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      Maternal Serum Concentrations of Selenium, Copper, and Zinc during Pregnancy Are Associated with Risk of Spontaneous Preterm Birth: A Case-Control Study from Malawi

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          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.

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          Most cited references33

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          New Ballard Score, expanded to include extremely premature infants

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            Copper, oxidative stress, and human health.

            Copper (Cu), a redox active metal, is an essential nutrient for all species studied to date. During the past decade, there has been increasing interest in the concept that marginal deficits of this element can contribute to the development and progression of a number of disease states including cardiovascular disease and diabetes. Deficits of this nutrient during pregnancy can result in gross structural malformations in the conceptus, and persistent neurological and immunological abnormalities in the offspring. Excessive amounts of Cu in the body can also pose a risk. Acute Cu toxicity can result in a number of pathologies, and in severe cases, death. Chronic Cu toxicity can result in liver disease and severe neurological defects. The concept that elevated ceruloplasmin is a risk factor for certain diseases is discussed. In this paper, we will review recent literature on the potential causes of Cu deficiency and Cu toxicity, and the pathological consequences associated with the above. Finally, we will review some of the potential biochemical lesions that might underlie these pathologies. Given that oxidative stress is a characteristic of Cu deficiency, the role of Cu in the oxidative defense system will receive special attention. The concept that excess Cu may be a precipitating factor in Alzheimer's disease is discussed.
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              Placental oxidative stress: from miscarriage to preeclampsia.

              To review the role of oxidative stress in two common placental-related disorders of pregnancy, miscarriage and preeclampsia. Review of published literature. Miscarriage and preeclampsia manifest at contrasting stages of pregnancy, yet both have their roots in deficient trophoblast invasion during early gestation. Early after implantation, endovascular trophoblast cells migrate down the lumens of spiral arteries, and are associated with their physiological conversion into flaccid conduits. Initially these cells occlude the arteries, limiting maternal blood flow into the placenta. The embryo therefore develops in a low oxygen environment, protecting differentiating cells from damaging free radicals. Once embryogenesis is complete, the maternal intervillous circulation becomes fully established, and intraplacental oxygen concentration rises threefold. Onset of the circulation is normally a progressive periphery-center phenomenon, and high levels of oxidative stress in the periphery may induce formation of the chorion laeve. If trophoblast invasion is severely impaired, plugging of the spiral arteries is incomplete, and onset of the maternal intervillous circulation is premature and widespread throughout the placenta. Syncytiotrophoblastic oxidative damage is extensive, and likely a major contributory factor to miscarriage. Between these two extremes will be found differing degrees of trophoblast invasion compatible with ongoing pregnancy but resulting in deficient conversion of the spiral arteries and an ischemia-reperfusion-type phenomenon. Placental perfusion will be impaired to a greater or lesser extent, generating commensurate placental oxidative stress that is a major contributory factor to preeclampsia. Miscarriage, missed miscarriage, and early- and late-onset preeclampsia represent a spectrum of disorders secondary to deficient trophoblast invasion.
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                Author and article information

                Contributors
                Journal
                J Pregnancy
                J Pregnancy
                JP
                Journal of Pregnancy
                Hindawi
                2090-2727
                2090-2735
                2020
                30 April 2020
                : 2020
                : 9435972
                Affiliations
                1Department of Obstetrics and Gynecology, College of Medicine, University of Malawi, P.O. Box 30055, Lilongwe, Malawi
                2TB/HIV Department, Malawi Liverpool Wellcome Trust Clinical Research Programme, Blantyre, Malawi
                3Malawi University of Science and Technology, P .O .Box 5196, Limbe, Malawi
                4Department of Laboratory Medicine, University Hospital of North Norway, Sykehusveien 38, NO-9038 Tromsø, Norway
                5The Norwegian University of Science and Technology, Trondheim, Norway
                Author notes

                Academic Editor: Fabio Facchinetti

                Author information
                https://orcid.org/0000-0001-6154-3613
                Article
                10.1155/2020/9435972
                7210528
                32411468
                4af7ec65-39fa-4f38-9881-72b5376a32c5
                Copyright © 2020 Grace Chiudzu et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 24 June 2019
                : 16 March 2020
                : 13 April 2020
                Funding
                Funded by: Safe Motherhood Malawi
                Categories
                Research Article

                Obstetrics & Gynecology
                Obstetrics & Gynecology

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