Editorials

Subclinical hypothyroidism after pre-eclampsia

BMJ 2009; 339 doi: https://doi.org/10.1136/bmj.b5183 (Published 08 December 2009) Cite this as: BMJ 2009;339:b5183
  1. Robyn A North, professor of maternal and fetal medicine1,
  2. Robert N Taylor, professor of gynaecology and obstetrics2
  1. 1Division of Reproduction and Endocrinology, King’s College London, St Thomas’ Hospital, London SE1 7EH
  2. 2Division of Reproductive Endocrinology, Emory University School of Medicine, Atlanta, GA 30322, USA
  1. robyn.north{at}kcl.ac.uk

    High concentrations of antiangiogenic factor may impair thyroid function during and after pregnancy

    Subclinical hypothyroidism—raised thyroid stimulating hormone in the presence of normal thyroid hormone concentrations—is common, being seen in 4-10% of non-pregnant women. These women are at risk of progressing to overt hypothyroidism. Subclinical hypothyroidism is most often caused by chronic autoimmune thyroiditis, but it also occurs after damage to thyroid tissue through surgery or radiation, or as a result of drugs interfering with thyroid function.1

    In the linked study (doi:10.1136/bmj.b4336), Levine and colleagues report a potential new mechanism for the development of subclinical hypothyroidism in women—pre-eclampsia related vascular injury within the thyroid secondary to high circulating concentrations of the antiangiogenic factor, soluble fms-like tyrosine kinase 1 (sFlt-1).2 Furthermore, their results suggest that the damage sustained may have long term effects on thyroid function.

    Although it has long been recognised that serum concentrations of thyroid stimulating hormone are increased in pre-eclampsia,3 Levine and colleagues report that the increased rate of subclinical hypothyroidism associated with pre-eclampsia (24% of 141 cases; adjusted odds ratio 2.2, 95% confidence interval 1.1 to 4.4) was not present in early pregnancy.2 The prevalence of thyroid peroxidase antibodies was similar in women …

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