Michael B Zimmermann1, Hans Burgi, Richard F Hurrell. 1. Laboratory for Human Nutrition, Swiss Federal Institute of Technology (Eidgenössische Technische Hochschule) Zürich, Schmelzbergstrasse 7, LFV E 19, CH-8092 Zürich, Switzerland. michael.zimmermann@ilw.agrl.ethz.ch
Abstract
CONTEXT: Pregnant women are often iron deficient, and iron deficiency has adverse effects on thyroid metabolism. Impaired maternal thyroid function during pregnancy may cause neurodevelopmental delays in the offspring. OBJECTIVE: Our objective was to investigate whether maternal iron status is a determinant of TSH and/or total T(4) (TT4) concentrations during pregnancy. DESIGN AND OUTCOME MEASURES: In a representative national sample of Swiss pregnant women (n = 365) in the second and third trimester, samples of urine and blood were collected, and data on maternal characteristics and supplement use were recorded. Concentrations of TSH, TT4, hemoglobin, mean corpuscular volume, serum ferritin, transferrin receptor, and urinary iodine were measured. Body iron stores were calculated and stepwise regressions performed to look for associations. RESULTS: Median urinary iodine was 139 mug/liter (range 30-433). In the third trimester, nearly 40% of women had negative body iron stores, 16% had a TT4 less than 100 nmol/liter, and 6% had a TSH more than 4.0 mU/liter. Compared with the women with positive body iron stores, the relative risk of a TT4 less than 100 nmol/liter in the group with negative body iron stores was 7.8 (95% confidence interval 4.1; 14.9). Of the 12 women with TSH more than 4.0 mU/liter, 10 had negative body iron stores. Serum ferritin, transferrin receptor, and body iron stores were highly significant predictors of TSH (standardized beta: -0.506, 0.602, and -0.589, respectively; all P < 0.0001) and TT4 (standardized beta: 0.679, -0.589, and 0.659, respectively; all P < 0.0001). CONCLUSION: Poor maternal iron status predicts both higher TSH and lower TT4 concentrations during pregnancy in an area of borderline iodine deficiency.
CONTEXT: Pregnant women are often iron deficient, and iron deficiency has adverse effects on thyroid metabolism. Impaired maternal thyroid function during pregnancy may cause neurodevelopmental delays in the offspring. OBJECTIVE: Our objective was to investigate whether maternal iron status is a determinant of TSH and/or total T(4) (TT4) concentrations during pregnancy. DESIGN AND OUTCOME MEASURES: In a representative national sample of Swiss pregnant women (n = 365) in the second and third trimester, samples of urine and blood were collected, and data on maternal characteristics and supplement use were recorded. Concentrations of TSH, TT4, hemoglobin, mean corpuscular volume, serum ferritin, transferrin receptor, and urinary iodine were measured. Body iron stores were calculated and stepwise regressions performed to look for associations. RESULTS: Median urinary iodine was 139 mug/liter (range 30-433). In the third trimester, nearly 40% of women had negative body iron stores, 16% had a TT4 less than 100 nmol/liter, and 6% had a TSH more than 4.0 mU/liter. Compared with the women with positive body iron stores, the relative risk of a TT4 less than 100 nmol/liter in the group with negative body iron stores was 7.8 (95% confidence interval 4.1; 14.9). Of the 12 women with TSH more than 4.0 mU/liter, 10 had negative body iron stores. Serum ferritin, transferrin receptor, and body iron stores were highly significant predictors of TSH (standardized beta: -0.506, 0.602, and -0.589, respectively; all P < 0.0001) and TT4 (standardized beta: 0.679, -0.589, and 0.659, respectively; all P < 0.0001). CONCLUSION: Poor maternal iron status predicts both higher TSH and lower TT4 concentrations during pregnancy in an area of borderline iodine deficiency.
Authors: Thomas W Bastian; Jeremy A Anderson; Stephanie J Fretham; Joseph R Prohaska; Michael K Georgieff; Grant W Anderson Journal: Endocrinology Date: 2012-10-09 Impact factor: 4.736
Authors: S L Carmichael; C Ma; S A Rasmussen; M L Cunningham; M L Browne; C Dosiou; E J Lammer; G M Shaw Journal: Am J Med Genet A Date: 2015-02-05 Impact factor: 2.802