5Normal physiology The hypothalamic pituitary axis Thyrotropin-releasing hormone (TRH)Produced in a tonic fashion in the paraventricular nucleus of the hypothalamus.TSH has an α and β subunit;β subunit confers specificity.TSH secretion regulated by negative feedback from circulating thyroid hormone, dopamine, and somatostatin.TSH then stimulates the thyroid gland to produce, as well as secrete, thyroxine(T4) and triiodothyronine (T3).
6The rate-limiting step is iodide trapping mediated by TSH.nonpregnant state, 80 mg/d to 100 mg/d of iodine taken up20% of the intake is cleared by the thyroid gland; remainder renally
8Physiologic adaptation during pregnancy increase in thyroid-binding globulinsecondary to an estrogenic stimulation of TBG synthesis and reduced hepatic clearance of TBG ;two to threefoldlevels of bound proteins, total thyroxine, and total triiodothyronine are increased and resin triiodothyronine uptake (RT3U) is decreasedbegins early in the first trimester, plateaus during midgestation, and persists until shortly after deliverydecrease in its hepatic clearance,estrogen-induced sialylationfree T4 and T3 increase slightly during the first trimester in response to elevated hCG. decline to nadir in third trimester
9human chorionic gonadotropin (hCG) intrinsic thyrotropic activitybegins shortly after conception, peaks around gestational week 10,declines to a nadir by about week 20directly activate the TSH receptorpartial inhibition of the pituitary gland (by cross-reactivity of the α subunit)transient decrease in TSH between Weeks 8 and 14mirrors the peak in hCG concentrations20% of normal women, TSH levels decrease to less than the lower limit of normal
11reduction in plasma iodide A decrease in basal TSH of 0.1 mU/L was observed for every 10,000 IU/L increment in hCGreduction in plasma iodidefetal :monodeiodinase types II and III in the placentaincreased maternal glomerular filtration rate-- increased renal clearance of iodide throughout pregnancytransplacental passage of T4 and iodide and placental metabolism of iodothyroninesstimulate the maternal thyroid ; depleting the maternal circulation of thyroid hormone and its precursors
12Hypothyroid;25% to 47% average dosage increase during pregnancy increased serum thyroid stimulating hormone (TSH) and thyroglobulin concentrations, relative hypothyroxinemia, and occasional goiter formationEsp. from area with borderline iodine sufficiencyassociated with increase in thyroid gland size in 15%
13EFFECTS OF PREGNANCY ON THYROID PHYSIOLOGY Physiologic ChangeThyroid-Related Consequences↑ Serum thyroxine-binding globulin↑ Total T4 and T3; ↑ T4 production↑ Plasma volume↑ T4 and T3 pool size; ↑ T4 production; ↑ cardiac outputD3 expression in placenta and (?) uterus↑ T4 productionFirst trimester ↑ in hCG↑ Free T4; ↓ basal thyrotropin; ↑ T4 production↑ Renal I- clearance↑ Iodine requirements↑ T4 production; fetal T4 synthesis during second and third trimesters↑ Oxygen consumption by fetoplacental unit, gravid uterus, and mother↑ Basal metabolic rate; ↑ cardiac output
15Hyperthyroidism and pregnancy 0.2% of pregnanciesprevalence 0.1% to 0.4%, with 85% Graves’ diseaseSingle toxic adenoma, multinodular toxic goiter, and subacute thyroiditisgestational trophoblastic disease,viral thyroiditis and tumors of the pituitary gland or ovary (struma ovarii)TSH is depressed and fT4 and fTI are increased.The RT3U that normally is decreased in pregnancy is increased in hyperthyroidism.
