(The fact that the thyroid gland does not produce enough thyroid hormone is called hypothyroidism.) Since overt hypothyroidism has been proven to be associated with poor pregnancy outcomes, maternal hypothyroidism (hypothyroidism during pregnancy) should be avoided by starting treatment as soon as it is detected during pregnancy.
It is known that subclinical hypothyroidism is more common than overt hypothyroidism. However, its association with poor pregnancy outcomes is contradictory. Cohort studies have shown an association between subclinical hypothyroidism and adverse pregnancy outcomes, but no such association has been demonstrated in randomized controlled studies. On the other hand, there is uncertainty about the benefits of treating pregnant women with subclinical hypothyroidism with oral L-thyroxine.
Since oral intake of L-thyroxine during pregnancy cannot cure fetal hypothyroidism (hypothyroidism in the unborn baby), it is not scientifically correct to say to a mother on L-thyroxine therapy that this treatment can also treat possible hypothyroidism in the fetus (unborn baby).
(The fact that the thyroid gland does not produce too much thyroid hormone is called hyperthyroidism.)
Although there are many causes of overt hyperthyroidism, it most often occurs due to Graves’ disease during pregnancy. Clinical hyperthyroidism during pregnancy can lead to miscarriage, pregnancy-related hypertension, preterm delivery, anemia, arrhythmias, and in more advanced cases, heart failure and thyroid crisis. For this reason, it is aimed to keep the mother in a mild hyperthyroid state by starting treatment as soon as it is detected during pregnancy. The most preferred medication in the treatment is propylthiouracil (PTU) because it crosses the placenta at minimal rates.
Hyperthyroidism in pregnancy is more common than Graves’s and the cause is hyperthyroidism due to hCG. Hyperthyroidism due to hCG is milder than Graves’ disease. hCG-dependent hyperthyroidism is temporary and often does not require treatment.
There is no evidence that the treatment of subclinical hyperthyroidism will have a positive effect on the course of pregnancy, and the treatment of subclinical hyperthyroidism during pregnancy is not recommended because the treatment may have potential adverse effects on the fetus.
In our country, scientific data are insufficient to recommend routine iodine supplementation to all pregnant women (during antenatal care). For this reason, large-scale and population-based studies are needed to determine the prevalence of iodine deficiency in pregnant women in our country.
If there is a known severe iodine deficiency in the area where the pregnant woman lives, iodine supplementation is definitely recommended in the prenatal period. It has been shown that mild to moderate iodine deficiency during pregnancy may have negative effects on neurological, behavioral and learning skills in the short and long term. However, the cause-effect relationship has not been fully proven.
The benefit of screening for thyroid dysfunction in the pregnant population has been proven to detect clinical hypothyroidism and initiate treatment early. This screening should preferably be done before conception (pregnancy occurs) or, if possible, at the beginning of pregnancy.
The usefulness of screening to detect subclinical hypothyroidism has not been proven because data are not yet available to demonstrate the benefit of subsequent thyroxine therapy.
Early pregnancy screening only requires measurement of TSH levels. Tests for free or total T4 are only required when there is a change in TSH. Similarly, its use in routine screening is not recommended, as there is insufficient evidence to recommend for or against screening for antithyroid antibodies in pregnancy.
Interpretation of thyroid hormone test results during pregnancy is different due to changes in thyroid physiology during pregnancy. Therefore, our recommendation is that each laboratory calculates the percentile values of its own pregnant study population for each of the 3 trimesters and reports the studied values in percentiles.
When the existing literature, guidelines and expert opinions are evaluated in general, it is revealed that it is not appropriate to screen all pregnant women with TSH in the first trimester. Screening with TSH should only be done in risky cases.
