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Autoimmune thyroid disease in pregnancy

Autoimmune hypothyroid disease can cause problems during pregnancy. 


An endocrinologist's practical approach to hypothyroidism in pregnancy

All aspects of thyroid physiology change during pregnancy which makes interpretation of thyroid function more difficult. The best way to monitor hypothyrodiism in pregnancy is the Free Thyroxine Index (FTI) which is a ratio of the total T4 and the T3 resin uptake. The FTI remains constant regardless if a patient is pregnant or not. This avoids the mis-diagnosis of 'hypothyroxinemia' based on direct Free T4 measurements. Previous recommendations had suggested the use of the direct Free T4 (FT4) assay, but this method is flawed if non pregnant reference ranges are used since the levels of FT4 decrease below the normal range in the second and third trimesters. Most national labs do have have pregnancy ranges for the direct Free T4. Free T4 by equilibrium dialysis is accurate but very expensive.


Details of normal thyroid hormone physiology changes during pregnancy 

There are a number of changes that occur with thyroid physiology in pregnancy that are related to the hormonal changes that occur in pregnancy. At the end of pregnancy thyroid physiology reverts back to normal thyroid physiology. There is a predictable sequence of events that occurs during different stages of pregnancy. Here are the important points. 

  1. Thyroid binding globulin (TBG) and albumin, which are the principle carrier proteins that allow thyroid hormone to transported in the blood, increase dramatically due to pregnancy.  The TBG concentrations rise because estrogen increases TBG production and TBG sialylation, which results in decreased clearance of TBG from the mother's system.  This normal condition of TBG excess leads to an increase in both serum total thyroxine (T4) and triiodothyronine (T3) concentrations, but not serum free T4 and T3 concentrations.
  2. The TSH receptor is stimulated by the pregnancy hormone human chorionic gonadotrophin (hCG) which comes from the fetal complex. This increase in HCG forces an increase the thyroid hormone production of the mother.  
  3. hCG has a weak, but measurable, thyroid-stimulating activity. Serum hCG concentrations increase soon after fertilization and peak at 10 to 12 weeks. During this period serum free T4 and T3 concentrations increase slightly, usually within the normal range which cross the placenta and provide the thyroid hormone for the fetus during this period of time. 
  4. The mother's thyroid hormone (T4 and T3)  is critical for first-trimester fetal brain development  The fetus does not produce any thyroid hormone until the 12th week of gestation when the fetal thyroid becomes capable of concentrating iodine. Thus, the fetus depends on the mother to provide extra thyroid hormone.