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The thyroid’s normal function is a prerequisite for a normal pregnancy and the delivery of a normal baby. This is very important especially during the first trimester of prepgnancy, during which the fetus’ brain is developed and the fetus is not yet capable of producing its own thyroid hormones.
In recent years there has been an increase in the frequency of autoimmune thyroiditis that is caused by antibodies attacking against the thyroid gland. It is thought that this increase may be due to the very sensitive lab tests that have become available and result in an increase of thyroid pill intake by women.
During pregnancy, the frequency of thyroid dysfunction is around 2 – 3%. Moreover, antithyroid autoantibodies have been in 5 – 15% of women of reproductive age even in those with normal thyroid values (free T3, free T4, TSH).
The malfunction of the thyroid and the antithyroid autoantibodies (antithyroid peroxidase autoantibodies – anti-TPO and antithyroglobulin antibodies – anti-TG) may cause unexplained infertility and are associated with complications during pregnancy.
During the first trimester of pregnancy, subclinical hypothyroidism without therapy and the presence of increased thyroid antibodies (anti-TPO and anti-TG) may be associated with miscarriage and recurrent miscarriage.
During the third trimester of pregnancy, sublinical hypothyroidism and increased thyroid antibodies have been associated with preeclampsia, placental abruption, premature delivery, before 37 weeks gestation, low neonatal weight (<2500g), increased risk of neonatal admission in the intensive care unit (NICU), increased risk of perinatal morbidity and mortality.
Endocrinologists believe that thyroid therapy during pregnancy should include women that suffer from subclinical hypothyroidism even if the TSH is slightly increased and cases of hyperthyroidism in combination with increased levels of anti-TPO and/or anti-TG antibodies.
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