Thyroid Disease in Pre- and Post-Pregnancy

Abstract

Thyroid dysfunction affects approximately 3% of pregnant women. Adequate thyroid hormone levels are important for fetal development. Normal physiological changes of pregnancy can contribute to subclinical hypothyroidism which may require treatment with thyroxine during pregnancy. Pre-existing hypothyroidism requires an increase in thyroxine dosage. Pre-existing hyperthyroidism may or may not require continued treatment with anti-thyroid medication, though these medications can rarely cause adverse fetal effects. Gestational hyperthyroidism must be distinguished from a new diagnosis of Graves’ disease in pregnancy. Gestational hyperthyroidism does not require treatment with anti-thyroid medication. Graves’ disease requires additional monitoring of mother and fetus and consideration of anti-thyroid medication. Post-partum thyroiditis is an underdiagnosed condition which can cause transient hyperthyroidism before recovery or hypothyroidism, or hypothyroidism without a hyperthyroid phase. Serial monitoring of thyroid function test is required. The vast majority of women with thyroid conditions can be managed to a successful pregnancy outcome.

Case Study 2–4. Answers

Case study 2: M.R symptoms of palpitations, difficulty sleeping, and not putting on weight are consistent with hyperthyroidism. Her thyroid function tests support this with an elevated thyroxine/T4 and supressed thyroid stimulating hormone levels. As she is in the first trimester, gestational hyperthyroidism caused by BHCG stimulation of the thyroid is the probable diagnosis. Although the condition is considered “benign” in that it does not cause fetal problems or long-term maternal problems, women can be significantly symptomatic. It is important to test for thyroid receptor antibodies to distinguish from the serious condition of Graves’ disease. A positive result for such antibodies should prompt immediate contact with a specialist. M.R should be counselled that the condition is self-limiting and likely to improve in the next 2–6 weeks as BHCGs levels fall in the second trimester. She should be encouraged to eat more and to activate social supports. Beta-blocker medication can be considered in severe cases for short-term use with the involvement of a medical practitioner.

Case study 3: K.P has subclinical hypothyroidism as defined by her thyroid stimulating hormone being marginally elevated and her thyroid stimulating hormone being in the normal range. Most women with this condition are asymptomatic. In the context of having a child with Autism Spectrum Disorder, K.P may be particularly concerned about anything she has read or heard regarding a link between “low thyroid levels” and “intellectual problems”. It is important to reassure K.P that this generally occurs in cases much more severe than her situation. K.P should be tested for thyroid peroxidase antibodies, the presence of these may indicate that she would benefit from post-partum monitoring for the development of post-partum thyroiditis or hypothyroidism. During pregnancy, a small dose of thyroxine (e.g. 50mcg daily) should be started with titration to the pregnancy-specific thyroid stimulating hormone targets outlined in this chapter, or as per local guidelines.

Case example 4: H’s symptom of losing hair is consistent with hyperthyroidism. Her difficulty in sleeping and concern about her child’s welfare may be expected with a newborn child, but may also be due or worsened by hyperthyroidism. It can be difficult to distinguish such a situation clinically, and therefore thyroid function and thyroid antibody tests, especially thyroid peroxidase antibodies, should be requested. Together these results (supressed thyroid stimulating hormone, elevated thyroxine/T4, positive thyroid peroxidase, and thyroglobulin antibodies) may indicate a diagnosis of post-partum thyroiditis. Serial clinical and biochemical monitoring of women with post-partum thyroiditis is required. In the long-term, hypothyroidism may develop and require treatment with thyroxine.