OBJECTIVE: To compare lipocalin-2 (LCN2) levels in pre-eclamptic women with those in healthy pregnant women, and to determine whether there is a correlation between LCN2 levels and the severity of the disease. METHODS: The study included 66 pregnant women: 22 healthy pregnant women (Group 1), 23 women with mild pre-eclampsia (Group 2), and 21 women with severe pre-eclampsia (Group 3). Pre-eclamptic women and normal controls were carefully matched for maternal age, gestational age, and body mass index (BMI). The maternal levels of plasma LCN2 were determined by enzyme-linked immunosorbent assay. RESULTS: Plasma LCN2 levels in the pre-eclamptic group were significantly lower than those in the healthy control group (p < 0.05). Although plasma LCN2 level was lower in the severe compared to the mild pre-eclamptic group, the difference was not statistically significant (p > 0.05). There was no significant correlation between LCN2 levels and the homeostasis model assessment of insulin resistance (HOMA-IR), BMI, triglyceride, gestational week at delivery, birth weight, and systolic and diastolic blood pressure in pre-eclamptic and healthy pregnant women (p > 0.05). CONCLUSIONS: Our results show that there are decreased concentrations of plasma LCN2 in pre-eclamptic subjects and this may indicate that LCN2 plays a role in the pathogenesis of pre-eclampsia. However, further experiments are needed to clarify this role.
OBJECTIVE: To compare lipocalin-2 (LCN2) levels in pre-eclamptic women with those in healthy pregnant women, and to determine whether there is a correlation between LCN2 levels and the severity of the disease. METHODS: The study included 66 pregnant women: 22 healthy pregnant women (Group 1), 23 women with mild pre-eclampsia (Group 2), and 21 women with severe pre-eclampsia (Group 3). Pre-eclamptic women and normal controls were carefully matched for maternal age, gestational age, and body mass index (BMI). The maternal levels of plasma LCN2 were determined by enzyme-linked immunosorbent assay. RESULTS: Plasma LCN2 levels in the pre-eclamptic group were significantly lower than those in the healthy control group (p < 0.05). Although plasma LCN2 level was lower in the severe compared to the mild pre-eclamptic group, the difference was not statistically significant (p > 0.05). There was no significant correlation between LCN2 levels and the homeostasis model assessment of insulin resistance (HOMA-IR), BMI, triglyceride, gestational week at delivery, birth weight, and systolic and diastolic blood pressure in pre-eclamptic and healthy pregnant women (p > 0.05). CONCLUSIONS: Our results show that there are decreased concentrations of plasma LCN2 in pre-eclamptic subjects and this may indicate that LCN2 plays a role in the pathogenesis of pre-eclampsia. However, further experiments are needed to clarify this role.