Antenatal thyroid hormone therapy and antithyroid drug use in Norway from 2004 to 2018

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Abstract

Objective

Thyroid disease during pregnancy is associated with adverse pregnancy outcomes and suboptimal fetal development. During the last decades, guidelines for diagnosing thyroid disease during pregnancy have changed considerably and there has been increased awareness. This study aimed to describe the prevalence of thyroid disease treatment over time among pregnant women in Norway.

Design

Nationwide register-based study.

Methods

We combined historical data from the Medical Birth Registry of Norway and the Norwegian Prescription Database, identifying pregnant women using thyroid therapy from 2004 to 2018.

Results

A total of 855,067 pregnancies were included in the analyses. The proportion of women using thyroid hormone replacement therapy during pregnancy increased from 1.46% ( n = 800) in 2004 to 3.57% ( n = 1940) in 2018. The proportion of women using antithyroid medications also increased from 0.04% ( n = 20) in 2004 to 0.10% ( n = 56). During these 15 years, the mean maternal age increased by 0.9 years. When adjusting for age, the risk for being on thyroid hormone replacement therapy during pregnancy increased by an average of 5% per year (odds ratio: 1.05, 95% CI: 1.05–1.05).

Conclusion

During the recent 15 years, there has been a substantial increase in the use of thyroid hormone therapy in Norwegian pregnant women. We speculate that this could be due to an increased awareness in combination with overdiagnosis because of inappropriate diagnostic criteria. To truly understand the possible causes and consequences of this development, further research is warranted.

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Most cited references 33

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2017 Guidelines of the American Thyroid Association for the Diagnosis and Management of Thyroid Disease During Pregnancy and the Postpartum.

Erik Alexander, Elizabeth N Pearce, Gregory A Brent … (2017)

Thyroid disease in pregnancy is a common clinical problem. Since the guidelines for the management of these disorders by the American Thyroid Association (ATA) were first published in 2011, significant clinical and scientific advances have occurred in the field. The aim of these guidelines is to inform clinicians, patients, researchers, and health policy makers on published evidence relating to the diagnosis and management of thyroid disease in women during pregnancy, preconception, and the postpartum period.

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Serum TSH, T(4), and thyroid antibodies in the United States population (1988 to 1994): National Health and Nutrition Examination Survey (NHANES III).

Lewis Braverman, Carole Spencer, Elaine Gunter … (2002)

NHANES III measured serum TSH, total serum T(4), antithyroperoxidase (TPOAb), and antithyroglobulin (TgAb) antibodies from a sample of 17,353 people aged > or =12 yr representing the geographic and ethnic distribution of the U.S. population. These data provide a reference for other studies of these analytes in the U.S. For the 16,533 people who did not report thyroid disease, goiter, or taking thyroid medications (disease-free population), we determined mean concentrations of TSH, T(4), TgAb, and TPOAb. A reference population of 13,344 people was selected from the disease-free population by excluding, in addition, those who were pregnant, taking androgens or estrogens, who had thyroid antibodies, or biochemical hypothyroidism or hyperthyroidism. The influence of demographics on TSH, T(4), and antibodies was examined. Hypothyroidism was found in 4.6% of the U.S. population (0.3% clinical and 4.3% subclinical) and hyperthyroidism in 1.3% (0.5% clinical and 0.7% subclinical). (Subclinical hypothyroidism is used in this paper to mean mild hypothyroidism, the term now preferred by the American Thyroid Association for the laboratory findings described.) For the disease-free population, mean serum TSH was 1.50 (95% confidence interval, 1.46-1.54) mIU/liter, was higher in females than males, and higher in white non-Hispanics (whites) [1.57 (1.52-1.62) mIU/liter] than black non-Hispanics (blacks) [1.18 (1.14-1.21) mIU/liter] (P < 0.001) or Mexican Americans [1.43 (1.40-1.46) mIU/liter] (P < 0.001). TgAb were positive in 10.4 +/- 0.5% and TPOAb, in 11.3 +/- 0.4%; positive antibodies were more prevalent in women than men, increased with age, and TPOAb were less prevalent in blacks (4.5 +/- 0.3%) than in whites (12.3 +/- 0.5%) (P < 0.001). TPOAb were significantly associated with hypo or hyperthyroidism, but TgAb were not. Using the reference population, geometric mean TSH was 1.40 +/- 0.02 mIU/liter and increased with age, and was significantly lower in blacks (1.18 +/- 0.02 mIU/liter) than whites (1.45 +/- 0.02 mIU/liter) (P < 0.001) and Mexican Americans (1.37 +/- 0.02 mIU/liter) (P < 0.001). Arithmetic mean total T(4) was 112.3 +/- 0.7 nmol/liter in the disease-free population and was consistently higher among Mexican Americans in all populations. In the reference population, mean total T(4) in Mexican Americans was (116.3 +/- 0.7 nmol/liter), significantly higher than whites (110.0 +/- 0.8 nmol/liter) or blacks (109.4 +/- 0.8 nmol/liter) (P < 0.0001). The difference persisted in all age groups. In summary, TSH and the prevalence of antithyroid antibodies are greater in females, increase with age, and are greater in whites and Mexican Americans than in blacks. TgAb alone in the absence of TPOAb is not significantly associated with thyroid disease. The lower prevalence of thyroid antibodies and lower TSH concentrations in blacks need more research to relate these findings to clinical status. A large proportion of the U.S. population unknowingly have laboratory evidence of thyroid disease, which supports the usefulness of screening for early detection.

