Thyroid Diseases During Pegnancy
Thyroid Diseases During Pegnancy
Thyroid Diseases During Pegnancy
and the puerperium. Uncorrected thyroid dysfunction in pregnancy has adverse effects on fetal and maternal well-being. The deleterious effects of thyroid dysfunction can also extend beyond pregnancy and delivery to affect neurointellectual development in the early life of the child. Demand for thyroid hormones is increased during pregnancy which may cause a previously unnoticed thyroid disorder to worsen. Still, the overall lack of evidence [2] precludes a recommendation for universal screening for thyroid disorder in all pregnant women.
iodine intake. A daily iodine intake of 250 mcg is recommended in pregnancy but this is not always achieved even in iodine sufficient parts of the world.
Thyroid hormone concentrations in blood are increased in pregnancy, partly due to the high levels of oestrogen and due to the weak thyroid stimulating effects of human chorionic gonadotropin(hCG) that acts like TSH. Thyroxine (T4) levels rise from about 612 weeks, and peak by mid-gestation; reverse changes are seen with TSH. Gestation specific reference ranges for thyroid function tests are not widely in use although many centres are now preparing them.
Hypothyroidism
Clinical evaluation
Hypothyroidism is common in pregnancy with an estimated prevalence of 2-3% and 0.3-0.5% for subclinical and overt hypothyroidism respectively.
[5]
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 presentation
of hypothyroidism in pregnancy is not always classical and may sometimes be difficult to distinguish from the symptoms of normal pregnancy. A high index of suspicion is therefore required especially in women at risk of thyroid disease e.g. women with a personal or family history of thyroid disease, goitre, or co-existing primary autoimmune disorder like type 1 diabetes.
pregnancy and is usually due to progressive thyroid destruction due to autoimmune thyroid disease. Several studies, mostly retrospective, have shown an association between overt hypothyroidism and adverse fetal and obstetric outcomes (e.g. Glinoer 1991).
[7]
asmiscarriages, anaemia in pregnancy, pre-eclampsia, abruptio placenta and postpartum haemorrhage can occur in pregnant women with overt hypothyroidism. Also, the offspring of these mothers can have complications such as premature birth, low birth weight and increased neonatal respiratory distress.
[8]
subclinical hypothyroidism. A three-fold risk of placental abruption and a two-fold risk of pre-term delivery were reported in mothers with subclinical hypothyroidism.
[10]
higher prevalence of subclinical hypothyroidism in women with pre-term delivery (before 32 weeks) compared to matched controls delivering at term. An association with adverse
obstetrics outcome has also been demonstrated in pregnant women with thyroid autoimmunity independent of thyroid function. Treatment of hypothyroidism reduces the risks of these adverse obstetric and fetal outcomes; a retrospective study of 150 pregnancies showed that treatment of hypothyroidism led to reduced rates of abortion and premature delivery. Also, a prospective intervention trial study showed that treatment of euthyroid antibody positive pregnant women led to fewer rates of miscarriage than non treated controls.
[11]
It has long been known that cretinism (i.e. gross reduction in IQ) occurs in areas of severe iodine deficiency due to the fact that the mother is unable to make T4 for transport to the fetus particularly in the first trimester. This neurointellectual impairment (on a more modest scale) has now been shown in an iodine sufficient area (USA) where a study showed that the IQ scores of 79 year old children, born to mothers with undiagnosed and untreated hypothyroidism in pregnancy, were seven points lower than those of children of matched control women with normal thyroid function in pregnancy.
[12]
weeks gestation was associated with an 8-10 point deficit in mental and motor function scores in infant offspring compared to children of mothers with normal thyroid function.
[14]
Even maternal
thyroid peroxidase antibodies were shown to be associated with impaired intellectual development in the offspring of mothers with normal thyroid function.
[15][16]
However, no association
was found between isolated maternal hypothyroxinaemia and adverse perinatal outcomes in 2 large US studies, studies. although the behavioural outcomes in the children were not tested in these
Levothyroxine is the treatment of choice for hypothyroidism in pregnancy. Thyroid function should be normalised prior to conception in women with pre-existing thyroid disease. Once pregnancy is confirmed the thyroxine dose should be increased by about 30-50% and subsequent titrations should be guided by thyroid function tests (FT4 and TSH) that should be monitored 4-6 weekly until euthyroidism is achieved. It is recommended that TSH levels are maintained below 2.5 mU/l in the first trimester of pregnancy and below 3 mU/l in later pregnancy.
[17]
The recommended
maintenance dose of thyroxine in pregnancy is about 2.0-2.4 mcg/kg daily. Thyroxine requirements may increase in late gestation and return to pre-pregnancy levels in the majority of women on delivery. Pregnant patients with subclinical hypothyroidism (normal FT4 and elevated TSH) should be treated since the condition is associated with maternal and fetal complications.
Hyperthyroidism
Clinical evaluation
Hyperthyroidism occurs in about 0.2-0.4% of all pregnancies. Most cases are due to Graves disease although less common causes (e.g. toxic nodules and thyroiditis) may be seen.
