desvenlafaxine 50 mg / d治疗的临床效用MDD:回顾两个随机安慰剂对照试验的执业医师。

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Reddy年代,凯恩C、B Pitrosky Musgnung J,尼南PT, Guico-Pabia CJ

desvenlafaxine 50 mg / d治疗的临床效用MDD:回顾两个随机安慰剂对照试验的执业医师。

咕咕叫地中海Res当今。2010年1月,26 (1):139 - 50。doi: 10.1185 / 03007990903408678。

PubMed ID
19919295 (在PubMed
]
文摘

背景:重度抑郁症(MDD)是一种常见的、严重损害的疾病。Desvenlafaxine(管理Desvenlafaxine琥珀酸)是第三serotonin-norepinephrine再摄取抑制剂(去甲肾上腺素重摄取抑制剂)批准在美国治疗的MDD。短期临床研究证明了有效性和安全性的50到400毫克/天的剂量,没有证据表明剂量大于50 mg / d带来额外的好处。目的:综述发表数据有效性、安全性和耐受性desvenlafaxine 50毫克/ d推荐治疗剂量的MDD和探讨临床实践方面的考虑。方法:系统回顾的MEDLINE、PsycINFO和PubMed通过2009年6月(年)使用desvenlafaxine条款执行,dv, ODV。入选标准的审查是一个双盲设计,安慰剂控制或活性对比组,50毫克的剂量desvenlafaxine集团和MDD登记患者的诊断。海报中如果他们报道了一项研究,随后发表在一份手稿。结果:总体的结果两个随机、安慰剂对照,8周的临床试验证明desvenlafaxine 50 mg / d MDD的功效。统计上显著的改进与安慰剂比较观察疗效测量(测量表汉密尔顿抑郁量表总分(ham - d (17));P < 0.05)。 Significant differences were observed on several secondary measures (Montgomery Asberg Depression Rating Scale scores in both trials [P < 0.05]; Clinical Global Impressions-Improvement scores [P < or = 0.01], Clinical Global Impressions-Severity scores [P < or = 0.01], HAM-D(17) response [P < or = 0.01] and remission [P < 0.05] in one trial each). Functional outcomes measures (Sheehan Disability Scale total and World Health Organization 5-Item Well-Being Index scores) were significant in both trials (P < 0.05). Safety results indicate desvenlafaxine treatment was safe and well tolerated; findings were consistent with the SNRI class. The generalizability of these findings is limited by the study protocols, which excluded patients with unstable comorbid medical conditions and also those with other Axis 1 and 2 psychiatric illnesses. Additionally, comparisons with other SNRIs are challenging given differences in study design. Desvenlafaxine can be initiated with the 50-mg/d therapeutic dose without titration and provides efficacy with rates of discontinuation due to treatment-emergent adverse events similar to placebo. In vitro data indicate desvenlafaxine has minimal inhibitory effects on cytochrome P450 (CYP) 2D6 and clinical studies show desvenlafaxine does not have a clinically relevant effect on CYP2D6 metabolism. In vitro data also indicate desvenlafaxine is not a substrate or inhibitor of the p-glycoprotein transporter. Plasma protein binding of desvenlafaxine is low (30%) and independent of drug concentration. Bioavailability is high at 80% after oral administration and is not affected by food. CONCLUSIONS: Desvenlafaxine 50 mg/d has demonstrated efficacy, safety, and tolerability for the treatment of MDD in two placebo-controlled trials. The metabolic profile of desvenlafaxine suggests a low risk of drug-drug interactions owing to minimal inhibitory effects on CYP2D6, lack of interaction with p-glycoprotein, and low protein binding.

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药物
药物靶点
药物 目标 类 生物 药理作用 行动
Desvenlafaxine Sodium-dependent去甲肾上腺素转运体 蛋白质 人类
是的
抑制剂
 细节
Desvenlafaxine Sodium-dependent羟色胺转运体 蛋白质 人类
是的
抑制剂
 细节