Iron Deficiency, An Independent Risk Factor for Isolated Hypothyroxinemia in Pregnant and Nonpregnant Women of Childbearing Age in China
Context:Isolated hypothyroxinemia during early pregnancy may irreversibly damage the neurodevelopment of offspring. However, the causes are not well clarified.Objective:To explore the association of iron deficiency (ID) with hypothyroid function of women in early pregnancy and nonpregnant women.Desi...
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| Published in | The journal of clinical endocrinology and metabolism Vol. 100; no. 4; pp. 1594 - 1601 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Oxford University Press
01.04.2015
Copyright by The Endocrine Society |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0021-972X 1945-7197 1945-7197 |
| DOI | 10.1210/jc.2014-3887 |
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| Abstract | Context:Isolated hypothyroxinemia during early pregnancy may irreversibly damage the neurodevelopment of offspring. However, the causes are not well clarified.Objective:To explore the association of iron deficiency (ID) with hypothyroid function of women in early pregnancy and nonpregnant women.Design:A total of 7953 pregnant women of ≤ 12 weeks gestation and 2000 childbearing-aged women were recruited. A subpopulation including 3340 pregnant women and 1052 nonpregnant women with sufficient iodine intake and negative thyroid peroxidase antibody were studied. Mild and severe cases of hypothyroxinemia were defined as free T4 levels below the 10th percentile and the 5th percentile, respectively, with normal TSH. Total body iron, serum ferritin, and serum transferrin receptor were used as indicators for iron nutrition.Results:Serum free T4 levels were significantly lower in both pregnant and nonpregnant women with ID compared with the corresponding groups without ID (both P < .05). The prevalence of mild and severe hypothyroxinemia was markedly higher in women with ID than those without, in both pregnant and nonpregnant women (all P < .01). Logistic regression indicated that ID was an independent risk factor for both mild and severe hypothyroxinemia in pregnancy (odds ratio [OR] = 2.440, 95% confidence interval [CI]: 1.324–4.496, P = .004; and OR = 3.278, 95% CI: 1.443–7.446, P = .005, respectively) and nonpregnancy (OR = 2.662, 95% CI: 1.330–5.329, P = .006; and OR = 3.254, 95% CI: 1.375–7.700, P = .007, respectively).Conclusions:An association between ID and isolated hypothyroxinemia was found in both pregnant and nonpregnant childbearing-aged women, independent of the effects of iodine and thyroid autoimmunity. We speculate that ID may be a pathogenic factor for hypothyroxinemia, even in pregnant women during the first trimester. |
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| AbstractList | Isolated hypothyroxinemia during early pregnancy may irreversibly damage the neurodevelopment of offspring. However, the causes are not well clarified.CONTEXTIsolated hypothyroxinemia during early pregnancy may irreversibly damage the neurodevelopment of offspring. However, the causes are not well clarified.To explore the association of iron deficiency (ID) with hypothyroid function of women in early pregnancy and nonpregnant women.OBJECTIVETo explore the association of iron deficiency (ID) with hypothyroid function of women in early pregnancy and nonpregnant women.A total of 7953 pregnant women of ≤ 12 weeks gestation and 2000 childbearing-aged women were recruited. A subpopulation including 3340 pregnant women and 1052 nonpregnant women with sufficient iodine intake and negative thyroid peroxidase antibody were studied. Mild and severe cases of hypothyroxinemia were defined as free T4 levels below the 10th percentile and the 5th percentile, respectively, with normal TSH. Total body iron, serum ferritin, and serum transferrin receptor were used as indicators for iron nutrition.DESIGNA total of 7953 pregnant women of ≤ 12 weeks gestation and 2000 childbearing-aged women were recruited. A subpopulation including 3340 pregnant women and 1052 nonpregnant women with sufficient iodine intake and negative thyroid peroxidase antibody were