Abstract

Preterm birth is delivery before 37 completed weeks. A study was conducted to evaluate the association of maternal serum concentrations of selenium, copper, and zinc and preterm birth. There were 181 women in this nested case-control study, 90/181 (49.7%) term and 91/181 (50.3%) preterm pregnant women. The overall mean serum concentration of selenium was 77.0, SD 19.4 μg/L; of copper was 2.50, SD 0.52 mg/L; and of zinc was 0.77, SD 0.20 mg/L with reference values of 47-142 μg/L, 0.76-1.59 mg/L, and 0.59-1.11 mg/L, respectively. For preterm birth, mean serum concentration for selenium was 79.7, SD 21.6 μg/L; for copper was 2.61, SD 0.57 mg/L; and for zinc was 0.81, SD 0.20 mg/L compared to that for term births: selenium (74.2; SD 16.5 μg/L; p = 0.058), copper (2.39; SD 0.43 mg/L; p = 0.004), and zinc (0.73; SD 0.19 mg/L; p = 0.006), respectively. In an adjusted analysis, every unit increase in maternal selenium concentrations gave increased odds of being a case OR 1.01 (95% CI: 0.99; 1.03), p = 0.234; copper OR 1.62 (95% CI: 0.80; 3.32), p = 0.184; zinc OR 6.88 (95% CI: 1.25; 43.67), p = 0.032. Results show that there was no deficiency of selenium and zinc and there were high serum concentrations of copper in pregnancy. Preterm birth was associated with higher maternal serum concentrations of copper and zinc.

Highlights

  • Preterm birth occurs before 37 completed weeks (259 days) after the first day of the last menstrual period preceding the pregnancy [1]

  • Contrary to the findings of other studies in the literature, this study found that the maternal serum concentration of zinc was higher in women with preterm birth than in those delivering at term, and a unit increase of zinc had a 7-fold increased risk of having a preterm birth

  • Copper, or zinc micronutrient deficiencies were found in the study population

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Summary

Introduction

Preterm birth occurs before 37 completed weeks (259 days) after the first day of the last menstrual period preceding the pregnancy [1]. A common pathway involving a cellular apoptosis-transmitting inflammatory signal, senescent placental cells, and its changes in the placental membrane was hypothesised to stimulate parturition both term and preterm [8]. This common pathway is believed to be stimulated by the premature aging of the placenta caused by oxidative stress [9]. The placenta is the main source of reactive oxygen species (ROS) which induces cellular damage

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