Thyroid dysfunction—changes in how well your thyroid gland works—can start during or after pregnancy in women who never had thyroid problems before. This occurs because pregnancy causes major changes in the levels of hormones made in the thyroid gland. When the thyroid makes too much of the thyroid hormones T3 and T4, it is called overactive thyroid or hyperthyroidism. This problem also causes very low levels of thyroid stimulating hormone TSH , a hormone that tells the thyroid to make T3 and T4. An overactive thyroid greatly increases metabolism how your body uses energy.
Birth defects caused by PTU can include Gravesdisease pregnancy anomalies abnormalities Granny from red riding hood the face or neck region and in the urinary system. All newborns of mothers with Graves disease who are positive for these antibodies should be checked for signs of thyroid problems and treated if necessary. How does pregnancy affect the thyroid? Overall risk of fetal complications associated with cordocentesis and intra-amniotic injection is low at 0. Cooper DS, Lauberg P. Gravesdisease pregnancy control of thyrotoxicosis is associated with pregnancy loss, pregnancy-induced hypertension, prematurity, low birth weight, intrauterine growth restriction, stillbirth, thyroid storm, and maternal congestive heart failure [ 27 — 29 ]. In the first trimester of pregnancy, the preferred drug to treat hyperthyroidism is propylthiouracil PTU. Diagnosis and Management of Hyperthyroidism in pregnancy: a review. Am J Cardiol.
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After the birth of my Gravezdisease daughter inI started suffering from a long list of symptoms and was ultimately diagnosed with Graves Disease. Graves' disease is triggered by some process in the body's immune system, which normally protects the body from infection. Your risk is higher if you: 1 Have a family history. Here is another post that Scaffolding tower essex about Gravesdisease pregnancy risks in those Gravesdisease pregnancy Hashi and although you do not have Hashis, the Gravesdisease pregnancy might be good as I believe some Gravesdisease pregnancy this may apply since you are now in a hypothyroid state with no thyroid. This skin condition is usually painless and relatively mild, but it can be painful for some. Severe emotional stress or trauma may trigger Graves' disease. I was put on a PTU 6 days a week at 50 mg. Lucy says:. Trokoudes, K. I want Gravesdisezse have a child but loosing hope with my condition I am only here to learn if you had any success Grqvesdisease improving your health. Treatments Gravrsdisease Graves' disease lower the amount of thyroid hormone in your body or block the action of thyroid hormone. These changes do not affect the pregnancy or your unborn baby. Yes, Unfortunately.
Data sharing not applicable to this article as no datasets were generated or analyzed during the current study.
- It is named after Robert Graves, an Irish physician, who described this form of hyperthyroidism about years ago.
- Doctors call it an autoimmune disorder, since the body essentially attacks itself rather than a bacteria or virus.
Data sharing not applicable to this article as no datasets were generated or analyzed during the current study. The paper will discuss preconception counseling, etiologies of hyperthyroidism, thyroid function testing, pregnancy-related complications, maternal management, including thyroid storm, anti-thyroid drugs and the complications for mother and fetus, fetal and neonatal thyroid function, neonatal management, and maternal post-partum management.
The key to a successful pregnancy begins with preconception counseling. GH affects 0. Establishing the correct diagnosis and effectively managing GH in pregnancy is challenging; pregnancy alters thyroid physiology and laboratory testing, antithyroid drugs ATDs are associated with teratogenicity, and maternal, fetal, and newborn complications are directly related to control of GH and in a few cases to the levels of serum maternal thyroid-stimulating immunoglobulin TSI [ 2 ].
All women of reproductive age with GH or past history of GH should receive preconception counseling. Women with GH should be advised to postpone conception and use contraception until GH is controlled. Persistently elevated TRAb levels during pregnancy are prognostic of fetal thyroid dysfunction [ 6 ].
Consequently, women with very elevated TRAb levels prior to conception may be better candidates for thyroidectomy. After surgery, TRAb levels decrease and normalize within months to one year [ 4 , 5 ].
Alternatively, women may switch to PTU once pregnant. Patients taking ATDs should use contraception and be counseled to pay close attention to menstrual cycles. A pregnancy test should be done immediately if there is a missed period.
