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求大神帮忙翻译一段英文，真心不会，谢谢
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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. |
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