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Iodine-deficiency disorders.

Michael Zimmermann, Pieter L. Jooste, Chandrakant S. Pandav (2008)

2 billion individuals worldwide have insufficient iodine intake, with those in south Asia and sub-Saharan Africa particularly affected. Iodine deficiency has many adverse effects on growth and development. These effects are due to inadequate production of thyroid hormone and are termed iodine-deficiency disorders. Iodine deficiency is the most common cause of preventable mental impairment worldwide. Assessment methods include urinary iodine concentration, goitre, newborn thyroid-stimulating hormone, and blood thyroglobulin. In nearly all countries, the best strategy to control iodine deficiency is iodisation of salt, which is one of the most cost-effective ways to contribute to economic and social development. When iodisation of salt is not possible, iodine supplements can be given to susceptible groups. Introduction of iodised salt to regions of chronic iodine-deficiency disorders might transiently increase the proportion of thyroid disorders, but overall the small risks of iodine excess are far outweighed by the substantial risks of iodine deficiency. International efforts to control iodine-deficiency disorders are slowing, and reaching the third of the worldwide population that remains deficient poses major challenges.

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Author and article information

Journal

Journal ID (nlm-ta): Endocr Connect

Journal ID (iso-abbrev): Endocr Connect

Journal ID (hwp): EC

Title: Endocrine Connections

Publisher: Bioscientifica Ltd (Bristol )

ISSN (Electronic): 2049-3614

Publication date (Electronic): 23 March 2022

Publication date Collection: 01 April 2022

Volume: 11

Issue: 4

Electronic Location Identifier: e210631

Affiliations

[1 ]Women’s Clinic , Innlandet Hospital Trust, Lillehammer, Norway

[2 ]Center for International Health , University of Bergen, Bergen, Norway

[3 ]Department of Microbiology , Innlandet Hospital Trust, Lillehammer, Norway

[4 ]Department of Medicine , Haugesund Hospital, Haugesund, Norway

[5 ]Department of Clinical Science , University of Bergen, Bergen, Norway

[6 ]Academic Center for Thyroid Diseases , Erasmus University Medical Center, Rotterdam, the Netherlands

[7 ]Department of Research , Innlandet Hospital Trust, Lillehammer, Norway

Author notes

Correspondence should be addressed to K S Bakken: kjersti.sletten.bakken@ 123456sykehuset-innlandet.no

Author information

Kjersti S Bakken http://orcid.org/0000-0001-9308-3367

Article

Publisher ID: EC-21-0631

DOI: 10.1530/EC-21-0631

PMC ID: 9066597

PubMed ID: 35324464

SO-VID: bf95edc8-25b3-40d3-81a9-393edf1bee2c

License:

This work is licensed under a Creative Commons Attribution 4.0 International License.

History

Date received : 15 February 2022

Date accepted : 23 March 2022

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