studied. Mild and severe cases of hypothyroxinemia were defined as free T4 levels below the 10th percentile and the 5th percentile, respectively, with normal TSH. Total body iron, serum ferritin, and serum transferrin receptor were used as indicators for iron nutrition.Serum free T4 levels were significantly lower in both pregnant and nonpregnant women with ID compared with the corresponding groups without ID (both P < .05). The prevalence of mild and severe hypothyroxinemia was markedly higher in women with ID than those without, in both pregnant and nonpregnant women (all P < .01). Logistic regression indicated that ID was an independent risk factor for both mild and severe hypothyroxinemia in pregnancy (odds ratio [OR] = 2.440, 95% confidence interval [CI]: 1.324-4.496, P = .004; and OR = 3.278, 95% CI: 1.443-7.446, P = .005, respectively) and nonpregnancy (OR = 2.662, 95% CI: 1.330-5.329, P = .006; and OR = 3.254, 95% CI: 1.375-7.700, P = .007, respectively).RESULTSSerum free T4 levels were significantly lower in both pregnant and nonpregnant women with ID compared with the corresponding groups without ID (both P < .05). The prevalence of mild and severe hypothyroxinemia was markedly higher in women with ID than those without, in both pregnant and nonpregnant women (all P < .01). Logistic regression indicated that ID was an independent risk factor for both mild and severe hypothyroxinemia in pregnancy (odds ratio [OR] = 2.440, 95% confidence interval [CI]: 1.324-4.496, P = .004; and OR = 3.278, 95% CI: 1.443-7.446, P = .005, respectively) and nonpregnancy (OR = 2.662, 95% CI: 1.330-5.329, P = .006; and OR = 3.254, 95% CI: 1.375-7.700, P = .007, respectively).An association between ID and isolated hypothyroxinemia was found in both pregnant and nonpregnant childbearing-aged women, independent of the effects of iodine and thyroid autoimmunity. We speculate that ID may be a pathogenic factor for hypothyroxinemia, even in pregnant women during the first trimester.CONCLUSIONSAn association between ID and isolated hypothyroxinemia was found in both pregnant and nonpregnant childbearing-aged women, independent of the effects of iodine and thyroid autoimmunity. We speculate that ID may be a pathogenic factor for hypothyroxinemia, even in pregnant women during the first trimester. Isolated hypothyroxinemia during early pregnancy may irreversibly damage the neurodevelopment of offspring. However, the causes are not well clarified. To explore the association of iron deficiency (ID) with hypothyroid function of women in early pregnancy and nonpregnant women. A total of 7953 pregnant women of ≤ 12 weeks gestation and 2000 childbearing-aged women were recruited. A subpopulation including 3340 pregnant women and 1052 nonpregnant women with sufficient iodine intake and negative thyroid peroxidase antibody were studied. Mild and severe cases of hypothyroxinemia were defined as free T4 levels below the 10th percentile and the 5th percentile, respectively, with normal TSH. Total body iron, serum ferritin, and serum transferrin receptor were used as indicators for iron nutrition. Serum free T4 levels were significantly lower in both pregnant and nonpregnant women with ID compared with the corresponding groups without ID (both P < .05). The prevalence of mild and severe hypothyroxinemia was markedly higher in women with ID than those without, in both pregnant and nonpregnant women (all P < .01). Logistic regression indicated that ID was an independent risk factor for both mild and severe hypothyroxinemia in pregnancy (odds ratio [OR] = 2.440, 95% confidence interval [CI]: 1.324-4.496, P = .004; and OR = 3.278, 95% CI: 1.443-7.446, P = .005, respectively) and nonpregnancy (OR = 2.662, 95% CI: 1.330-5.329, P = .006; and OR = 3.254, 95% CI: 1.375-7.700, P = .007, respectively). An association between ID and isolated hypothyroxinemia was found in both pregnant and nonpregnant childbearing-aged women, independent of the effects of iodine and thyroid autoimmunity. We speculate that ID may be a pathogenic factor for hypothyroxinemia, even in pregnant women during the first trimester. Context:Isolated hypothyroxinemia during early pregnancy may