Maternal plasma fetal DNA as a marker for preterm labour

TN Leung, J Zhang, TK Lau, NM Hjelm, YMD Lo - The Lancet, 1998 - thelancet.com
TN Leung, J Zhang, TK Lau, NM Hjelm, YMD Lo
The Lancet, 1998thelancet.com
Confidential Enquires into Maternal Deaths have highlighted the need for adequate
treatment of thromboembolic disease, a major cause of maternal death in the UK. 1 Low-
molecular-weight heparin (LMWH) is effective, safe, and associated with fewer side-effects
than unfractionated heparin for the treatment of acute deep vein thrombosis and pulmonary
thromboembolism in nonpregnant women. 2, 3 LMWHs are commonly used for
thromboprophylaxis during pregnancy, 3 but unfractionated heparin is the mainstay of …
Confidential Enquires into Maternal Deaths have highlighted the need for adequate treatment of thromboembolic disease, a major cause of maternal death in the UK. 1 Low-molecular-weight heparin (LMWH) is effective, safe, and associated with fewer side-effects than unfractionated heparin for the treatment of acute deep vein thrombosis and pulmonary thromboembolism in nonpregnant women. 2, 3 LMWHs are commonly used for thromboprophylaxis during pregnancy, 3 but unfractionated heparin is the mainstay of treatment for antenatal venous thromboembolism. The monitoring of unfractionated heparin by activated partial thromboplastin time can, however, be difficult in late pregnancy, when an apparent heparin resistance occurs because of increased fibrinogen and factor VIII. 4, 5 To date there has been no report of LMWH for treatment of deep venous thrombosis or pulmonary thromboembolism in pregnancy. We treated with subcutaneous enoxaparin, a LMWH, two women with antenatal deep vein thrombosis and two with antenatal pulmonary thromboembolism, objectively confirmed by ultrasound or ventilation-perfusion lung scintigraphy. The starting dose was 1 mg/kg every 12 h, based on the early pregnancy weight, since LMWH does not cross the placenta. We measured anti-Xa activity by chromogenic substrate assay (target therapeutic range 0· 4–1· 0 U/mL 3 h after injection). In one woman (weight 94 kg), the start dose was decreased from 100 mg to 80 mg twice daily since the peak concentration of anti-Xa on 100 mg was 1· 2 U/mL; the resultant peak concentration of anti-Xa on 80 mg was 1· 0 U/mL. In the other three women, the start dose of enoxaparin produced satisfactory peak concentrations of anti-Xa. We measured blood platelets, activated partial thromboplastin times, and anti-Xa concentrations before and weekly during treatment, and all of the women were continued on enoxaparin until delivery,(times between thromboembolism and delivery 1, 2, 4, and 8 weeks). The women were taught to self-inject, and three were managed as outpatients until delivery at term. The dose of enoxaparin was decreased to 40 mg every 12 h during labour, and recommenced immediately after delivery. Two
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