16Hyperthyroidism and pregnancy serum TSH value <0.01 mU/L and also a high serum free T4 valuemay be difficult to determine the causethyroid radionuclide imaging is contraindicated in pregnant women.Measurement of thyrotropin receptor antibody (thyroid stimulating immunoglobulins) Graves' disease during pregnancytransient hyperthyroidism in hyperemesis gravidarum and gestational transient thyrotoxicity (GET)
17Hyperthyroidism and pregnancy Severe maternal hyperthyroidismincreased risk of stillbirthpreterm deliveryintrauterine growth restrictionPreeclampsiaheart failurespontaneous abortionFetal thyroid hyperfunction or hypofunction caused by TSHRAbsFetal goiter from excessive antithyroid drug treatmentNeonatal thyrotoxicosisIncreased perinatal and maternal mortalityDecreased IQ of offspring because of excessive use of antithyroid drugs
18Transient hyperthyroidism during pregnancy & gestational transient thyrotoxicity (GET) hyperemesis gravidarumsevere nausea and vomiting leading to a 5% loss of body weight, dehydration, and ketosis.absence of goiter and ophthalmopathy, and absence of the common symptoms and signs of hyperthyroidismhigher serum hCG and estradiol concentrations60% have a subnormal serum TSH level (< 0.4 mU/L),50% have an elevated serum free T4 concentrationSeverity positively correlated with maternal free T4 levels but not to thyroid function.12% elevated free T3 indexbelieved to be related to hCG stimulation of the thyroid glandNormalization of T4 levels by midgestation.Treatment is supportive care
19GET first trimester related to hCG stimulation of the thyroid gland symptoms of hyperthyroidism and elevated free T4 levels.The thyroid gland usually is not enlargedresolution of symptoms parallels the decline in hCG levelsusually resolves spontaneously by 20 weeks’ gestationbeyond 20 weeks,repeat evaluation for other causes
20Trophoblastic hyperthyroidism hydatidiform mole (molar pregnancy) & choriocarcinoma.high serum hCG concentrations and abnormal hCG isoforms55 to 60 percent had clinically evident hyperthyroidismnormal thyroid gland and few symptoms of thyroid hormone excess.some :findings of hyperthyroidism and a diffuse goiterophthalmopathy is not presentNausea and vomiting may predominate
21subclinical hyperthyroidism associated with osteoporosis, cardiovascular morbidity, and progression to overt thyrotoxicosis and thyroid failure.not associated with adverse pregnancy outcomesdoes not warrant treatment.
22Graves’ disease 95% of thyrotoxicosis during pregnancy. activity level fluctuate during gestation, withexacerbation during the first trimestergradual improvement during the latter half.exacerbation shortly after deliveryclinical scenarios.stable Graves’ disease receiving thionamide therapy with exacerbation during early pregnancy.in remission with a relapse of disease.without prior history diagnosed with Graves’ disease de novo during pregnancy.
23Graves’ disease Diagnosis difficult :hypermetabolic symptoms in normal pregnancythyroid examination: goiter (with or without bruit)suppressed serum TSH level and usually elevated free and total T4 serum concentrations.TSH receptor antibodiescomplications related to the duration and control of maternal hyperthyroidismautoantibodies mimic TSH can cross the placenta and cause neonatal Graves’ disease
25Graves’ disease Neonatal thyrotoxicosis : 1% of infants occur in euthyroid mother or has had surgical or radioactive 131I treatments before pregnancyfetal ultrasound to exclude evidence of fetal thyrotoxicosis (eg, an anterior fetal neck mass) or fetal tachycardia.fetal goiter, advanced bone age, poor growth, and craniosynostosis, Cardiac failure and hydropsFetal blood sampling — Fetal blood for thyroid function tests by percutaneous umbilical vein sampling after 20 weeks of gestationHigh maternal TSH receptor-stimulating antibody levels Fetal signs suggestive of thyroid disease History of a prior baby with hyperthyroidism
26Thyroid storm obstetric emergency extreme metabolic state 10% of pregnant women with hyperthyroidismhigh risk of maternal cardiac failure.fever, change in mental status, seizures, nausea, diarrhea, and cardiac arrhythmias.inciting event (eg, infection, surgery, labor/delivery) and a source of infectiontreatment immediately, even if serum free T4, free T3, and TSH levels are not known.untreated thyroid storm can be shock, stupor, and coma.