The risk of birth defects from ATDs is greatest during weeks 6—10 [ 7 ]. Causes of Hyperthyroidism in Pregnancy [ 33 ]. The clinical course is closely correlated with hCG levels, which begin to rise at week 7 of gestation. Symptoms spontaneously resolve as serum concentration of hCG decreases between weeks 14 and 20 [ 10 ].
Trophoblastic disease i. TRAb are typically absent. In very symptomatic patients a trial of beta-blocker may provide relief. In pregnancy, propranolol is preferred as atenolol has been associated with decreased birth weight [ 12 , 13 ]. Women with a prior history of GTT have a higher likelihood of having a repeat episode [ 9 ].
As described above, the signs and symptoms of GH in pregnancy are similar to those of a non-pregnant GH patient. The diagnosis of GH should be suspected in a hyperthyroid pregnant woman who 1 was having symptoms prior to pregnancy 2 had a prior diagnosis of hyperthyroidism, and 3 had a previous birth to an infant with thyroid dysfunction.
The small increase in GH incidence and worsening of GH symptoms described in early pregnancy may be from the stimulation of the thyroid gland by hCG or elevation in TRAb levels during the first trimester [ 14 — 16 ]. As pregnancy progresses, changes in the immunologic response lead to improvement in symptoms.
Postpartum, a rebound of the immune system can lead to exacerbation of GH [ 17 ]. In the latter half of pregnancy, increased thyroid-binding globulin TBG and decreased serum albumin concentration can affect the widely available FT4 automated immunoassays resulting in significant variability between assays [ 19 — 21 ]. FT4 concentration also continuously declines throughout pregnancy [ 21 ]. Consequently, assay and trimester-specific pregnancy reference ranges are necessary if FT4 is used.
After week 16, the non-pregnancy reference range may be adjusted by a factor of 1. One exception is in the diagnosis of an autonomous functioning nodule predominantly secreting T3. TRAb is useful in confirming the diagnosis of GH [ 5 ]. During pregnancy, TRAb crosses the placenta and may induce fetal hyperthyroidism.
TRAb levels over 3 times the upper limit of normal are associated with hyperthyroidism in the fetus and newborn [ 5 ]. While TBII is unable to differentiate between stimulating or blocking antibodies, in a patient who is thyrotoxic an elevated TBI is due to the presence of stimulating TRAb in the majority of cases. Poor control of thyrotoxicosis is associated with pregnancy loss, pregnancy-induced hypertension, prematurity, low birth weight, intrauterine growth restriction, stillbirth, thyroid storm, and maternal congestive heart failure [ 27 — 29 ].
Women with uncontrolled GH are 9. However, if disease is controlled during pregnancy, they are 2. Mothers with uncontrolled GH are also The rate of fetal demise and stillbirth in mothers with poorly controlled GH is 5. ATDs remain the treatment of choice for GH during pregnancy. Care must be taken to avoid overtreatment with ATD. Fetal hypothyroidism is an indication to decrease or stop ATD. Maternal TRAb serum concentration greater than 3 times the upper limit of the reference range in the third trimester is a risk factor for neonatal hyperthyroidism [ 32 , 38 — 40 ].
Thyroidectomy in the second trimester is an effective option if a woman is unable to tolerate ATDs, non-consistent with drug therapy, requiring very high doses of ATDs, has a large goiter, or allergic to ATD. TS is a rare complication of uncontrolled GH. Given its rarity, the incidence of TS in pregnancy is not clear.
Davis et al. TS may occur when a chronically hyperthyroid patient encounters an additional stress or precipitating event i. Patients with TS present with tachycardia, thermic dysregulation, and altered mental status. If not adequately treated, TS can lead to multi-organ failure including congestive heart failure. Biochemical testing reveals suppressed TSH and elevated T4.
Management of Thyroid Storm [ 34 , 63 ]. ATD remains the mainstay treatment of women with GH during pregnancy. PTU and MMI are equally effective, cross the placenta at comparable rates, and may produce fetal hypothyroidism with or without goiter. However, other studies have not shown any difference in rates of congenital malformations between those treated with MMI or PTU and the general population [ 54 ]. Prior to the onset of fTH production, the fetus relies on TH from the mother via transplacental passage [ 60 ].
