Objective Insulin-like growth factor-1 (IGF-1) and IGF binding protein-1 (IGFBP-1) may be important determinants of glucose homeostasis. We examined the association between circulating concentrations of IGF-1, IGFBP-1 in early pregnancy and development of

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.