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Editorials

Mild thyroid dysfunction in pregnancy and children’s educational performance

BMJ 2018; 360 doi: https://doi.org/10.1136/bmj.k636 (Published 20 February 2018) Cite this as: BMJ 2018;360:k636
  1. Fanni Päkkilä, researcher
  1. University of Oulu and Oulu University Hospital, Department of Obstetrics and Gynaecology and Medical Research Centre, FI-90014 Oulu, Finland
  1. Correspondence to: F Päkkilä fanni.pakkila{at}oulu.fi

No evidence of a link up to age 15

Thyroid dysfunction is a common endocrinological problem during pregnancy, as 0.2% to 0.6% of pregnancies involve overt hypothyroidism (thyroid stimulating hormone concentrations exceeding reference intervals and free thyroxine concentrations below reference intervals) and an additional 3.5% to 18.0% of pregnancies are affected by subclinical hypothyroidism (elevated thyroid stimulating hormone concentrations but normal free thyroxine concentrations).1 Untreated overt hypothyroidism increases the risk of difficulty conceiving and of many adverse obstetrical and child outcomes, including impaired neuropsychological development.2 The consequences of subclinical thyroid dysfunction, especially with regard to cognitive outcomes for the child, are not that well established.2

A growing number of observational studies describe small but somewhat worrisome associations between mild maternal thyroid underfunction during pregnancy and juvenile cognitive development problems.2

In this issue, Nelson and colleagues (doi:10.1136/bmj.k452) present study assessing maternal thyroid function tests during early pregnancy and the school attainment of children from 54 months to 15 years of age drawn from the prospective Avon Longitudinal Study of Parents and Children birth cohort.3 In this well researched cohort of 4461 mother-child pairs collected in 1991–92 Nelson and colleagues reassuringly found no clinically important association between mild maternal hypothyroidism and attainment at school.3

This study has many strengths. Thyroid function tests for thyroid stimulating hormone, free thyroxine, and thyroid peroxidase antibodies were assessed mostly during the first trimester, which is the most crucial time for fetal neurodevelopment. Mothers with a known thyroid disease were excluded. Children’s school performance data came from the National Pupil Database, which covers England’s state schools (84.3% of pupils in the Avon Longitudinal Study of Parents and Children cohort area). The database records five age specific national curriculum assessments, ranging from school entry to the end of secondary school at age 15.

In this study, mild maternal thyroid dysfunction during pregnancy was not associated with children’s performance on any of the assessments.3 These findings are in line with one large previous study of maternal thyroid function in early pregnancy and children’s school performance at ages 8 and 16.4

The topic is of international interest because screening for thyroid stimulating hormone in early pregnancy is currently recommended by the American and European Thyroid Associations only if the mother has risk factors for thyroid disease such as past or current symptoms of thyroid disease, family history, known thyroid antibody positivity, or previous autoimmune disorders.25 So far, the evidence concerning maternal thyroid dysfunction and cognitive development in offspring has not swayed clinical guidelines towards universal thyroid stimulating hormone screening.2

Randomised controlled trials of antenatal screening and treatment of mild maternal thyroid dysfunction have not shown improvements in cognitive function among children of women treated with levothyroxine.67 These studies have been criticised for the late timing of screening and treatment, as studies of pregnant women miss the crucial time of conception and very early fetal development. But we still lack convincing evidence that treating mild maternal thyroid dysfunction in early pregnancy is beneficial for either mother or child.2

Further complicating the screening discussion, some studies have suggested that the risk of adverse outcomes for children is not a threshold effect operating only above the upper reference limit for thyroid stimulating hormone, but rather rises continuously as thyroid stimulating hormone increases.1 Longer follow-up is likely to yield greater insight into how seriously these small statistical increases in risk should be considered. Nelson and colleagues analysed their data comprehensively using various thyroid stimulating hormone cut-off values, and they also analysed thyroid stimulating hormone and free thyroxine concentrations as continuous variables without finding any association with educational attainment.3

Defining abnormal levels of thyroid stimulating hormone is difficult during pregnancy, and reliable references ranges are not always available. Stimulation of the thyroid by physiological human chorionic gonadotropin suppresses thyroid stimulating hormone levels especially during the first trimester, and this response can be abnormal among thyroid peroxidase antibody positive women.8 Many other factors such as ethnicity, body mass index, age, and iodine intake also affect normal individual levels of thyroid stimulating hormone.2

Given these complexities, it is no wonder that the question of universal screening for thyroid stimulating hormone divides professional opinion. The challenge in prenatal care is to identify women at risk for thyroid diseases as early as possible, even before pregnancy is confirmed. More clinical trials of screening and treatment and especially prepregnancy cohort studies are now required. In the meantime, Nelson and colleagues’ study adds important observational evidence that mild maternal thyroid dysfunction during early pregnancy does not seem to adversely affect children’s educational attainment.3

Acknowledgments

I thank docent Tuija Männistö, MD, PhD, for her comments and insight regarding this editorial.

Footnotes

  • Research, doi: 10.1136/bmj.k452
  • Competing interests: I have read and understood the BMJ Group policy on declaration of interests and declare none.

  • Provenance and peer review: Commissioned; not peer reviewed

  • Copyright statement: The Corresponding Author has the right to grant on behalf of all authors and does grant on behalf of all authors, a worldwide license to the Publishers and its licensees in perpetuity, in all forms, formats and media (whether known now or created in the future), to i) publish, reproduce, distribute, display and store the Contribution, ii) translate the Contribution into other languages, create adaptations, reprints, include within collections and create summaries, extracts and/or, abstracts of the Contribution, iii) create any other derivative work(s) based on the Contribution, iv) to exploit all subsidiary rights in the Contribution, v) the inclusion of electronic links from the Contribution to third party material where-ever it may be located; and, vi) licence any third party to do any or all of the above.

References

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