- Flare up of Grave's disease .
- Distinguish postpartum by iodine or technetium scan high uptake in Grave's disease) and absent thyroid stimulating antibodies in postpartum thyroiditis.
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Thyroid Disease in Pregnancy
Main and Danish guidelines by the web master
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Thyroid Function During Normal Pregancy
Serum TBG concentrations rise almost two-fold and leads to an increase in both serum total thyroxine (T4) and Tri-iodothyronine (T3) but not free T4 and T3 (See normal lab values). TSH falls in the first trimester but may rise in early pregnancy and increase in the third trimester. Similarly the normal range for free (T3) and (T4) are reduced in the end of pregnancy (see normal lab values). Hyperthyroidism
Hyperthyroidism complicating pregnancy occurs in 0.2% of pregnancies most often (95%) Grases' Graves' thyroid disease (autoimmune disease with stimulating antibodies). Other causes are toxic adenomas and subacute lymphocystic thyroidism. Some antibodies can inhibit fetal thyroidism. Autoimmune thyroid disease is common in pregnancy. The thyroid peroxidase antibodies (TPA) or antibodies against thyreoglubin is associated with a significant increase in miscarriage rate. Pregnancy complicated with poorly controlled hyperthyroidism is associated with increase rate of spontaneous abortion, preterm delivery, IUGR, stillbirth, preeclampsia, congestive heart failure. Crisis are seldom: Precipitated by , infection and preeclampsia. Exacerbation may occur in the first trimester and improvement in the last half of pregnancy (TSH receptor stimulating antibodies may fall). Diagnosis Raised T3 and T4 and TSH fall (see normal lab values) present of TRAb and goiter and present of TRAb autoimmunity. Normally diagnosed before pregnancy but can be revealed in pregnancy (most often take place in the first or the beginning of the second trimester). Symptoms Exophthalmos (may occur before hyperthyroidism) tremor, lid lag, weight loss, tachycardia. Treatment The goal is to keep the mothers euthyroid with free T4 in the high normal range using the lowest drug dose.
Both prophylthiouracil (PTU) and Methimazole (MMI) cross the placenta and can cause fetal hypothyroidism and goiter. PTU has generally been preferred because it has not been associated with fetal scalp defects - aplasia cutis or choanal or esophageal atresia which very rarely has been seen with MMI. PTU has a shorter halflife and more bound to albumin which may result in less fetal hypothyroidism. Women on maintenance dose of MMI need not be switch to PTU in pregnancy. Newly diagnosed thyrotoxicosis should be aggressively treated with PTU 450 mg or MMI 45 mg for 4-6 weeks before reduction in dose. Doses of PTU £ 150 mg/day or MMI £ 45 are unlikely to cause problems in the fetus. And these doses are safe for breastfeeding (only 0.07% of the maternal dose is consumed by the fetus). If higher dose, the thyroid function should be checked in the neonate. Combined therapy with Thyroxin "block and replace therapy" has no place (fetal thyroidism). b-blockers Often used in early management for symptoms and discontinued once there is clinical improvement, usually after 3 weeks. Can occasionally cause IUGR, hypoglycemia, respiratory depression and tachycardia. Surgery Rarely indicated. Usually reserved for those with dysplasia or stridor and those who has or develop allergies to antithyroid drugs (1-5%). Best performed in the II trimester, if necessary. May be associated with increased risk of abortion and preterm labor. Radioactive Iodine Contraindicated in pregnancies and 4 months after treatment. Fetal and neonatal Grave´s disease 1-5% have hyperthyroidism due to transplacental transfer of TSH receptor-stimulating antibodies (TRAb). Half life is long (Weeks) and symptoms seen up to 6 weeks post partum. Values five-fold and more are predictive. Low < 20 l minimal risk. Symptoms: Symptoms: High fetal heart rate (> 160 beats/min, fetal goiter, fetal hydrops, pretem delivery, advanced bone age, IUGR fetal deaths and craniosynostosis are manifestations of fetal thyrotoxicosis (seldom). Fetal blood sampling for thyroid function test may be considered. Propylthiouracil and Methimaxol as well as betablockers (Propranolol) may be given to mothers to treat fetuses who have severe tachycardia or very poor growth. The pediatrician should be informed whenever there is a history of maternal thyroid disease without treatment, as the mortality rate of the newborn is almost 15%. The treatment is only needed for a few weeks. NB! In case of unexplained fetal tachycardia and goiter, TRAB should be measured. In case of struma and treatment with antithyreoid medicine which can block the infants thyreoid gland. The infant can develop slight but transiant hypofunction. If the mother has TRAb antibodies the baby can later develop hyperthyroidism. Yodine uptake: recommended dose 2250 µ/d. The prevalende: overt (0,3-0,5%), subclinical 2-3%
Lethargy, tiredness, hairless, dry skin, constipation, carpal tunnel syndrome, fluid retention and goiter Cases: Most common Hashimoto's thyroiditis or and Grave's disease. Others are atropic thyoriditis or iatrogenic (thyroidectomy, radioactive therapy) and related to drugs (iodine, lithium anti-thyroid drugs). Diagnosis: Low free T4 and raised TSH (see normal lab values) suggest primary hypothyreodisme, overt if free T4 are clearly below normal and subclinical if free T4 is normal. Treatment: The goal of therapy is to normalize the mother's serum TSH concentration, low in the normal range and free Ty in the upper 1/3 of the normal range. Small amount of thyroxine cross the placenta but no risk for thyrotoxicosis of the fetus. Most have maintenance dose of 100-150 mg/day. Starting dose normal 100-150 mg/day.
Should be evaluated in the same way as if the woman is not pregnant. Radionuclide scanning is contraindicated. Thyroid function test should be performed to exclude a toxic nodule or Hashimoto's thyroiditis. A raised Thyroglobulin titre (-100 mg (L) is suggestive of malignancy. Ultrasound: Cystic lesions more likely to be benign. Surgery in case of malignancy performed in the II or III trimester with Thyroxine given postoperative to suppress TSH since residual tumor is usually TSH dependent. (1) Albalovich M et al. Management of Thyroid Dysfunction durin g Pregnancy and Postpartum: An Endocrine Society Clinial Practice Guideline. J.Clin. Endocrinol. Metab. , 92 (suppl. 8) s. 1-47, 2007 (2) Nelson-Piercy C. Handbook of Obstetric Medicine. Second Edition, By Martin Dunitz, Ltd., published in the United Kingdom in 2002. (3) www.uptodate.com 2007
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