Fetal risks in mothers with GH include hyperthyroidism due to inappropriate transplacental passage of maternal TRAb and hypothyroidism due to excessive maternal administration of ATD. During routine OB visits, antepartum surveillance should include assessment of fetal heart rate, typically performed with handheld doppler monitor.
Fetal tachycardia is concerning for a thyroid etiology. Other causes of tachycardia such as infection, medications cocaine, terbutaline , obstetric conditions placental abruption, fetal bleeding , and fetal tachyarrhythmias should be ruled out [ 62 ].
As discussed previously, maternal serum TRAb titers provide useful prognostic information. TRAbs can cross the placenta and act to stimulate or block fetal thyroid hormone production once the fetal thyroid gland becomes functional [ 1 , 2 ]. Women with a prior fetus or neonate with a thyroid disorder, TRAb greater than 3 times the ULN, fetal tachycardia, and poorly controlled hyperthyroidism should have a FUS.
The earliest sonographic sign of fetal thyroid dysfunction is fetal goiter, which appears as a solid neck mass [ 56 , 64 ]. Less commonly, fetal thyrotoxicosis can lead to heart failure, fetal hydrops, and fetal demise [ 63 ].
Fetal goiter can cause fetal, obstetric, and neonatal complications including polyhydramnios secondary to reduced swallowing ability, cervical dystocia, and mechanical obstruction of the fetal airway respectively [ 58 , 66 , 67 ].
Cesarean delivery may be preferred due to high risk of labor dystocia from a deflexed head [ 68 ]. Signs of hypothyroidism on FUS include fetal goiter, growth restriction, and delayed bone age [ 63 ]. ATD dose reduction or discontinuation should restore normal fetal thyroid function and decrease the size of the fetal goiter [ 56 ]. Rarely, intra-amniotic levothyroxine injections in conjunction with reduction of ATD dose may be indicated as combination therapy may lead to faster resolution of fetal goiter and recovery from hypothyroidism [ 67 ].
In the rare circumstance where the diagnosis remains unclear, cordocentesis remains the method of choice for confirmation of fetal thyroid status [ 1 , 2 , 57 , 64 ]. Known as fetal blood sampling, cordocentesis involves US guided placement of a needle into the fetal circulation usually through direct placement into a free loop of umbilical cord or at the cord insertion site.
Alternatively, TH concentrations in the amniotic fluid can be measured [ 58 , 65 ]. While less hazardous, amniotic fluid hormone levels have not been validated as a reliable measure of fetal thyroid function [ 56 ]. Injection of levothyroxine into the umbilical vein should be restricted to cases of confirmed fetal hypothyroidism and progressive polyhydramnios in spite of repeated intra-amniotic injections [ 56 , 69 ]. Overall risk of fetal complications associated with cordocentesis and intra-amniotic injection is low at 0.
The change in size of fetal goiter and extent of polyhydramnios help determine the response to treatment [ 64 ]. Repeat cordocentesis may be necessary to monitor therapy [ 70 ]. The lowest dose necessary to normalize the fetal heart rate — beats per minute should be used [ 1 ]. Care must be taken to prevent inducing fetal hypothyroidism due to excessive administration of ATD. Progressive or complex thyroid illness during pregnancy warrants consideration of consultation with a pediatric endocrinologist prior to delivery [ 2 ].
Newborns of hyperthyroid mothers should be evaluated soon after birth. Neonates are at risk of hypothyroidism secondary to maternal ATD therapy, central hypothyroidism from untreated mothers via suppression of fetal TSH production that impairs the hypothalamic-pituitary-thyroid maturation [ 1 , 71 ] and hyperthyroidism after the effect of maternal ATDs dissipates [ 33 ].
FT4 measurement at birth should be repeated between days 3 and 5 of life and continuously followed if elevated [ 40 ]. TRAb positive neonates without biochemical or clinical evidence of thyroid dysfunction should have weekly clinical and laboratory follow up until the TRAb test becomes negative [ 40 ]. Some hyperthyroid neonates are first diagnosed at birth. Signs of neonatal thyrotoxicosis include tachycardia, tachypnea, pulmonary arterial hypertension, systemic hypertension and heart failure.