27Guidelines for clinical management of maternal hyperthyroidism during pregnancy 1. Use the lowest dosage of thionamide (preferably PTU) to maintain maternal total T4 concentrations in the upper one third of normal to slightly elevated range for pregnancy.Normal range of total T4 during pregnancy is estimated to be 1.5 times the nonpregnant state2. Monitor maternal total T4 serum concentration every 2–4 weeks, and titrate thionamide as necessary.Monitoring serum TSH may become useful later.Shane O. LeBeau, Endocrinol Metab Clin N Am35 (2006) 117–136
28Guidelines for clinical management of maternal hyperthyroidism during pregnancy 3. Measure TSH receptor antibodies (thyroid-stimulating immunoglobulins or TSH receptor binding inhibitory immunoglobulins) at 26–28 weeks to assess risk of fetal/neonatal hyperthyroidism.TSH receptor antibody measurement is crucial in hypothyroid levothyroxine-treated women with a prior history of Graves’ disease, who do not appear thyrotoxic.4. Perform fetal ultrasound at weeks 26–28 to assess potential fetal response to thionamide treatment and effect of TSH receptor antibodies on fetal thyroid function
29Guidelines for clinical management of maternal hyperthyroidism during pregnancy 5. Consider thyroidectomy if persistently high doses of thionamide (PTU > 600 mg/d or MMI > 40 mg/d) are required,or if the patient cannot tolerate thionamide therapy.6. β-Adrenergic blocking agents and low doses of iodine may be used perioperatively to control hyperthyroid state.7. Check fetal cord blood at delivery for TSH and T4.
30Treatment Thionamides propylthiouracil (PTU) and methimazole(MMI) Both cross the placenta with equal transfer kinetics.Both can cause fetal goiter and hypothyroidism, usually mild and transient & dose-dependentmedian time to normalization of maternal thyroid function7 weeks with PTU and 8 weeks with MMIPTU more highly bound to albumintheorize that MMI crosses the placenta in higher concentrations
31Treatment Thionamides maternal :rash rare birth defects in MMI: aplasia cutis, choanal atresia,esophageal atresia, and minor dysmorphic featuresLow thyroid function at birth ½ neonates whose mothers received PTU or MMI and had serum T4 concentrations within the normal (non-pregnant) rangenormal IQ scoresGraves’ disease may amelioratethionamide discontinued in 30% during the final weeksfall in serum TSH receptor-stimulating antibody concentrations and a rise in TSH receptor-blocking antibodies.Graves' hyperthyroidism can worsen postpartumdo not recommend the use of T4 with thionamide therapy during pregnancy.
32Treatment β-Adrenergic blockers Iodides weaned as soon as the hyperthyroidism is controlledoccasional cases of neonatal growth restriction, hypoglycemia, respiratory depression, and bradycardiaincreased frequency of first-trimester miscarriagesavoiding in the first trimesterIodidespast reports of neonatal hypothyroidism after exposure to iodinelow-dose potassium iodide may be consideredPreparation for thyroidectomythionamide-intolerant patients refusing surgery.
33Treatment Surgery Subtotal thyroidectomy : persistently high dosages of thionamides (PTU > 600 mg/d, MMI > 40 mg/d) are required to control maternal diseaseallergic or intolerant of both thionamidesnoncompliant with medical therapycompressive symptomssecond trimester, before gestational week 24prepared with a β-adrenergic blocking agent and a 10- to 14-day course of potassium iodide
34Treatment Radioactive iodine therapy Nursing contraindicated fetal thyroid gland begins to concentrate iodine after gestational week 10, Fetal thyroid tissue is present by 10 to 12 weekspredisposing to congenital hypothyroidismNursingBreast feeding in mothers taking PTU or MMI is safeThyroid function in newborn infants is unaffectedPTU is preferred because it is less concentrated in breast milk
35Hypothyroidism in pregnancy elevated serum TSH concentration:2.5% of pregnanciesIn iodine-sufficient environmentHashimoto’s thyroiditisprior radioactive iodine treatmentsurgical ablation of Graves’ diseaseless common causes: overtreatment of hyperthyroidism with thionamides, transient hypothyroidism owing to postpartum thyroiditis, medications that alter the absorption or metabolism of levothyroxine, and pituitary/hypothalamic disease)
36Hypothyroidism in pregnancy diagnosisSymptoms masked by the hypermetabolic state of pregnancy.20% to 30% overt hypothyroidism develop symptomsweight gain, lethargy, decrease in exercise capacity, and intolerance to cold,constipation, hoarseness, hair loss, brittle nails, dry skin, goiter, or delay in the relaxation phase of the deep tendon reflexesElevated serum TSH concentrationCentral hypothyroidism do not manifest an elevated serum TSH level
