急！来士普对治疗惊恐和焦虑有用没啊？谢谢！急！

呼呼猫

我不知道该不该吃..........谢谢！
急！来士普对治疗惊恐和焦虑有用没啊？

晔阳

来士普

来源：新特药房药讯         浏览:2693   发布时间：2006-8-4 11:54:00

                                                                                                                                                                                                          商品名:来士普
通用名:艾司西酞普兰
英文商品名exapro
英文通用名:Escitalopram
【作用机制】
艾司西酞普兰增进中枢神经系统5-羟色胺（5-HT）能的作用，抑制5-羟色胺的再摄取，临床用于抑郁症的治疗。动物研究表明，艾司西酞普兰为选择性5-羟色胺再摄取抑制剂（SSRI），而对去甲肾上腺素和多巴胺再摄取作用微弱，其作用为西酞普兰右旋对映体作用的100倍。艾司西酞普兰对5-羟色胺1-7受体或其他受体包括α和β肾上腺素、多巴胺1-5、组胺1、蕈毒碱1-5和苯二氮卓受体无作用或非常小，另外对Na+、K+、Cl-和Ca++离子通道无作用。
【适应证】
1. 重症抑郁症（MDD）的治疗：重症抑郁症主要表现显著或持久的情绪低落或燥动情绪（至少持续2周），主要包括以下症状：情绪低落、兴趣减少、体重或食欲明显变化、失眠或嗜睡、精神运动兴奋或迟缓、过度疲劳、内疚或自卑感、思维迟缓或注意力不集中、自杀企图或念头。
2 、广泛性焦虑（GAD）：表现为过度的焦虑和烦恼，至少持续6个月。主要有以下症状：烦燥不安、易疲劳、注意力不集中、兴奋、肌肉紧张和睡眠障碍。
【用法与用量】
1.重症抑郁症：起始剂量一日一次10mg，一周后可以增至一日一次20mg,早晨或晚上口服。一般情况下应持续几个月甚至更长时间的治疗。老年患者或肝功能不全者建议一日一次10mg·，轻度或中度肾功能不全者无需调节剂量。严重肾功能不全者慎用。2.广泛性焦虑：起始剂量一日一次10mg，一周后可以增至一日一次20mg，早晨或晚上口服。至少停用单胺氧化酶抑制剂（MAOI）14天后才可以调换本药，同样，停用本药14天后才可以用单胺氧化酶抑制剂。停药时应逐渐减量。
【药物不良反应】
约5％的患者有失眠、阳萎、恶心、便秘、多汗、口干、疲劳、嗜睡。约2％的患者有头痛、上呼吸道感染、背痛、咽炎和焦虑等。偶见报道可引起躁狂或轻度躁狂或低钠血。有惊厥史的患者应慎用。实验室参数没有明显的改变。心电图无明显异常。
【药物相互作用】 禁与单胺氧化酶抑制剂并用， 与酒精和中枢神经系统药物（例如抗抑郁药）并用时应慎重。与阿司匹林、华法令等抗凝血药合用时可能引起上消化道出血的危险应慎用。锂盐可能增加艾司西肽普兰的作用，合用时应慎用。酶诱导剂卡马西平可能增加艾司西肽普兰的代谢，两者合用时应增加后者的剂量。与美托洛尔合用对患者的血压和心率没有明显影响。艾司西肽普兰不应与西肽普兰合用。
【注意事项】
肝、肾功能不全者，有惊厥史或心脏病患者、甲状腺疾病、电解质紊乱、有其他精神疾病（例如双相情感障碍）或自杀念头者应慎用。 服药期间不宜操作机器， 孕妇或哺乳期妇女应慎用，对婴幼儿的安全性没有临床资料。对本品或西肽普兰过敏的患者应禁用
HistoryEscitalopram was developed in a close cooperation between Lundbeckand Forest Laboratories. Its development was initiated in the summer of1997, and the resulting new drug application was submitted to the FDAin March 2001. The short time (3.5 years) it took to developescitalopram can be attributed to the previous extensive experience ofLundbeck and Forest with citalopram, which has similar pharmacology.[3]FDA issued the approval of escitalopram for major depression in August2002 and for generalized anxiety disorder in December 2003.Escitalopram can be considered an example of "lifecycle management"[4]- the strategy pharmaceutical companies use in order to extend thelifetime of a drug, in this case of the citalopram franchise.Escitalopram is an enantiomer of citalopram,used for the same indication, and for that reason it required lessinvestment and less time to develop. Two years after escitalopram'slaunch, when the patent on citalopram expired, the escitalopram salessuccessfully made up for the loss. On May 23, 2006, the FDA approved a generic version of escitalopram by Teva.[5] However, on July 14 of that year, the U.S. District Court of Delaware decided in favor of Lundbeck regarding the patent infringement dispute and ruled the patent on escitalopram valid.[6]
Despite the drug's similarity, preclinical as well as various clinical studies (including double-blinded studies) have shown differentiated effects of citalopram and escitalopram,[7] as well as a clinical superiority compared with a variety of other SSRIs, such as paroxetine,[8] especially in severely depressed patients and sertraline. Compared with newer serotonin-norepinephrine reuptake inhibitors such as venlafaxine[9] and duloxetine[10] escitalopram was shown to be at least as effective.

