Objective: We investigated whether levels of annexin A5,evidence for resistance to annexin A5 activity, and levels antiannexin A5 antibodies might be altered in women with a history of recurrent spontaneous pregnancy ...Objective: We investigated whether levels of annexin A5,evidence for resistance to annexin A5 activity, and levels antiannexin A5 antibodies might be altered in women with a history of recurrent spontaneous pregnancy losses. Study design: These annexin A5 parameters were assayed in 70 nonpregnant women with a history of ≥3 recurrent spontaneous pregnancy losses (cases) and 50 women without adverse pregnancy history (control subjects). Results: Cases had significantly lower plasma annexin A5 levels than control subjects (median, 4.7 ng/mL [range, 0.3-40.4 ng/mL] vs 6.7 ng/mL [range, 0.7-56.0]; P = .01), significantly reduced anticoagulant ratios (188%[range, 119%-279%] vs 238%[range, 159%-286%]; P < .0001), and reduced binding of annexin A5 to phospholipid (6.3 ng/aliquot phospholipid [range, 1.5-16.4 ng/aliquot phospholipid] vs 9.7 ng/aliquot phospholipid (range, 3.5-17.0 ng/aliquot phospholipid]; P = .0002). There were no significant differences in anti-annexin A5 antibody levels. Conclusion: Reduction of annexin A5 and interference with its anticoagulant and binding activities are associated significantly with a history of recurrent spontaneous pregnancy losses. These data support the concept of a significant role for annexin A5 in the maintenance of pregnancy.展开更多
Objective: This study was undertaken to evaluate the association between protein Z concentration and pregnancy complications. Study design: A prospective case-control study was conducted over a 2-year period to evalua...Objective: This study was undertaken to evaluate the association between protein Z concentration and pregnancy complications. Study design: A prospective case-control study was conducted over a 2-year period to evaluate the prevalence of protein Z deficiency in pregnancy complications. Protein Z levels were measured at the time of diagnosis of complications such as preeclampsia, intrauterine growth restriction, and intrauterine fetal demise. Protein Z deficiency was defined as a plasma level below 1.2 mg/L. In addition to patients presenting with pregnancy complications, healthy age-matched nonpregnant and pregnant women were invited to participate. Results: A total of 145 women were included in the study: 50 nonpregnant women, 34 healthy pregnant women, 29 women with preeclampsia, 25 women presented with intrauterine growth restriction, and 7 women with intrauterine fetal demise. The median protein Z level was similar in healthy pregnant and nonpregnant women (1.63 0.47-3.1 mg/L and 1.69 0.7-3 mg/L, respectively). Three women with normal pregnancies had a low protein Z level (8.8%), compared with 8 patients presenting with intrauterine growth restriction (33.3%) and 8 patients with intrauterine fetal demise (50%). Compared with normal pregnancy, the frequency of decreased protein Z was significantly higher in cases of intrauterine growth restriction and in intrauterine fetal demise (relative risk RR 1.96, 95%CI 1.16-3.32; P = .041 and RR 3.36, 95%CI 1.65-6.8; P = .0031, respectively), but not in preeclampsia (RR 1.6, 95%CI 0.9-2.8; P = .23). Placenta histologic examination revealed vascular lesions in 50%of patients with protein Z deficiency and in 33%of patients with normal levels of protein Z (RR 0.84; 95%CI 0.6-1.2). Conclusion: Protein Z deficiency is associated with late fetal demise and intrauterine growth restriction. The pathophysiologic role of protein Z deficiency, either congenital or caused by the presence of specific antibodies remains unclear and should be further investigated.展开更多
文摘Objective: We investigated whether levels of annexin A5,evidence for resistance to annexin A5 activity, and levels antiannexin A5 antibodies might be altered in women with a history of recurrent spontaneous pregnancy losses. Study design: These annexin A5 parameters were assayed in 70 nonpregnant women with a history of ≥3 recurrent spontaneous pregnancy losses (cases) and 50 women without adverse pregnancy history (control subjects). Results: Cases had significantly lower plasma annexin A5 levels than control subjects (median, 4.7 ng/mL [range, 0.3-40.4 ng/mL] vs 6.7 ng/mL [range, 0.7-56.0]; P = .01), significantly reduced anticoagulant ratios (188%[range, 119%-279%] vs 238%[range, 159%-286%]; P < .0001), and reduced binding of annexin A5 to phospholipid (6.3 ng/aliquot phospholipid [range, 1.5-16.4 ng/aliquot phospholipid] vs 9.7 ng/aliquot phospholipid (range, 3.5-17.0 ng/aliquot phospholipid]; P = .0002). There were no significant differences in anti-annexin A5 antibody levels. Conclusion: Reduction of annexin A5 and interference with its anticoagulant and binding activities are associated significantly with a history of recurrent spontaneous pregnancy losses. These data support the concept of a significant role for annexin A5 in the maintenance of pregnancy.
文摘Objective: This study was undertaken to evaluate the association between protein Z concentration and pregnancy complications. Study design: A prospective case-control study was conducted over a 2-year period to evaluate the prevalence of protein Z deficiency in pregnancy complications. Protein Z levels were measured at the time of diagnosis of complications such as preeclampsia, intrauterine growth restriction, and intrauterine fetal demise. Protein Z deficiency was defined as a plasma level below 1.2 mg/L. In addition to patients presenting with pregnancy complications, healthy age-matched nonpregnant and pregnant women were invited to participate. Results: A total of 145 women were included in the study: 50 nonpregnant women, 34 healthy pregnant women, 29 women with preeclampsia, 25 women presented with intrauterine growth restriction, and 7 women with intrauterine fetal demise. The median protein Z level was similar in healthy pregnant and nonpregnant women (1.63 0.47-3.1 mg/L and 1.69 0.7-3 mg/L, respectively). Three women with normal pregnancies had a low protein Z level (8.8%), compared with 8 patients presenting with intrauterine growth restriction (33.3%) and 8 patients with intrauterine fetal demise (50%). Compared with normal pregnancy, the frequency of decreased protein Z was significantly higher in cases of intrauterine growth restriction and in intrauterine fetal demise (relative risk RR 1.96, 95%CI 1.16-3.32; P = .041 and RR 3.36, 95%CI 1.65-6.8; P = .0031, respectively), but not in preeclampsia (RR 1.6, 95%CI 0.9-2.8; P = .23). Placenta histologic examination revealed vascular lesions in 50%of patients with protein Z deficiency and in 33%of patients with normal levels of protein Z (RR 0.84; 95%CI 0.6-1.2). Conclusion: Protein Z deficiency is associated with late fetal demise and intrauterine growth restriction. The pathophysiologic role of protein Z deficiency, either congenital or caused by the presence of specific antibodies remains unclear and should be further investigated.