37Hypothyroidism in pregnancy Pregnancy outcomedepends on the severity of disease and adequacy of treatmentGestational hypertension in overtly hypothyroid women (36%) vs subclinical disease (25%) or the general population (8%)Overt hypothyroid vs subclinical disease,increased use of cesarean section because of fetal distressplacental abruption, anemia, andpostpartum hemorrhage increased rates of miscarriage, preeclampsia,placental abruption, growth restriction, prematurity and stillbirthsfetuses are at risk for impaired neurologic development low-birth-weight neonates
38Hypothyroidism in pregnancy TSH can be elevated with or without suppressed levels of free T4.antithyroid autoantibodies (eg, antithyroglobulin, antithyroidperoxidase) are presentelevated creatine phosphokinase, cholesterol, and liver function tests5% to 8% prevalence of hypothyroidism in type I diabetesmellitus and women who have type I diabetes have a 25% risk of developing postpartum thyroid dysfunction
39Causes of hypothyroidism Worldwide, the most common is iodine deficiency.impaired neurologic development; severe mental retardation, deafness,muteness, and pyramidal or extrapyramidal syndromes;Hashimoto’s thyroiditisIdiopathic hypothyroidism; atrophic thyroid glandand absent antithyroid antibodies.131I treatment for Graves’ disease and thyroidectomyDrugs interfere with the metabolism of thyroid hormones
40Subclinical hypothyroidism normal free T4 levelelevated TSH above the upper limit of reference range (4.5–10.0mIU/L)thresholds based on gestational age.TSH in the first half of pregnancy is 3.0 mIU/Lprevalence of subclinical hypothyroidism 2–5%increased risk of placental abruption and preterm birthimportant to monitor TSH and free T4 levels.2–5% progress to overt hypothyroidism each year
41Isolated maternal hypothyroxinemia normal TSHfree T4 below 0.86 ng/dl.In the first half of pregnancy,prevalence 1.3%.not associated with adverse perinatal outcome
42Guidelines for clinical management of maternal hypothyroidism during pregnancy 1. Check serum TSH level as soon as pregnancy is confirmed.2. For newly diagnosed hypothyroid women, initial levothyroxine dosage is based on severity of hypothyroidism. For overt hypothyroidism, administer 2 mcg/kg/d. If TSH is < 10 mU/L, initial dose of 0.1 mg/d may be sufficient.3. For previously diagnosed hypothyroid women, monitor serum TSH every 3–4 weeks during first half of pregnancy and every 6 weeks thereafter.4. Adjust levothyroxine dosage to maintain serum TSH ≤ 2.5 mU/L.5. Monitor serum TSH and total T4 levels 3–4 weeks after every dosage adjustment. When levothyroxine dosage achieves equilibrium, resume monitoring TSH aloneShane O. LeBeau, Endocrinol Metab Clin N Am35 (2006) 117–136
43Treatment6. Levothyroxine ingestion should be separated from prenatal vitamins containing iron, iron and calcium supplements,and soy products by at least 4 hours to ensure adequate absorption.7. After delivery, reduce levothyroxine to prepregnancy dosage, and check serum TSH in 6 weeksadjusting levothyroxine1. TSH < 10 mU/L, increase 0.05 mg/d.2. TSH =10–20 mU/L, increase mg/d.3. TSH > 20 mU/L, increase 0.1 mg/d.normal range for total T4 concentrations during pregnancy is 1.5 times the nonpregnantiodine :prenatal vitamin 220 mg/day
44Postpartum thyroid disease Postpartum thyroiditisDx: documenting abnormal TSH (elevated or suppressed) levels during the first year postpartum in the absence of positive TSI or a toxic nodulehypo- or hyperthyroidismclassic presentation :transient hyperthyroid phase that occurs 6 weeks to 6 months postpartumfollowed by a hypothyroid phase that lasts for up to 1 year postpartum
45Postpartum thyroiditis autoimmune disorder with a self-limited hyperthyroid phasewithin one year after parturition.PresentationsTransient hyperthyroidism aloneTransient hypothyroidism aloneTransient hyperthyroidism followed by hypothyroidism and then recovery.can also occur after spontaneous or induced abortion3 to 16 percenthigher, up to 25 percent, in women with type 1 diabetes mellitus ,and in women with positive antithyroid antibodies (normal thyroid function)
46Postpartum thyroiditis like painless thyroiditisvariant form of chronic autoimmune thyroiditis (Hashimoto's thyroiditis).high serum concentrations of anti-peroxidase antibodiesmany eventually become hypothyroid or have a goiterhigh serum antithyroid antibody concentrations early in pregnancydecline later (as immunologic tolerance increases during pregnancy)rise again after deliverysubclinical thyroid autoimmune disease early in pregnancy and soon afterProgression to permanent hypothyroidismrelated to higher TSH concentrations and the antiperoxidase antibody titermaternal age and female sex of the infantPostpartum thyroiditis is likely to recur after subsequent pregnancies
47distinguished from Graves' hyperthyroidism, hyperthyroidism in postpartum thyroiditis is usually mild (both clinically and biochemically),thyroid enlargement is minimalGraves' ophthalmopathy is absent.by reevaluation in three to four weeks: postpartum thyroiditis improvedlymphocytic hypophysitis,TSH normal or low, low free T4postpartum thyroiditis, TSH elevated with decreased FT4.
