較簡單,分子量較小。

合成过程[编辑]

甲基苯丙胺与甲卡西酮(methcathinone)、苯丙胺、以及其它兴奋剂的结构相似,可以用化学还原方法从麻黄碱伪麻黄碱制得。大多数制备的原料属于日用品或可以从商店直接买到。因此合成甲基苯丙胺显得简单易行。在网络上可以找到许多转化合成方法,通常不大可信。最有经验的行家或求教于化学课,或从那些生产安非他命的人员那儿学来。几乎每一种方法都要用到高度危险的化学品和流程。大多数的生产方法涉及到将麻黄碱/伪麻黄碱分子中羟基氢化。在美国最通常的方式用到红,形成氢碘酸。另一个日渐普遍的方法是使用Birch还原法[50],用一次性锂电池中的金属锂替代金属钠(金属钠较难获得)。Birch还原法是极其危险的,因为碱金属和无水液氨都有极高的反应性。而且当加入反应物时,液氨的温度使其极易爆沸。另一种方法是苯基丙酮甲胺还原胺化反应(Borch还原)[51],所用的都是美国缉毒局的I级化学品。其他较不常见的方法使用其他的氢化法,比如用氢气和催化剂。


历史[编辑]

甲基苯丙胺苯丙胺的化學結構非常相似。甲基苯丙胺是由日本化學家長井長義英语長井長義於1893年自麻黃鹼成功合成。1919年由緒方章日语緒方章完成了結晶化。

冰毒的正式學名是甲基安非他命,是一種強力興奮劑,能刺激中樞神經活動,化學結構與人體的腎上腺素類似。由於外貌上為無色的粒狀透明晶體,故俗稱為「冰」。冰毒在發明之初,乃是戰爭時期用作減低士兵勞累,非自然地提升作戰能力的手段以增加其作戰效率,苯丙胺還被提供給必須超長時間工作的軍需廠工人使用,因而成癮者不計其數。戰後,掌握制造方法者開始自行生產並非法販售予平民,冰毒開始被濫用,作為派對藥物,其成癮問題和害處才開始漸漸浮現。由於成癮者向醫療機構求助的數字越來越大,令政府開始關注濫用問題,並研究對社會造成的危害。

甲基苯丙胺在第二次世界大戰分別由同盟國軸心國以Pervitin[52]之註冊名稱分發予前線,納粹軍廣發甲基苯丙胺予士兵以作興奮劑之用,特別是在蘇德戰爭時的黨衛隊人員及德意志國防軍希特勒亦曾注射甲基苯丙胺。日本曾给士兵服用冰毒以提高戰鬥力。1941年武田製藥與大日本製藥(日本住友製藥)曾出產市販品,以及提供必須超長時間工作的軍需工廠工人使用,故在日本本土、臺灣、及日佔區都遺留下許多成癮患者。

1950年代,美国政府颁布法令将甲基苯丙胺规定为处方药,根据1951年出版的Arthur Grollman所著的《病理与药理学》一書,它可用于治疗嗜睡、后脑炎、帕金森综合症、酒精中毒,以及肥胖症。

1960年代,製造甲基苯丙胺的地下工廠開始普遍;1962年,冰毒首次作为一种违法毒品,被旧金山的摩托车黑帮制造出来,并在美国太平洋沿岸四处分发。这个黑帮很快便有了大批仿效者:制作冰毒所需要的原料非常普通,并且容易得到,比如外用酒精、碱液、麻黄碱和伪麻黄碱;最后一种当时作为非处方药供应。于是,作坊式实验室曾经生产了大量的违法甲基苯丙胺;墨西哥黑帮把大量廉价品带进了墨西哥。可以放进导管中抽吸的结晶甲基苯丙胺块在1980年代的夏威夷出现,并很快蔓延到美国大陆地区,成为最受欢迎的毒品种类。及至1980年,非醫療使用激增。其中,加州的聖地牙哥市更被稱爲北美的冰毒聖地(英國《經濟學人》,1989年12月2日號)。

