Thyroid disease in pregnancy may affect maternal and child health before and after childbirth. Thyroid disorders are common in women of childbearing age and for this reason are usually present as a recurrent disease in pregnancy and puerperium. Uncorrected thyroid dysfunction in pregnancy has adverse effects on the fetus and maternal well-being. The damaging effects of thyroid dysfunction can also extend beyond pregnancy and childbirth to influence neurointellectual development early in a child's life. Because elevated globulin binds to thyroxine, increased placenta type 3 deioidinase and placental transfer to maternal to fetal thyroxine, thyroid hormone demand increases during pregnancy. The necessary increase in thyroid hormone production is facilitated by high concentrations of human chorionic gonadotropin (hCG), which bind to the TSH receptor and stimulate the maternal thyroid to increase the maternal thyroid hormone concentration by about 50%. If the necessary thyroid function improvement can not be met, this may cause undetected thyroid disorders (imld) to worsen and become apparent as a pregnancy thyroid disease. Currently, there is insufficient evidence to suggest that screening for thyroid dysfunction is beneficial, especially since treatment of thyroid hormone supplementation may come with an overtreatment risk. After the woman gives birth, about 5% develops postpartum thyroiditis which can occur up to nine months later. It is characterized by a brief period of hyperthyroidism followed by a period of hypothyroidism; 20-40% remains permanent hypothyroid.
Video Thyroid disease in pregnancy
Tiroid dalam kehamilan
Fetal thyroxine is fully obtained from maternal sources early in pregnancy because the fetal thyroid gland only works in the second trimester of pregnancy. Because thyroxine is important for fetal neural development, it is important that delivery of maternal thyroxine to the fetus is confirmed early in pregnancy. In pregnancy, loss of urinary iodide and feto-placental units contributes to a state of relative iodine deficiency. Thus, pregnant women need additional iodine intake. Daily iodine intake of 250 Ã,Âμg is recommended in pregnancy but this is not always achieved even in a sufficient iodine portion of the world.
Thyroid hormone concentration in the blood increases in pregnancy, in part because of the high levels of estrogen and because of the weak thyroid stimulation effect of human chorionic gonadotropin (hCG) acting like TSH. Thyroxine (T4) levels increase from about 6-12 weeks, and peak in mid-gestation; reverse changes seen with TSH. The specific reference range for gestation for thyroid function tests is not widely used although many centers are now preparing it.
Maps Thyroid disease in pregnancy
Hypothyroidism Clinical evaluation
Hypothyroidism is common in pregnancies with an estimated prevalence of 2-3% and 0.3-0.5% for subclinical and overt hypothyroidism respectively. Endemic iodine deficiency accounts for most of the hypothyroidism in pregnant women around the world while chronic autoimmune thyroiditis is the most common cause of hypothyroidism in the ample part of iodine in the world. Presentation of hypothyroidism in pregnancy is not always classical and is sometimes difficult to distinguish from normal pregnancy symptoms. Therefore, a high index of suspicion is required, especially in women at risk for thyroid disease, eg. women with a personal or family history of thyroid disease, mumps, or an existing primary autoimmune disorder such as type 1 diabetes.
The risk of hypothyroidism in fetal and maternal well-being
Hypothyroidism is diagnosed by recording high TSH associated with subnormal T4 concentrations. Subclinical hypothyroidism (SCH) is present when TSH is high but T4 levels are within the normal range but are normally normally low. Schz is the most common form of hypothyroidism in pregnancy and is usually due to progressive thyroid destruction due to autoimmune thyroid disease.
Some studies, mostly retrospectively, have shown a link between overt hypothyroidism and fetal and obstetric outcomes (eg Glinoer 1991). Maternal complications such as miscarriage, anemia in pregnancy, preeclampsia, placental abrupio, and postpartum haemorrhage may occur in pregnant women with blatant hypothyroidism. Also, the offspring of these mothers can have complications such as preterm birth, low birth weight and increased neonatal respiratory distress. Similar complications have been reported in women with subclinical hypothyroidism. The threefold risk of placental abruption and twice the risk of preterm delivery is reported in women with subclinical hypothyroidism. Other studies have shown a higher prevalence of subclinical hypothyroidism in women with preterm labor (before 32 weeks) compared with appropriate controls at delivery. The association with adverse obstetric outcomes has also been demonstrated in pregnant women with thyroid autoimmunity independent of thyroid function. Treatment of hypothyroidism reduces the risk of adverse obstetric and fetal outcomes; a retrospective study of 150 pregnancies showed that hypothyroidism treatment led to reduced abortion rates and premature births. Also, prospective intervention trial studies have shown that the treatment of pregnant women positive for euthyroid antibodies causes fewer rates of miscarriage than untreated controls.
It has long been known that cretinism (ie, gross abatement in IQ) occurs in areas of severe iodine deficiency due to the fact that mothers can not make T4 for transport to the fetus especially in the first trimester. This neuroinecual disorder (on a simpler scale) has now been demonstrated in a sufficient iodine region (USA) where a study shows that the IQ score of children aged 7-9 years, born from mothers with undiagnosed and untreated hypothyroidism in pregnancy, is seven points lower than children of control women who match the normal thyroid function in pregnancy. Another study showed that persistent hypothyroidemia in 12 weeks' gestation was associated with an 8-10-point deficit in mental and motor function scores in infants compared with children of mothers with normal thyroid function. Even maternal thyroid peroxidase antibodies have been shown to be associated with intellectual developmental disorders in maternal offspring with normal thyroid function. Interestingly, it has been shown that only maternal FT4 levels are associated with child IQ and brain morphological results, compared with maternal TSH levels.