48Postpartum thyroiditis antithyroids :no role.Hypothyroid :may require treatment and somesignificant rate of residual hypothyroidismRecommend:maintain thyroxine until childbearing is complete, with an attempt to wean off medication 1 year after the last deliveryPostpartum--signs/symptoms of thyroid dysfunctionsymptoms mimic normal postpartum changesTSH, free T4, and antithyroid antibodies levelspostpartum depression and postpartum thyroiditis
49Postpartum Graves’ disease 60% Graves’ disease in the reproductive years; postpartum onseteuthyroid patients with Graves’ disease with TSIincreased risk of developing recurrent Graves’ disease if antithyroid medication was withheldTSIs differentiate postpartum Graves’ disease from postpartum thyroiditis with a hyperthyroid component.
50Thyroid cancer Thyroid tumors ;most common endocrine neoplasms. thyroid cancer accounts for 1% of all cancers. ¾ women; 1/2 reproductive years.biopsy ,Serum TSH and free T4 levels,ultrasonography & Fine needle aspirationRadionucleotide scanning is contraindicated during pregnancymalignant or suspicious for papillary cancer, surgery at the earliest safe periodno evidence that pregnancy causes a reactivation of thyroid cancer or that exposure to radioactive iodine poses a risk to future pregnanciesmaintained on thyroid replacement therapy with monitoring of TSH and free T4 levels every 8 weeks.
52Euthyroidism with autoimmune thyroid disease increased risk for spontaneous miscarriage, subclinical hypothyroidism, and postpartum thyroiditisIncrease in serum TSH levelsmost normalpresence of antithyroid antibodieslack of thyroidal reserve in response to the stimulatory effects of pregnancy.
53Euthyroidism with autoimmune thyroid disease recommend initiating levothyroxine therapy in women with antithyroid antibodiesbefore pregnancyTSH level greater than 2.5 mU/L.Serum TSH should be monitored throughout pregnancy in all antithyroid antibody–positive womenmaintain the TSH concentration at 2.5 mU/L or less.