[edit] PharmacologyEscitalopram acts by increasing intrasynaptic levels of theneurotransmitter serotonin by blocking the reuptake of theneurotransmitter into the neuron. Of the SSRIs currently on the marketescitalopram has the highest affinity for the human serotonin transporter (SERT). Remarkably, another enantiomer of citalopram (R-citalopram)counteracts to a certain degree the serotonin-enhancing action ofescitalopram. As a result, escitalopram is a more potent antidepressantthan citalopram, which is a mixture of escitalopram and R-citalopram.In order to explain this phenomenon, researchers from Lundbeck proposedthat escitalopram enhances its own binding via an additionalinteraction with another allosteric site on the transporter.[11] Further research by the same group showed that R-citalopram also enhances binding of escitalopram,[12]and therefore the allosteric interaction cannot explain the observedcounteracting effect. However, in the most recent paper the sameauthors again reversed their findings and reported that R-citalopram decreases binding of escitalopram to the transporter.[13]Although allosteric binding of escitalopram to the serotonintransporter is of unquestionable research interest, its clinicalrelevance is unclear since the binding of escitalopram to theallosteric site is at least 1000 times weaker than to the primarybinding site.
In vitro studies using human liver microsomes indicated that CYP3A4 and CYP2C19 are the primary isozymes involved in the N-demethylation of escitalopram.

[edit] Side effects and drug interactionsMain article: Selective serotonin reuptake inhibitor
The side effect profile of escitalopram is close to that of other SSRIs, with nausea, somnolence, and gastrointestinal side effects reported as relatively common. Escitalopram, like other SSRIs, has been shown to cause sexual side effects in many patients.[14]Escitalopram is not associated with significant weight gain. Forexample, 0.6 kg mean weight change after 6 months of treatment withescitalopram for depression was insignificant and similar to that withplacebo (0.2 kg).[15] 1.4-1.8 kg mean weight gain was reported in 8-month trials of escitalopram for depression,[16] and generalized anxiety disorder (引起焦虑）.[17]A 52-week trial of escitalopram for the long-term treatment ofdepression in elderly also found insignificant 0.6 kg mean weight gain.[18] Escitalopram may help reduce weight in those treated for binge eating associated obesity.[19] It may also cause dizziness after exercise in children.[citation needed]
A meta-analysis of clinical trials database conducted by theescitalopram manufacturer Lundbeck found no indication thatescitalopram would provoke suicidal behaviour compared with placebo in patients with major depressive disorder and anxiety disorders, on the contrary, suicidal thoughts in the escitalopram group were significantly decreased.[20]An analysis conducted by the FDA found a statistically insignificant1.5 to 2.4-fold, depending on the statistical technique used, increaseof suicidality among the adults treated with escitalopram forpsychiatric indications.[21][22][23] Similarly, the UK MHRAdata indicate an 80% increase of suicide-related events, not reachingstatistical significance, in the escitalopram vs placebo patients.[24]The authors of a related study note the general problem withstatistical approaches—due to the rarity of suicidal events in clinicaltrials, it is hard to draw firm conclusions with a sample smaller thantwo million patients.[25] A single case report described a patient developing suicidal ideation after beginning treatment with escitalopram, and suicidal ideation disappearing after stopping the treatment.[26]
Escitalopram should be taken with caution when using St John's wort.[27]

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