[18]
hyperthyroidism from the hyperdynamic state of pregnancy. Distinctive clinical features of Graves disease include the presence of ophthalmopathy, diffuse goitre and pretibial myxoedema. Also, hyperthyroidism must be distinguished from gestational transient thyrotoxicosis, a self-limiting hyperthyroid state due to the thyroid stimulatory effects of beta-hCG . This distinction is important since the latter condition is typically mild and will not usually require specific antithyroid treatment. Hyperthyroidism due to Graves disease may worsen in the first trimester of pregnancy, remit in later pregnancy, and subsequently relapse in the postpartum.
mothers with Graves disease. Rarely neonatal hypothyroidism may also be observed in the infants of mothers with Graves hyperthyroidism. This may result from transplacental transfer of circulating maternal anti-thyroid drugs, pituitary-thyroid axis suppression from transfer of maternal thyroxine.
suffer severe adverse reactions to anti-thyroid drugs and this is best performed in the second trimester of pregnancy.Radioactive iodine is absolutely contraindicated in pregnancy and the puerperium. If a woman is already receiving carbimazole, a change to propylthiouracil (PTU) is recommended but this should be changed back to carbimazole after the first trimester. This is because carbimazole can rarely be associated with skin and also mid line defects in the fetus but PTU long term also can cause liver side effects in the adult. Carbimazole and PTU are both secreted in breast milk but evidence suggests that antithyroid drugs are safe during lactation.
[22]
mothers have received antithyroid drugs in pregnancy. Current guidelines suggest that a pregnant patient should be on PTU during the first trimester of pregnancy due to lower tetragenic effect and then be switched to methimazole during the second and third trimester due to lower liver dysfunction side effects.
Postpartum Thyroiditis
Postpartum thyroid dysfunction (PPTD) is a syndrome of thyroid dysfunction occurring within the first 12 months of delivery as a consequence of the postpartum immunological rebound that follows the immune tolerant state of pregnancy. PPTD is a destructive thyroiditis with similar pathogenetic features to Hashimotos thyroiditis.
[23]
The disease is very common with a prevalence of 5-9% of unselected postpartum women. Typically there is a transient hyperthyroid phase that is followed by a phase of hypothyroidism. Permanent hypothyroidism occurs in as much as 30% of cases after 3 years, and in 50% at 7 10 years. The hyperthyroid phase will not usually require treatment but, rarely, propanolol may be used for symptom control in severe cases. The hypothyroid phase should be treated with thyroxine if patients are symptomatic, planning to get pregnant, or if TSH levels are above 10 mU/L. Long-term follow up is necessary due to the risk of permanent hypothyroidism. Nearly all the women with PPTD have positive TPO antibodies. This marker can be a useful screening test in early pregnancy as 50% of women with antibodies will develop thyroid dysfunction postpartum.
In addition some but not all studies have shown an association between PPTD and depression so that thyroid function should be checked postpartum in women with mood changes.
These normal hormonal changes can sometimes make thyroid function tests during pregnancy difficult to interpret. Thyroid hormone is critical to normal development of the babys brain and nervous system. During the first trimester, the fetus depends on the mothers supply of thyroid hormone, which comes through the placenta. At around 12 weeks, the babys thyroid begins to function on its own. The thyroid enlarges slightly in healthy women during pregnancy, but not enough to be detected by a physical exam. A noticeably enlarged thyroid can be a sign of thyroid disease and should be evaluated. Thyroid problems can be difficult to diagnose in pregnancy due to higher levels of thyroid hormone in the blood, increased thyroid size, fatigue, and other symptoms common to both pregnancy and thyroid disorders.
Hyperthyroidism
What causes hyperthyroidism in pregnancy?
Hyperthyroidism in pregnancy is usually caused by Graves disease and occurs in about one of every 500 pregnancies. Graves disease is an autoimmune disorder. Normally, the immune system protects people from infection by identifying and destroying bacteria, viruses, and other potentially harmful foreign substances. But in autoimmune diseases, the immune system attacks the bodys own cells and organs. With Graves disease, the immune system makes an antibody called thyroid -stimulating immunoglobulin (TSI), sometimes called TSH receptor antibody, which mimics TSH and causes the thyroid to make too much thyroid hormone. In some people with Graves disease, this antibody is also associated with eye problems such as irritation, bulging, and puffiness. Although Graves disease may first appear during pregnancy, a woman with preexisting Graves disease could actually see an improvement in her symptoms in her second and third trimesters. Remissiona disappearance of signs and symptomsof Graves disease in later pregnancy may result from the general suppression of the immune system that occurs during pregnancy. The disease usually worsens again in the first few months after delivery. Pregnant women with Graves disease should be monitored monthly.