美國到1983年才制定法律管制持有甲基苯丙胺的前驅體和製造設備。1986年,美國制定了一份聯邦管制藥物取締法,名爲Federal Controlled Substance Analogue Enforcement Act,以打擊“設計毒品”(designer drugs)泛濫。儘管如此,吸食甲基苯丙胺仍在美國郊區(尤其是中西部和南部)上升,直至今日。而各州都在加緊立法打擊。

参见[编辑]

備註[编辑]

  1. ^ Synonyms and alternate spellings include: metamfetamine (International Nonproprietary Name (INN)), N-methylamphetamine, desoxyephedrine, Syndrox, Methedrine, and Desoxyn.[10][11][12] Common slang terms for methamphetamine include: speed, meth, crystal, crystal meth, glass, shards, ice, and tic[13] and, in New Zealand, "P".[14]
  2. ^ The active ingredient in some OTC inhalers in the United States is listed as levmetamfetamine, the INN and USAN英语United States Adopted Name of levomethamphetamine.[16][17]
  3. ^ NMDA受體是電壓相依型配体门控离子通道英语ligand-gated ion channels,需要同时结合谷氨酸和共激动剂(D-絲氨酸甘氨酸)來打開離子通道[41]

來源群組[编辑]

  1. ^ [7][23][27][28][29][30][31]

参考文献[编辑]

脚注[编辑]

  1. ^ 1.0 1.1 Toxicity. Methamphetamine. PubChem Compound. National Center for Biotechnology Information. [31 December 2013]. 
  2. ^ Adderall XR Prescribing Information (PDF). United States Food and Drug Administration: 12–13. December 2013 [30 December 2013]. 
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  16. ^ Part 341 – cold, cough, allergy, bronchodilator, and antiasthmatic drug products for over-the-counter human use. Code of Federal Regulations Title 21: Subchapter D – Drugs for human use. United States Food and Drug Administration. April 2015 [7 March 2016]. Topical nasal decongestants --(i) For products containing levmetamfetamine identified in 341.20(b)(1) when used in an inhalant dosage form. The product delivers in each 800 milliliters of air 0.04 to 0.150 milligrams of levmetamfetamine. 
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  19. ^ 19.0 19.1 Malenka RC, Nestler EJ, Hyman SE. 15. (编) Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience 2nd. New York: McGraw-Hill Medical. 2009: 370. ISBN 978-0-07-148127-4. Unlike cocaine and amphetamine, methamphetamine is directly toxic to midbrain dopamine neurons. 
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    Neuropsychological studies have detected deficits in attention, working memory, and decision-making in chronic METH addicts ...
    There is compelling evidence that the negative neuropsychiatric consequences of METH abuse are due, at least in part, to drug-induced neuropathological changes in the brains of these METH-exposed individuals ...
    Structural magnetic resonance imaging (MRI) studies in METH addicts have revealed substantial morphological changes in their brains. These include loss of gray matter in the cingulate, limbic and paralimbic cortices, significant shrinkage of hippocampi, and hypertrophy of white matter (Thompson et al., 2004). In addition, the brains of METH abusers show evidence of hyperintensities in white matter (Bae et al., 2006; Ernst et al., 2000), decreases in the neuronal marker, N-acetylaspartate (Ernst et al., 2000; Sung et al., 2007), reductions in a marker of metabolic integrity, creatine (Sekine et al., 2002) and increases in a marker of glial activation, myoinositol (Chang et al., 2002; Ernst et al., 2000; Sung et al., 2007; Yen et al., 1994). Elevated choline levels, which are indicative of increased cellular membrane synthesis and turnover are also evident in the frontal gray matter of METH abusers (Ernst et al., 2000; Salo et al., 2007; Taylor et al., 2007).
     
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    About 5–15% of the users who develop an amphetamine psychosis fail to recover completely (Hofmann 1983) ...
    Findings from one trial indicate use of antipsychotic medications effectively resolves symptoms of acute amphetamine psychosis.
     
