Unresolved questions in managing hypothyroidism during pregnancyBMJ 2007; 335 doi: https://doi.org/10.1136/bmj.39189.513935.BE (Published 09 August 2007) Cite this as: BMJ 2007;335:300
- Daniel Glinoer, chief of division1,
- Marcos Abalovich, associate professor of internal medicine2
- 1Division of Endocrinology, Department of Internal Medicine, University Hospital Saint Pierre, B-1000 Brussels, Belgium
- 2Division of Endocrinology, Carlos Durand Hospital, Buenos Aires, Argentina
- Correspondence to:
Diagnosing and managing hypothyroidism during pregnancy can be problematic. The scenario box on this page illustrates some typical problems encountered and raises pertinent questions concerning good medical practice. In this article, we define autoimmune thyroiditis as the presence of measurable circulating antithyroid autoantibodies (to thyroglobulin or thyroperoxidase), irrespective of abnormalities of thyroid function. Subclinical hypothyroidism is defined as an increase in serum thyroid stimulating hormone (TSH; usually 4-10 mU/l) associated with normal concentrations of serum thyroxine and triiodothyronine. Overt hypothyroidism is defined as an increase in serum TSH (usually >10 mU/l) associated with a decreased concentration of thyroxine, as a result of negative feedback; at that stage, most patients have symptoms and benefit from treatment.
Mrs SC, aged 29 years, has a family history of goitre. Nine months after a first delivery in 1999, she had positive antithyroid peroxidase antibodies and a serum thyroid stimulating hormone (TSH) concentration of 3.1 mU/l. No treatment was given, but she was told that she should have her thyroid function monitored, advice that she did not follow. Two years later, when she was six weeks pregnant, she was diagnosed with hypothyroidism of autoimmune origin: serum TSH 150 mU/l, free thyroxine 2.6 pmol/l (normal 10-26), antithyroid peroxidase antibodies 990 U/ml (normal <60). She presented with severe hypothyroidism during the first weeks of pregnancy, although we cannot tell whether it was present before conception (though this is likely) or developed after the onset of pregnancy. Treatment with thyroxine was started immediately, and thyroid function returned to normal and remained so throughout the remainder of her pregnancy (table 1⇓). Delivery was full term and obstetrically uneventful. After parturition, the mother's thyroid function was equilibrated with 75 µg thyroxine/day. Six months postpartum, TSH rose transiently to 10.4 mU/l, as a result of postpartum thyroiditis, and thyroxine was …
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