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Hypothyroidism is common in pregnancy with an estimated prevalence of 2-3% and 0.3-0.5% for subclinical and overt hypothyroidism respectively. [8] Endemic iodine deficiency accounts for most hypothyroidism in pregnant women worldwide while chronic autoimmune thyroiditis is the most common cause of hypothyroidism in iodine sufficient parts of the world.
The thyroid may enlarge slightly in healthy women during pregnancy, but not enough to be felt. These changes do not affect the pregnancy or unborn baby. Yet, untreated thyroid problems can threaten pregnancy and the growing baby. Symptoms of normal pregnancy, like fatigue, can make it easy to overlook thyroid problems in pregnancy. [1]
A suppressed TSH could represent the hyperthyroid phase, but warrants further testing to investigate for possible Graves' disease. [6] A normal TSH with persistent symptoms could represent the shift between phases and requires repeat testing 4–6 weeks later; an elevated TSH at this time could indicate the hypothyroid phase. [6]
Subclinical hyperthyroidism in pregnancy is associated with an increased risk of pre-eclampsia, low birth weight, miscarriage and preterm birth. [50] Propylthiouracil is the preferred treatment of hyperthyroidism (both overt and subclinical) in the first trimester of pregnancy as it is associated with less birth defects than methimazole. [50]
The diagnosis of hyperthyroidism is confirmed by blood tests that show a decreased thyroid-stimulating hormone (TSH) level and elevated T 4 and T 3 levels. TSH is a hormone made by the pituitary gland in the brain that tells the thyroid gland how much hormone to make. When there is too much thyroid hormone, the TSH will be low.
Fasting in healthy, euthyroid people causes reduced T3 and elevated rT3, although TSH is usually unchanged. [3] [5] [10] Even moderate weight loss can lower T3. [2] This may be primarily via reduced levels of leptin (the satisfaction hormone). Low leptin levels can downregulate hypothalamic TRH neurons and cause a reduction in TSH.
The increase in kidney clearance during pregnancy causes more iodide to be excreted and causes relative iodine deficiency and as a result an increase in thyroid size. Estrogen-stimulated increase in thyroid-binding globulin (TBG) leads to an increase in total thyroxine (T4), but free thyroxine (T4) and triiodothyronine (T3) remain normal. [5]
Thyroid hormones, T4 and TSH, diffuse across the placenta traveling from the mother to fetus for 10–12 weeks before the fetus’s own thyroid gland can begin synthesizing its own thyroid hormones. [2] The mother continues to supply some T4 to the fetus even after he/she is able to synthesize his/her own.