They may also be small for gestational age with accelerated bone maturation and craniosynostosis [ 34 , 63 ]. Follow up is necessary until the hyperthyroidism resolves which may take months.
Therapy should be initiated within two weeks of life for optimal outcomes and the infant should be followed for the first three years of life [ 2 ]. PPT classically begins with a transient hyperthyroid phase followed by transient hypothyroidism before a return to euthyroidism.
Breastfeeding has been shown to be safe in mothers taking ATDs in appropriate doses. Studies of infants exposed to ATDs in breast milk in doses sufficient to control maternal GH had normal thyroid function and normal intellectual development [ 79 , 80 ].
Doses should be split into 2 to 3 doses and administered after the mother has breastfed. The goal in the care of women with GH is the delivery of a euthyroid healthy newborn to a healthy mother. Establishing the diagnosis of GH can be challenging for the physician. Maintaining euthyroidism throughout pregnancy is key to reducing the risk of maternal, fetal, and newborn complications.
Take care, Katie. In addition to causing heart problems and osteoporosis, Graves' disease in women can cause: Problems with your menstrual period. You may also be at higher risk for preeclampsia , placental abruption or miscarriage. Graves' disease resources. Your doctor should discuss each of the treatment options with you including the logistics, benefits and potential side effects, expected speed of recovery and costs.
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Graves Disease in Pregnancy - Health Encyclopedia - University of Rochester Medical Center
Graves disease is a condition where the thyroid gland makes too much thyroid hormone. This is called hyperthyroidism or overactive thyroid. A healthy thyroid gland works normally in pregnancy. It tends to run in families. The symptoms of hyperthyroidism may look like other health conditions. Always see your healthcare provider for a diagnosis. The healthcare provider will ask about your health history. He or she will also do a physical exam, and ask about symptoms.
The goal of treatment is to keep the thyroid hormone levels normal. Treatment may include:. Some medicines cross the placenta and may not be safe for the baby.
Radioactive iodine damages the overactive thyroid cells. But this treatment is not safe in pregnancy. If you have Graves disease, you can take steps to have a healthy pregnancy. Get early prenatal care and work with your healthcare provider to manage the disease. Graves disease usually gets worse in the first half of pregnancy. It gets better in the second half, and then gets worse again after delivery.
It is important to keep your thyroid levels normal. Hyperthyroidism that is out of control may lead to preterm birth. This is birth before 37 weeks of pregnancy.
It can also lead to low birth weight of the baby. Some pregnant women have a severe life-threatening form of hyperthyroidism called thyroid storm. This is a condition in which there are very high levels of thyroid hormone. Medicines to treat hyperthyroidism may harm your developing baby and newborn. Anti-thyroid medicine may also cause low levels of thyroid hypothyroidism in the developing baby and newborn.
It is usually short-term and does not cause problems for the baby, but careful monitoring is important. Bring someone with you to help you ask questions and remember what your provider tells you. At the visit, write down the name of a new diagnosis, and any new medicines, treatments, or tests. Also write down any new instructions your provider gives you. Know why a new medicine or treatment is prescribed, and how it will help you.
Also know what the side effects are. Know what to expect if you do not take the medicine or have the test or procedure. If you have a follow-up appointment, write down the date, time, and purpose for that visit. Search Encyclopedia. Graves Disease in Pregnancy What is Graves disease? What causes Graves disease in pregnancy? Who is at risk for Graves disease in pregnancy? What are the symptoms of Graves disease?
How is Graves disease in pregnancy diagnosed? How is Graves disease in pregnancy treated? Surgery to remove part of the thyroid the part that is overactive Radioactive iodine damages the overactive thyroid cells. What are possible complications of Graves disease in pregnancy? Key points about Graves disease in pregnancy Graves disease is a condition where the thyroid gland makes too much thyroid hormone.
Before your visit, write down questions you want answered. Ask if your condition can be treated in other ways.