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  37. ^ Malenka RC, Nestler EJ, Hyman SE. Chapter 15: Reinforcement and Addictive Disorders. (编) Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience 2nd. New York, USA: McGraw-Hill Medical. 2009: 386. ISBN 978-0-07-148127-4. Currently, cognitive–behavioral therapies are the most successful treatment available for preventing the relapse of psychostimulant use. 
  38. ^ Stoops WW, Rush CR. Combination pharmacotherapies for stimulant use disorder: a review of clinical findings and recommendations for future research. Expert Rev Clin Pharmacol. May 2014, 7 (3): 363–374. PMC 4017926. PMID 24716825. doi:10.1586/17512433.2014.909283. Despite concerted efforts to identify a pharmacotherapy for managing stimulant use disorders, no widely effective medications have been approved. 
  39. ^ Perez-Mana C, Castells X, Torrens M, Capella D, Farre M. Efficacy of psychostimulant drugs for amphetamine abuse or dependence. Cochrane Database Syst. Rev. September 2013, 9: CD009695. PMID 23996457. doi:10.1002/14651858.CD009695.pub2. To date, no pharmacological treatment has been approved for [addiction], and psychotherapy remains the mainstay of treatment. ... Results of this review do not support the use of psychostimulant medications at the tested doses as a replacement therapy 
  40. ^ Forray A, Sofuoglu M. Future pharmacological treatments for substance use disorders. Br. J. Clin. Pharmacol. February 2014, 77 (2): 382–400. PMC 4014020. PMID 23039267. doi:10.1111/j.1365-2125.2012.04474.x. 
  41. ^ 41.0 41.1 Malenka RC, Nestler EJ, Hyman SE. Chapter 5: Excitatory and Inhibitory Amino Acids. (编) Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience 2nd. New York, USA: McGraw-Hill Medical. 2009: 124–125. ISBN 978-0-07-148127-4. At membrane potentials more negative than approximately −50 mV, the Mg2+ in the extracellular fluid of the brain virtually abolishes ion flux through NMDA receptor channels, even in the presence of glutamate. ... The NMDA receptor is unique among all neurotransmitter receptors in that its activation requires the simultaneous binding of two different agonists. In addition to the binding of glutamate at the conventional agonist-binding site, the binding of glycine appears to be required for receptor activation. Because neither of these agonists alone can open this ion channel, glutamate and glycine are referred to as coagonists of the NMDA receptor. The physiologic significance of the glycine binding site is unclear because the normal extracellular concentration of glycine is believed to be saturating. However, recent evidence suggests that D-serine may be the endogenous agonist for this site. 
  42. ^ Kanehisa Laboratories. Amphetamine – Homo sapiens (human). KEGG Pathway. 10 October 2014 [31 October 2014]. Most addictive drugs increase extracellular concentrations of dopamine (DA) in nucleus accumbens (NAc) and medial prefrontal cortex (mPFC), projection areas of mesocorticolimbic DA neurons and key components of the "brain reward circuit". Amphetamine achieves this elevation in extracellular levels of DA by promoting efflux from synaptic terminals. ... Chronic exposure to amphetamine induces a unique transcription factor delta FosB, which plays an essential role in long-term adaptive changes in the brain. 
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  47. ^ 47.0 47.1 47.2 47.3 Shoptaw SJ, Kao U, Heinzerling K, Ling W. Shoptaw SJ, 编. Treatment for amphetamine withdrawal. Cochrane Database Syst. Rev. 2009, (2): CD003021. PMID 19370579. doi:10.1002/14651858.CD003021.pub2. The prevalence of this withdrawal syndrome is extremely common (Cantwell 1998; Gossop 1982) with 87.6% of 647 individuals with amphetamine dependence reporting six or more signs of amphetamine withdrawal listed in the DSM when the drug is not available (Schuckit 1999) ... Withdrawal symptoms typically present within 24 hours of the last use of amphetamine, with a withdrawal syndrome involving two general phases that can last 3 weeks or more. The first phase of this syndrome is the initial "crash" that resolves within about a week (Gossop 1982;McGregor 2005) 
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