Management of hypothyroidism in pregnancy
Medications to treat hypothyroidism have been found to be safe during pregnancy. Levothyroxine is the treatment of choice for hypothyroidism in pregnancy. Thyroid function should be normalized before conception in women with pre-existing thyroid disease. Once the pregnancy is confirmed, the thyroxine dose should be increased by about 30-50% and subsequent titration should be guided by a thyroid function test (FT4 and TSH) that should be monitored for 4-6 weeks until euthyroidism is achieved. It is recommended that TSH levels be maintained below 2.5 mU/l in the first trimester of pregnancy and below 3 mU/l in subsequent pregnancies. The recommended dose of thyroxine maintenance in pregnancy is about 2.0-2.4 Âμg/kg daily. Thyroxin requirements may increase in late pregnancy and return to pre-pregnancy levels in most women during labor. Pregnant patients with subclinical hypothyroidism (normal FT4 and high TSH) should be treated as well, since supplementation with levothyroxine in such cases results in a significantly higher birth rate, with a relative 2.76 chance.
Hyperthyroidism
Clinical evaluation
Hyperthyroidism occurs in about 0.2-0.4% of all pregnancies. Most cases are caused by Graves' disease even though less common causes (eg toxic nodules and thyroiditis) can be seen. The clinical judgment itself is sometimes inadequate in distinguishing hyperthyroidism from hyperdynamic state of pregnancy. The typical clinical features of Graves' disease include the presence of ophthalmopathy, diffuse goitre, and pretibial myxoedema. Also, hyperthyroidism should be distinguished from gestational transient tirotoksikosis, self-limiting hyperthyroid state due to the beta-hCG thyroid stimulation effect. This difference is important because the latter condition is usually mild and usually does not require specific antithyroid therapy. Zinc red cells can also be useful in distinguishing both. Hyperthyroidism due to Graves' disease may worsen in the first trimester of pregnancy, further in subsequent pregnancies, and then relapse in the postpartum.
The risk of hyperthyroidism in fetal and maternal well-being
Uncontrolled hyperthyroidism in pregnancy is associated with an increased risk of severe preeclampsia and up to a fourfold increased risk of low birth weight birth. Some of these unfavorable outcomes are more marked in women who are diagnosed for the first time in pregnancy. A recent study also indicates that normal high maternal FT4 levels are associated with decreased IQ of children and gray matter and cortical volume, similar to the effects of hypothyroidism.
Uncontrolled and untreated maternal hyperthyroidism may also lead to fetal and neonatal hyperthyroidism due to transplacental transfer of TSH stimulant receptor antibodies (TRAb). Clinical neonatal hyperthyroidism occurs in about 1% of infants born to mothers with Graves' disease. Unusual neonatal hypothyroidism may also be observed in infants of mothers with Graves hyperthyroidism. This may be the result of transplacental transfers from circulating maternal anti-thyroid drugs, suppression of thyroid-thyroid axis from maternal thyroxine transfer.
Management of hyperthyroidism in pregnancy
Ideally a woman who is known to have hyperthyroidism should seek pre-pregnancy advice, although there is no evidence for its benefits. Suitable education should eliminate the fears common to these women. She should be referred for specialist treatment for frequent checks of her thyroid status, evaluation of thyroid antibodies and close monitoring of her medicinal needs. Medical therapy with anti-thyroid drugs is a treatment option for hyperthyroidism in pregnancy. Metimazole and propylthiouracil (PTU) are effective in preventing pregnancy complications by hyperthyroidism. Surgery is considered for patients suffering severe adverse reactions to anti-thyroid drugs and this is best done in the second trimester of pregnancy. Radioactive iodine is completely contraindicated in pregnancy and the puerperium. If a woman has received carbimazole, a change to propylthiouracil (PTU) is recommended but this should be changed back to carbimazole after the first trimester. This is because carbimazole is rarely associated with the skin and also the midline defect in the fetus but long-term PTU may also cause adverse effects on the liver in adults. Carbimazole and PTU are both secreted in breast milk but evidence suggests that antithyroid drugs are safe during lactation. There is no adverse effect on the development of IQ or psychomotor in children whose mothers have received antithyroid drugs in pregnancy.
Current guidelines show that a pregnant patient should be in PTU during the first trimester of pregnancy due to a lower tetragenic effect and then switch to methimazole during the second and third trimesters due to the adverse side effects of liver dysfunction.
Postpartum thyroiditis
Postpartum thyroid dysfunction (PPTD) is a syndrome of thyroid dysfunction occurring within the first 12 months of labor as a consequence of a postpartum immunologic rebound following a pregnancy immune tolerance state. PPTD is a destructive thyroiditis with a pathogenetic feature similar to Hashimoto's thyroiditis.
This disease is very common with the prevalence of 5-9% of unpointed postpartum women. There is usually a transient hyperthyroid phase followed by a hypothyroidism phase. Permanent hypothyroidism occurs in 30% of cases after 3 years, and 50% at 7-10 years. The hyperthyroid phase usually does not require treatment but, rarely, propanolol can be used for symptom control in severe cases. The hypothyroid phase should be treated with thyroxine if the patient is symptomatic, planning to become pregnant, or if the TSH level is above 10 mU/L. Long-term follow-up is necessary because of the risk of permanent hypothyroidism.
Almost all women with PPTD have positive TPO antibodies. These markers can be a useful screening test in early pregnancy because 50% of women with antibodies will develop postnatal thyroid dysfunction. In addition to some but not all studies show the relationship between PPTD and depression so that the function of the thyroid should be examined postpartum in women with mood changes.
References
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