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Rarely, hyperthyroidism in pregnancy is caused by hyperemesis gravidarum severe nausea and vomiting that can lead to weight loss and dehydration. This extreme nausea and vomiting is believed to be triggered by high levels of hCG, which can also lead to temporary hyperthyroidism that goes away during the second half of pregnancy.
preeclampsiaa dangerous rise in blood pressure in late pregnancy thyroid storma sudden, severe worsening of symptoms miscarriage premature birth low birth weight
If a woman has Graves disease or was treated for Graves disease in the past with surgery or radioactive iodine, the TSI antibodies can still be present in the blood, even when thyroid levels are normal. The TSI antibodies she produces may travel across the placenta to the babys bloodstream and stimulate the fetal thyroid. If the mother is being treated with antithyroid medications, hyperthyroidism in the baby is less likely because these medications also cross the placenta. Women who have had surgery or radioactive iodine treatment for Graves disease should inform their health care provider, so the baby can be monitored for thyroid-related problems later in the pregnancy. Hyperthyroidism in a newborn can result in rapid heart rate, which can lead to heart failure; early closure of the soft spot in the skull; poor weight gain; irritability; and sometimes an enlarged thyroid that can press against the windpipe and interfere with breathing. Women with Graves disease and their newborns should be closely monitored by their health care team.
Rarely, in a woman with hyperthyroidism, free T 4 levels can be normal but T3 levels are high. Because of normal pregnancy-related changes in thyroid function, test results must be interpreted with caution. TSI test. If a woman has Graves disease or has had surgery or radioactive iodine treatment for the disease, her doctor may also test her blood for the presence of TSI antibodies.
Hypothyroidism
What causes hypothyroidism in pregnancy?
Hypothyroidism in pregnancy is usually caused by Hashimotos disease and occurs in three to five out of every 1,000 pregnancies. Hashimotos disease is a form of chronic inflammation of the thyroid gland.
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Like Graves disease, Hashimotos disease is an autoimmune disorder. In Hashimotos disease, the immune system attacks the thyroid, causing inflammation and interfering with its ability to produce thyroid hormones. Hypothyroidism in pregnancy can also result from existing hypothyroidism that is inadequately treated or from prior destruction or removal of the thyroid as a treatment for hyperthyroidism.
Postpartum Thyroiditis
Points to Remember
Thyroid disease is a disorder that results when the thyroid gland produces more or less thyroid hormone than the body needs. Pregnancy causes normal changes in thyroid function but can also lead to thyroid disease. Uncontrolled hyperthyroidism during pregnancy can lead to serious health problems in the mother and the unborn baby. During pregnancy, mild hyperthyroidism does not require treatment. More severe hyperthyroidism is treated with antithyroid medications, which act by interfering with thyroid hormone production. Uncontrolled hypothyroidism during pregnancy can lead to serious health problems in the mother and can affect the unborn babys growth and brain development. Hypothyroidism during pregnancy is treated with synthetic thyroid hormone, thyroxine (T 4). Postpartum thyroiditisinflammation of the thyroid glandcauses a brief period of hyperthyroidism, often followed by hypothyroidism that usually goes away within a year. Sometimes the hypothyroidism is permanent.
There are no side effects for the mother or the baby as long as the proper dose is used. In the case where hypothyroidism in the mother is NOT detected, the thyroid will still develop normally in the baby. Women with previously treated hypothyroidism should be aware that their dose of medication may have to be increased during pregnancy. They should contact their doctor, who should check their blood level of TSH periodically throughout pregnancy to see if their medication dose needs adjustment. Thyroid function tests should continue to be reviewed every 2 to 3 months throughout the pregnancy. After delivery, the thyroxine dose should be returned to the pre-pregnancy dose and thyroid function tests reviewed two months later.
The only common side effect of radioactive iodine treatment is underactivity of the thyroid gland, which occurs because too many thyroid cells were destroyed. This can be easily and safely treated with levothyroxine. There is no evidence that radioactive iodine treatment of hyperthyroidism interferes with a woman's future chances of becoming pregnant and delivering a healthy baby.
Fatigue Insomnia Nervousness Irritability Hypothyroidism Fatigue Depression Easily upset Trouble losing weight Postpartum thyroiditis goes away on its own after 1 to 4 months. While it is active, however, women often benefit from treatment for their thyroid hormone excess or deficiency. Some of the symptoms caused by too much thyroid hormone, such as tremor or palpitations, can be improved promptly by medications called beta-blockers(eg, propranolol). Antithyroid drugs, radioactive iodine, and surgery do not need to be considered because this form of hyperthyroidism is only temporary. If thyroid hormone deficiency develops, it can be treated for one to six months with levothyroxine. Women who have had an episode of postpartum thyroiditis are very likely to develop the problem again after future pregnancies. Although each episode usually resolves completely, one out of four women with postpartum thyroiditis goes on to develop a permanently underactive thyroid gland in future. Of course, levothyroxine fully corrects their thyroid hormone deficiency, and when used in the correct dose, can be safely taken without side effects or complications.
Rarely, a baby may be born without a thyroid gland. This birth defect is notcaused by thyroid problems in the mother. If an infant's hypothyroidism is not recognized and treated promptly, he/she will not develop normally. Therefore, all newborn babies in the United States routinely have a blood test to be sure that hypothyroidism is diagnosed and treated. Most thyroid medications will have no effect on the baby. The exception to this generality is the administration of radioactive iodine to the mother during pregnancy. Radioactive iodine can cross the placenta and it can destroy thyroid cells in the fetus.