irreversibly damage the neurodevelopment of offspring. However, the causes are not well clarified.Objective:To explore the association of iron deficiency (ID) with hypothyroid function of women in early pregnancy and nonpregnant women.Design:A total of 7953 pregnant women of ≤ 12 weeks gestation and 2000 childbearing-aged women were recruited. A subpopulation including 3340 pregnant women and 1052 nonpregnant women with sufficient iodine intake and negative thyroid peroxidase antibody were studied. Mild and severe cases of hypothyroxinemia were defined as free T4 levels below the 10th percentile and the 5th percentile, respectively, with normal TSH. Total body iron, serum ferritin, and serum transferrin receptor were used as indicators for iron nutrition.Results:Serum free T4 levels were significantly lower in both pregnant and nonpregnant women with ID compared with the corresponding groups without ID (both P < .05). The prevalence of mild and severe hypothyroxinemia was markedly higher in women with ID than those without, in both pregnant and nonpregnant women (all P < .01). Logistic regression indicated that ID was an independent risk factor for both mild and severe hypothyroxinemia in pregnancy (odds ratio [OR] = 2.440, 95% confidence interval [CI]: 1.324–4.496, P = .004; and OR = 3.278, 95% CI: 1.443–7.446, P = .005, respectively) and nonpregnancy (OR = 2.662, 95% CI: 1.330–5.329, P = .006; and OR = 3.254, 95% CI: 1.375–7.700, P = .007, respectively).Conclusions:An association between ID and isolated hypothyroxinemia was found in both pregnant and nonpregnant childbearing-aged women, independent of the effects of iodine and thyroid autoimmunity. We speculate that ID may be a pathogenic factor for hypothyroxinemia, even in pregnant women during the first trimester. CONTEXT:Isolated hypothyroxinemia during early pregnancy may irreversibly damage the neurodevelopment of offspring. However, the causes are not well clarified. OBJECTIVE:To explore the association of iron deficiency (ID) with hypothyroid function of women in early pregnancy and nonpregnant women. DESIGN:A total of 7953 pregnant women of ≤ 12 weeks gestation and 2000 childbearing-aged women were recruited. A subpopulation including 3340 pregnant women and 1052 nonpregnant women with sufficient iodine intake and negative thyroid peroxidase antibody were studied. Mild and severe cases of hypothyroxinemia were defined as free T4 levels below the 10th percentile and the 5th percentile, respectively, with normal TSH. Total body iron, serum ferritin, and serum transferrin receptor were used as indicators for iron nutrition. RESULTS:Serum free T4 levels were significantly lower in both pregnant and nonpregnant women with ID compared with the corresponding groups without ID (both P < .05). The prevalence of mild and severe hypothyroxinemia was markedly higher in women with ID than those without, in both pregnant and nonpregnant women (all P < .01). Logistic regression indicated that ID was an independent risk factor for both mild and severe hypothyroxinemia in pregnancy (odds ratio [OR] = 2.440, 95% confidence interval [CI]1.324–4.496, P = .004; and OR = 3.278, 95% CI1.443–7.446, P = .005, respectively) and nonpregnancy (OR = 2.662, 95% CI1.330–5.329, P = .006; and OR = 3.254, 95% CI1.375–7.700, P = .007, respectively). CONCLUSIONS:An association between ID and isolated hypothyroxinemia was found in both pregnant and nonpregnant childbearing-aged women, independent of the effects of iodine and thyroid autoimmunity. We speculate that ID may be a pathogenic factor for hypothyroxinemia, even in pregnant women during the first trimester. |
| Author | Xie, Xiaochen Zhou, Weiwei Meng, Tao Du, Jianling Zhang, Xiaomei Yang, Liu Fan, Chenling Teng, Weiping Li, Chenyan Li, Chenyang Xu, Bin Mao, Jinyuan Bi, Lihua Gao, Zhengnan Wang, Weiwei Yu, Xiaohui Liu, Aihua Shan, Zhongyan Zhang, Shaowei Teng, Xiaochun |
