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求大神幫忙翻譯一段英文,真心不會,謝謝
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Because in clinical practice, it is not possible to measure LMWH levels directly; pharmacokinetic studies have used such surrogate markers of activity as anti-Xa activity, but there are a number of difficulties with this. First, anti-Xa activity represents the amount of heparin present, rather than the degree of antithrombotic effect. Second, at equivalent anti-Xa activities, antifactor IIa activity of different products shows marked variations. Finally, conflicting evidence exists about whether anti-Xa levels predict for bleedingcomplications clinically. Several studies have looked at the pharmacokinetics and dynamics of different LMWHs in patients with CKD stages 1 to 3. In patients enrolled in the TIMI IIA trial, (aspirin plus enoxaparin), pharmacokinetic and pharmacodynamic profiles after enoxaparin therapy were assessed. Patients with an sCr level of 2.0 mg/dL or greater [177 mol/L] were excluded from the trial. CrCl was the most influential factor on enoxaparin clearance, area under the curve, and anti-Xa activity. Drug clearance was decreased by 22% in patients with a CrCl less than 40 mL/min (0.67mL/s) compared with those with greater CrCls (mean, 88 mL/min [1.47 mL/s]). The linear character of the elimination curve (Fig 2) led the investigators to extrapolate that enoxaparin clearance would be reduced by approximately 50% in patients with a CrCl less than 20 mL/min (0.33mL/s). Although numbers were small, patients with a CrCl less than 40 mL/min (0.67 mL/s) had greater trough and peak anti-Xa activity compared with those with normal renal function (P=0.0017 and P =0.0044, respectively) and were more likely to experience major hemorrhagic events. |
禁蟲 (正式寫手)
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Because in clinical practice, it is not possible to measure LMWH levels directly; pharmacokinetic studies have used such surrogate markers of activity as anti-Xa activity, but there are a number of difficulties with this. First, anti-Xa activity represents the amount of heparin present, rather than the degree of antithrombotic effect. Second, at equivalent anti-Xa activities, antifactor IIa activity of different products shows marked variations. Finally, conflicting evidence exists about whether anti-Xa levels predict for bleeding complications clinically. 因為臨床試驗尚不能直接測量低分子肝素的水平。 藥物代謝動力學領域曾經(jīng)有研究使用這種活性替代物來代替抗Xa因子活性。然而此方法任存在一些困難。首先抗Xa因子活性反映的是肝素的存在量而不是抗血栓作用的程度。其次在同等的抗Xa活性作用下,不同的產(chǎn)品IIa抗體因素的活性有明顯的差異。最后抗Xa因子水平預測是否會導致出血并發(fā)癥臨床上還存在爭議。 Several studies have looked at the pharmacokinetics and dynamics of different LMWHs in patients with CKD stages 1 to 3. In patients enrolled in the TIMI IIA trial, (aspirin plus enoxaparin), pharmacokinetic and pharmaco dynamic profiles after enoxaparin therapy were assessed. Patients with an sCr level of 2.0 mg/dL or greater [ 177 mol/L] were excluded from the trial. 一些研究者對CKD處于1-3期的患者在不同的低分子量肝素的條件下的藥代動力學和動態(tài)進行了研究。運用TIMI IIA試驗,使用阿司匹林加依諾肝素,對患者經(jīng)依諾肝素治療后的藥代動力和藥效數(shù)據(jù)進行了評估。sCr 水平在2.0 mg/dL 或者大于[ 177 mol/L]的患者排除在此實驗之外. CrCl was the most influential factor on enoxaparin clearance, area under the curve, and anti-Xa activity. Drug clearance was decreased by 22% in patients with a CrCl less than 40 mL/min (0.67mL/s) compared with those with greater CrCls (mean, 88 mL/min [1.47 mL/s]). CrCl是伊諾肝素清除性,曲線下面積和抗Xa活性三者最大的影響因素。與患者CrCl在高于88 mL/min [1.47 mL/s]的情況下相比, CrCl少于40 mL/min (0.67mL/s)的患者藥物的清除率下降了22%。 The linear character of the elimination curve (Fig 2) led the investigators to extrapolate that enoxaparin clearance would be reduced by approximately 50% in patients with a CrCl less than 20 mL/min (0.33mL/s). Although numbers were small, patients with a CrCl less than 40 mL/min (0.67 mL/s) had greater trough and peak anti-Xa activity compared with those with normal renal function (P =0.0017 and P =0.0044, respectively) and were more likely to experience major hemorrhagic events. 研究者根據(jù)消除曲線(見圖2)的線性特征推斷當患者CrCl少于20 mL/min (0.33mL/s)時依諾肝素的清除率可以下降大約50%。與腎功能正常者(P = 0.0017,P = 0.0044,分別)相比,雖然這種情況很少, CrCl小于40 mL/min (0.67 mL/s) 患者有更大的波谷和高抗Xa活性并且伴有大出血的可能性比較大。 |
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