541. HYPOTHYROIDISM AND PREGNANCY: MATERNAL AND FETAL ASPECTS CLINICAL PRACTICE GUIDELINE Management of Thyroid Dysfunction during Pregnancy and Postpartum: An Endocrine Society Clinical Practice Guideline1. HYPOTHYROIDISM AND PREGNANCY: MATERNALAND FETAL ASPECTSmaternal hypothyroidism should be avoided.Targeted case finding is recommended at the first prenatalvisit or at diagnosis of pregnancyIf hypothyroidism diagnosed before pregnancy, adjust preconception T4 dose to reach a TSH ≤2.5 U/ml before pregnancy.T4 dose incremented by 4–6 wk gestation and 30–50% increase in dosage.If overt hypothyroidism is diagnosed during pregnancy, thyroid function tests should be normalized as rapidly as possible.The T4 dosage should be titrated to rapidly ,maintain serum TSH ≤ 2.5 U/ml in the first trimester (or 3 U/ml in the second and third trimesters) or to trimester-specific normal TSH ranges.Thyroid function tests remeasured within 30–40 d.Abalovich et al. • Guideline: Thyroid Dysfunction during and after PregnancyJ Clin Endocrinol Metab, August 2007, 92(8) (Supplement):S1–S47
551.1.6. Subclinical hypothyroidism ;associated with an Women with thyroid autoimmunity who are euthyroid in the early stages of pregnancy are at risk of developing hypothyroidism and should be monitored for elevation of TSH above the normal rangeSubclinical hypothyroidism ;associated with anadverse outcome for both the mother and offspring.T4 treatment - improve obstetrical outcome but has not been proved to modify long-term neurological development in the offspring.Recommends T4 replacement in women with subclinical hypothyroidism.After delivery, most hypothyroid women need adecrease in the T4 dosage they received during pregnancy
562. MANAGEMENT OF MATERNAL HYPERTHYROIDISM: MATERNAL (A) AND FETAL (B) ASPECTS 2.1.a.1. subnormal serum TSHhyperthyroidism must be distinguished from both normal physiology during pregnancy and hyperemesis gravidarumDifferentiation of Graves’ disease from gestational thyrotoxicosis by evidence of autoimmunity, a goiter, and presence of TRAb.2.1.a.2. For overt hyperthyroidism due to Graves’ disease or hyperfunctioning thyroid nodules,ATD therapy should be either initiated (for those with new diagnoses) or adjusted (for those with a prior history)maintain the maternal thyroid hormone levels for free T4 in the upper nonpregnant reference range.2.1.a.3. methimazole may be associated with congenital anomalies, propylthiouracil should be used as a first-line drug,especially during first-trimester organogenesis.Methimazole may be prescribed if propylthiouracil is not available or if a patient cannot tolerate or has an adverse response to propylthiouracil
572.1.a.4. Subtotal thyroidectomy for maternal Graves’ disease if 1) a patient has a severe adverse reaction to ATD therapy,2)persistently high doses of ATD are required3) a patient is not adherent to ATD therapy and has uncontrolled hyperthyroidism.optimal timing of surgery is in the second trimester.2.1.a.5. no evidence that treatment of subclinical hyperthyroidism improves pregnancy outcome2.1.b.1 TRAb (either TSH receptor-stimulating or –binding antibodies) freely cross the placenta and can stimulate the fetal thyroid.These antibodies should be measured before pregnancy or by the end of the second trimester in mothers with current Graves’ disease, with a history of Graves’ disease and treatment with 131I or thyroidectomy, or with a previous neonate with Graves’ disease.Women who have a negative TRAb and do not require ATD have a very low risk of fetal or neonatal thyroid dysfunction.
582.1.b.2. 131I should not be given to a woman who is or may be pregnant. radiation danger to the fetus, including thyroid destruction if treated after the 12th week of gestation.There are no data for or against recommending termination of pregnancy after 131I exposure2.1.b.3. In women with elevated TRAb or in women treated with ATD, fetal ultrasound should be performed to look for evidence of fetal thyroid dysfunctiongrowth restriction, hydrops, presence of goiter, or cardiac failure.2.1.b.4. Umbilical blood sampling should be considered only if the diagnosis of fetal thyroid disease is not reasonably certain from the clinical data and if the information gained would change the treatment.2.1.b.5. All newborns of mothers with Graves’ disease should be evaluated for thyroid dysfunction and treated if necessary
593. GESTATIONAL HYPEREMESIS AND HYPERTHYROIDISM 3.1. Thyroid function tests should be measured in all patients with hyperemesis gravidarum (5% weight loss, dehydration, and ketonuria)3.2. Few women with hyperemesis gravidarum will require ATD treatment.Overt hyperthyroidism believed due to coincident Graves’ disease should be treated with ATD.Gestational hyperthyroidism with clearly elevated thyroid hormone levels (free T4 above the reference range or total T4 150% of top normal pregnancy value and TSH 0.1 U/ml) and evidence of hyperthyroidism may require treatment as long as clinically necessary4. AUTOIMMUNE THYROID DISEASE AND MISCARRIAGE4.1. universal screening for antithyroid antibodies and possible treatment cannot be recommended at this time.