Previous thyroid dysfunction/surgery (due to the 33% rate of hypothyroidism after lobectomy)
Family history of thyroid disease presence of goiter
Thyroid Antibodies positivity, especially thyroid peroxidase autoantibodies (TPOAb increases the risk of hypothyroidism and odds ratio: 40 when compared with TPOAb (+) versus (-))
Presence of clinical signs/symptoms of hypothyroidism
Type I diabetes (due to the increase in the rate of hypothyroidism to 16%)
History of miscarriage and preterm birth
Presence of vitiligo, adrenal insufficiency, hypoparathyroidism, atrophic gastritis, pernicious anemia, systemic sclerosis, SLE, Sjögren’s syndrome associated with autoimmune thyroid dysfunction
Presence of infertility (although the rates of overt and subclinical hypothyroidism have a wide range of 1-43%)
those who had head and neck irradiation (67% of the prevalence of hypothyroidism in 8-year follow-up)
Morbidly obese people with a BMI (body mass index) >40 (due to the detection of 13-19.5% hypothyroidism)
Women over the age of 30 (The rate of serum TSH value being 5 and above in the age of 18-24 is 4%, while at the age of 30 it is 7% and above)
Amiodarone treatment applications (14-18% hyperthyroidism-hypothyroidism)
Lithium use (6-52% hypothyroidism)
Exposure to iodinated contrast agents (up to 6 weeks before pregnancy that reveals 20% thyroid dysfunction)
Living in areas with moderate iodine deficiency
0.1 – 2.5 mU/L for the first trimester
0.2 – 3.0 mU/L for the second trimester
0.3 – 3.0 mU/L for third trimester
As with non-pregnant women, elevated TSH blood levels make the diagnosis of primary hypothyroidism in pregnant women. There is insufficient evidence to support routine screening with thyroid autoantibodies alone in the first trimester of pregnancy, therefore it is not recommended.
In the current literature, it has not been clearly demonstrated which is the best screening strategy, whether TSH alone, anti-TPO antibody alone, or TSH plus anti-TPO antibody.
TSH > 2.5-10.0 mU/L with normal free T4: Subclinical hypothyroidism
Low free T4 levels with TSH > 2.5-10.0 mU/L: Clinical (overt) hypothyroidism
TSH ≥ 10.0 mU/L, regardless of free T4 level: Clinical (overt) hypothyroidism
However, care should be taken when interpreting free T4 levels during pregnancy, and trimester-specific intervals determined by each laboratory for itself should be taken as reference. Alternatively, new reference ranges can be used in the 2nd and 3rd trimesters, which are obtained by multiplying the pre-pregnancy total T4 reference intervals by a factor of 1.5. Free T4 index can be another alternative reference value that can be used during pregnancy.
Since overt hypothyroidism has been proven to be associated with poor pregnancy outcomes, maternal hypothyroidism should be avoided by starting treatment as soon as it is detected during pregnancy.
All pregnant women with newly diagnosed overt hypothyroidism should be treated with thyroid hormone (thyroxine, T4). T4 dose, TSH 2.5 mIU/liter in the first trimester; In the 2nd and 3rd trimesters, it should be adjusted to keep it below 3 mIU/liter (or trimester-specific TSH limits). Thyroid function tests should be re-evaluated within 30-40 days of starting treatment and then every 4-6 weeks thereafter.
Routine iodine supplementation is not required when using levothyroxine to treat cases with hypothyroidism due to any cause.
Since there are no studies of pregnancy outcomes in pregnant euthyroid women with positive TG-antibodies, it is not recommended to treat these patients with levothyroxine.
If the diagnosis of hypothyroidism is made before pregnancy, the T4 dose should be adjusted so that TSH remains below 2.5mIU/liter in the preconceptional period.
After delivery, most hypothyroid women need to reduce the dose given during pregnancy to pre-pregnancy levels.
Treatment of isolated hypothyroxinemia is currently not recommended due to the lack of sufficient evidence for its effects and inconsistencies in free T4 measurement.
Since there is a greater demand on the thyroid during pregnancy and there is evidence that euthyroid women with autoimmune thyroid disease in the early stages of pregnancy are at greater risk for subclinical hypothyroidism or overt hypothyroidism in later gestational weeks, TSH monitoring is mandatory in these women every 4-6 weeks. .
Although the current literature data is limited, pregnancy loss is higher in first trimester pregnant women with negative thyroid antibody and TSH value between 2.5-5 mIU/l compared to first trimester pregnant women with negative thyroid antibody and TSH value below 2.5mIU/l. However, levothyroxine treatment is controversial since the efficacy of the treatment could not be demonstrated in these cases. Studies are needed to evaluate the efficacy of treatment in these cases.
When the existing literature, guidelines and expert opinions are evaluated in general, it is revealed that it is not appropriate to screen all pregnant women with TSH in the first trimester. Screening with TSH should be done in risky cases.
Since maternal oral L-thyroxine intake cannot cure fetal hypothyroidism in intrauterine life, it is not scientifically correct to say to a mother who is receiving L-thyroxine therapy for any thyroid dysfunction, that this treatment can also treat a possible hypothyroidism in the fetus.
Source: This guide has been prepared by the Perinatal Medicine Foundation based on the Perinatal Thyroid Workshop Report published in the Journal of Perinatology Volume 23, Issue 2, August 2015. Detailed information can be obtained from www.perinataldergi.com