| AuthorAffiliation | Endocrine Institute and Liaoning Provincial Key Laboratory of Endocrine Diseases (X.Y., Z.S., Chenyan.L., J.M., W.W., X.X., A.L., X.T., C.F., W.T.), Department of Endocrinology and Metabolism, The First Hospital of China Medical University, Shenyang 110001, China; Shenyang Womenʼs and Childrenʼs Hospital (W.Z., Chenyang.L.), Shenyang 110011, China; Department of Obstetrics and Gynecology (B.X.), No. 202 Hospital of Peopleʼs Liberation Army, Shenyang 110003, China; Dalian Obstetrics and Gynecology Hospital (L.B.), Dalian 116033, China; Department of Obstetrics and Gynecology (T.M.), The First Hospital of China Medical University, Shenyang 110001, China; Department of Endocrinology (J.D.), The First Affiliated Hospital of Dalian Medical University, Dalian 116011, China; Department of Endocrinology (S.Z.), No. 202 Hospital of Peopleʼs Liberation Army, Shenyang 110003, China; Department of Endocrinology (Z.G.), Dalian Municipal Central Hospital Affiliated of Dalian Medical University, Dali |
| AuthorAffiliation_xml | – name: Endocrine Institute and Liaoning Provincial Key Laboratory of Endocrine Diseases (X.Y., Z.S., Chenyan.L., J.M., W.W., X.X., A.L., X.T., C.F., W.T.), Department of Endocrinology and Metabolism, The First Hospital of China Medical University, Shenyang 110001, China; Shenyang Womenʼs and Childrenʼs Hospital (W.Z., Chenyang.L.), Shenyang 110011, China; Department of Obstetrics and Gynecology (B.X.), No. 202 Hospital of Peopleʼs Liberation Army, Shenyang 110003, China; Dalian Obstetrics and Gynecology Hospital (L.B.), Dalian 116033, China; Department of Obstetrics and Gynecology (T.M.), The First Hospital of China Medical University, Shenyang 110001, China; Department of Endocrinology (J.D.), The First Affiliated Hospital of Dalian Medical University, Dalian 116011, China; Department of Endocrinology (S.Z.), No. 202 Hospital of Peopleʼs Liberation Army, Shenyang 110003, China; Department of Endocrinology (Z.G.), Dalian Municipal Central Hospital Affiliated of Dalian Medical University, Dalian 116033, China; Department of Endocrinology (X.Z.), The First Hospital of Dandong, Dandong118000, China; and Shenyang Women and Children Health Care Center (L.Y.), Shenyang 110032, China |
| Author_xml | – sequence: 1 givenname: Xiaohui surname: Yu fullname: Yu, Xiaohui organization: 1Endocrine Institute and Liaoning Provincial Key Laboratory of Endocrine Diseases (X.Y., Z.S., Chenyan.L., J.M., W.W., X.X., A.L., X.T., C.F., W.T.), Department of Endocrinology and Metabolism, The First Hospital of China Medical University, Shenyang 110001, China – sequence: 2 givenname: Zhongyan surname: Shan fullname: Shan, Zhongyan email: shanzhongyan@medmail.com.cn organization: 1Endocrine Institute and Liaoning Provincial Key Laboratory of Endocrine Diseases (X.Y., Z.S., Chenyan.L., J.M., W.W., X.X., A.L., X.T., C.F., W.T.), Department of Endocrinology and Metabolism, The First Hospital of China Medical University, Shenyang 110001, China – sequence: 3 givenname: Chenyan surname: Li fullname: Li, Chenyan organization: 1Endocrine Institute and Liaoning Provincial Key Laboratory of Endocrine Diseases (X.Y., Z.S., Chenyan.L., J.M., W.W., X.X., A.L., X.T., C.F., W.T.), Department of Endocrinology and Metabolism, The First Hospital of China Medical University, Shenyang 110001, China – sequence: 4 givenname: Jinyuan surname: Mao fullname: Mao, Jinyuan organization: 1Endocrine Institute and Liaoning Provincial Key Laboratory of Endocrine Diseases (X.Y., Z.S., Chenyan.L., J.M., W.W., X.X., A.L., X.T., C.F., W.T.), Department of Endocrinology and Metabolism, The First Hospital of China Medical University, Shenyang 110001, China – sequence: 5 givenname: Weiwei surname: Wang fullname: Wang, Weiwei organization: 1Endocrine Institute and Liaoning Provincial Key Laboratory of Endocrine Diseases (X.Y., Z.S., Chenyan.L., J.M., W.W., X.X., A.L., X.T., C.F., W.T.), Department of Endocrinology and Metabolism, The First Hospital of China Medical University, Shenyang 110001, China – sequence: 6 givenname: Xiaochen surname: Xie fullname: Xie, Xiaochen organization: 1Endocrine Institute and Liaoning Provincial Key Laboratory of Endocrine Diseases (X.Y., Z.S., Chenyan.L., J.M., W.W., X.X., A.L., X.T., C.F., W.T.), Department of Endocrinology and Metabolism, The First Hospital of China Medical University, Shenyang 110001, China – sequence: 7 givenname: Aihua surname: Liu fullname: Liu, Aihua organization: 