605. THYROID NODULES AND CANCER 5.1. Fine-needle aspiration (FNA) cytology should be performed for thyroid nodules larger than 1 cm.Ultrasound-guided FNA minimizing inadequate sampling.5.2. When nodules are discovered in the first or early second trimester to be malignant on cytopathological analysis or exhibit rapid growth,surgery should be offered in the second trimester before fetal viability.For papillary cancer or follicular neoplasm without evidence of advanced diseaseprefer to wait until the postpartum period for definitive surgeryreassured that most well differentiated thyroid cancers are slow growingsurgical treatment soon after delivery is unlikely to adversely affect prognosis
615.3. administer thyroid hormone to achieve a suppressed but detectable TSH in pregnant women with a previously treated thyroid cancer or an FNA positive for or suspicious for cancer and those who elect to delay surgical treatment until postpartum.High-risk patients benefit from a greater degree of TSH suppressionfree T4 or total T4 levels should ideally not be increased above the normal range for pregnancy.5.4. RAI administration with 131I should not be given to women who are breastfeeding.pregnancy should be avoided for 6 months to 1 yr in women with thyroid cancer who receive therapeutic RAI doses to ensure stability of thyroid function and confirm remission of thyroid cancer.
626. IODINE NUTRITION DURING PREGNANCY 6.1. Women of childbearing age ; average iodine intake 150 g/d.pregnancy and breastfeeding women should increase intake to 250 g6.2. Iodine intake during pregnancy and breastfeeding should not exceed twice the daily recommended nutritional intake for iodine, i.e. 500 g iodine per day6.3. To assess the adequacy of the iodine intake during pregnancy in a population, urinary iodine concentration should be measured in a cohort of the population.Urinary iodine concentration should ideally range between 150 and 250 g/liter.6.4. To reach the daily recommended nutrient intake for iodine, multiple means must be considered, tailored to the iodine intake level in a given population.1) countries with iodine sufficiency and/or with a well established universal salt iodization (USI) program,2) countries without a USI program or an established USI program where the coverage is known to be only partial, and finally3) remote areas with no accessible USI program and difficult socioeconomic conditions.
637. POSTPARTUM THYROIDITIS 7.1. There are insufficient data to recommend screening of all women for PPT.7.2. Women known to be thyroid peroxidase antibody positive should have a TSH performed at 3 and 6 months postpartum7.3. The prevalence of PPT in women with type 1 diabetes is 3-fold greater than in the general population.Postpartum screening (TSH determination) is recommended for women with type 1 diabetes mellitus at 3 and 6 months postpartum7.4. Women with a history of PPT have a markedly increased risk of developing permanent primary hypothyroidism in the 5- to 10-yr period after the episode of PPT.An annual TSH level should be performed in these women.
647.5. Asymptomatic women with PPT who have a TSH above the reference range but less than 10 U/ml and who are not planning a subsequent pregnancy do not necessarily require intervention but should be remonitored in 4–8 wk.Symptomatic women and women with a TSH above normal and who are attempting pregnancy should be treated with levothyroxine.7.6. There is insufficient evidence to conclude whether an association exists between postpartum depression and either PPT or thyroid antibody positivity (in women who did not develop PPT).women with postpartum depression should be screened for hypothyroidism and appropriately treated.
658. SCREENING FOR THYROID DYSFUNCTION DURING PREGNANCY 1. Women with a history of hyperthyroid or hypothyroid disease, PPT, or thyroid lobectomy.2. Women with a family history of thyroid disease.3. Women with a goiter.4. Women with thyroid antibodies (when known).5. Women with symptoms or clinical signs suggestive of thyroid underfunction or overfunction, including anemia,elevated cholesterol, and hyponatremia.
666. Women with type I diabetes. 7. Women with other autoimmune disorders.8. Women with infertility who should have screening with TSH as part of their infertility work-up.9. Women with previous therapeutic head or neck irradiation.10. Women with a history of miscarriage or preterm delivery.
67References1. LeBeau& Mandel.Thyroid Disorders During Pregnancy.Endocrinol Metab Clin N Am 35 (2006) 117–136.2. Neale et al. Thyroid Disease in Pregnancy.Clin Perinatol 34 (2007) 543–557.3. Abalovich et al. • Guideline: Thyroid Dysfunction during and after Pregnancy. J Clin Endocrinol Metab, August 2007, 92(8) (Supplement):S1–S47.4. Kronenber: Williams Textbook of Endocrinology, 11th ed.5. Up To Date ver.15.1