1Endocrine Institute and Liaoning Provincial Key Laboratory of Endocrine Diseases (X.Y., Z.S., Chenyan.L., J.M., W.W., X.X., A.L., X.T., C.F., W.T.), Department of Endocrinology and Metabolism, The First Hospital of China Medical University, Shenyang 110001, China – sequence: 8 givenname: Xiaochun surname: Teng fullname: Teng, Xiaochun organization: 1Endocrine Institute and Liaoning Provincial Key Laboratory of Endocrine Diseases (X.Y., Z.S., Chenyan.L., J.M., W.W., X.X., A.L., X.T., C.F., W.T.), Department of Endocrinology and Metabolism, The First Hospital of China Medical University, Shenyang 110001, China – sequence: 9 givenname: Weiwei surname: Zhou fullname: Zhou, Weiwei organization: 2Shenyang Women's and Children's Hospital (W.Z., Chenyang.L.), Shenyang 110011, China – sequence: 10 givenname: Chenyang surname: Li fullname: Li, Chenyang organization: 2Shenyang Women's and Children's Hospital (W.Z., Chenyang.L.), Shenyang 110011, China – sequence: 11 givenname: Bin surname: Xu fullname: Xu, Bin organization: 3Department of Obstetrics and Gynecology (B.X.), No. 202 Hospital of People's Liberation Army, Shenyang 110003, China – sequence: 12 givenname: Lihua surname: Bi fullname: Bi, Lihua organization: 4Dalian Obstetrics and Gynecology Hospital (L.B.), Dalian 116033, China – sequence: 13 givenname: Tao surname: Meng fullname: Meng, Tao organization: 5Department of Obstetrics and Gynecology (T.M.), The First Hospital of China Medical University, Shenyang 110001, China – sequence: 14 givenname: Jianling surname: Du fullname: Du, Jianling organization: 6Department of Endocrinology (J.D.), The First Affiliated Hospital of Dalian Medical University, Dalian 116011, China – sequence: 15 givenname: Shaowei surname: Zhang fullname: Zhang, Shaowei organization: 7Department of Endocrinology (S.Z.), No. 202 Hospital of People's Liberation Army, Shenyang 110003, China – sequence: 16 givenname: Zhengnan surname: Gao fullname: Gao, Zhengnan organization: 8Department of Endocrinology (Z.G.), Dalian Municipal Central Hospital Affiliated of Dalian Medical University, Dalian 116033, China – sequence: 17 givenname: Xiaomei surname: Zhang fullname: Zhang, Xiaomei organization: 9Department of Endocrinology (X.Z.), The First Hospital of Dandong, Dandong118000, China – sequence: 18 givenname: Liu surname: Yang fullname: Yang, Liu organization: 10Shenyang Women and Children Health Care Center (L.Y.), Shenyang 110032, China – sequence: 19 givenname: Chenling surname: Fan fullname: Fan, Chenling organization: 1Endocrine Institute and Liaoning Provincial Key Laboratory of Endocrine Diseases (X.Y., Z.S., Chenyan.L., J.M., W.W., X.X., A.L., X.T., C.F., W.T.), Department of Endocrinology and Metabolism, The First Hospital of China Medical University, Shenyang 110001, China – sequence: 20 givenname: Weiping surname: Teng fullname: Teng, Weiping email: twp@vip.163.com organization: 1Endocrine Institute and Liaoning Provincial Key Laboratory of Endocrine Diseases (X.Y., Z.S., Chenyan.L., J.M., W.W., X.X., A.L., X.T., C.F., W.T.), Department of Endocrinology and Metabolism, The First Hospital of China Medical University, Shenyang 110001, China |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25599388$$D View this record in MEDLINE/PubMed |
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| Copyright | Copyright © 2015 by the Endocrine Society 2015 Copyright © 2015 by The Endocrine Society Copyright © 2015 by the Endocrine Society |
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| SubjectTerms | Adult Autoimmunity China - epidemiology Female Ferritin Humans Hypothyroidism Hypothyroidism - blood Hypothyroidism - epidemiology Hypothyroidism - etiology Iodide peroxidase Iodine Iron Iron - deficiency Pregnancy Pregnancy Complications - blood Pregnancy Complications - epidemiology Pregnancy Trimester, First - blood Risk Factors Thyroid Thyroid Function Tests Thyroid gland Thyroid-stimulating hormone Thyroxine Thyroxine - blood Young Adult |
| Title | Iron Deficiency, An Independent Risk Factor for Isolated Hypothyroxinemia in Pregnant and Nonpregnant Women of Childbearing Age in China |
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