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Thyroid Disease in Pregnancy
Josephine Carlos-Raboca, MD, FPCP, FPSEM Section of Endocrinology, Diabetes and Metabolism History has always associated thyroid with pregnancy.The ancient Greeks tied a reed around a woman’s neck to determine pregnancy; if it broke she is pregnant.Today, goiter is not a nessary companion of pregnancy. Studies show that thyroid increases in volume by 13% not clinically detectable. An increase by more than 20% can be detected but occurs only in iodine deficient populations. Metabolic alterations whether as physiologic response to stress or otherwise can uncover latent thyroid disorders in a pregnant woman. Makati Medical Center
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Outline Thyroid Physiology in Pregnancy Maternal Fetal
Gestational Thyrotoxicosis Grave’s Disease in Pregnancy Hypothyroidism Postpartum thyroiditis
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Pregnancy and Thyroid Function
The production, circulation and disposal of thyroid hormones are all altered during pregnancy. History has always associated thyroid with pregnancy.The ancient Greeks tied a reed around a woman’s neck to determine pregnancy; if it broke she is pregnant.Today, goiter is not a nessary companion of pregnancy. Studies show that thyroid increases in volume by 13% not clinically detectable. An increase by more than 20% can be detected but occurs only in iodine deficient populations. Metabolic alterations whether as physiologic response to stress or otherwise can uncover latent thyroid disorders in a pregnant woman.
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H - P Thyroid Axis
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Thyroid Hormone production
TRH - hypothalamus TSH - pituitary TSH – receptor on thyroid cell Thyroglobulin (Tg) - thyroid Thyroid peroxidase - thyroid Iodine T4(80%) T3 (20%) In non pregnant 150 ug/day
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Maternal Physiology Thyroid circulation Thyroxine clearance rate
Dietary iodine requirement hCG mediated thyroid stimulation
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Thyroid circulation T4 and T3 are highly bound to proteins:
Thyroid binding globulin (TBG)( 70%) Transthyretin (TBPA) Albumin Unbound Free T4(0.02%) Free T3 (0.3%)
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Thryoxine binding globulin(TBG)
Increased serum (TBG) due to estrogen induced sialylation of the protein which leads to decreased renal clearance and longer half life ( from normal 15 minutes, increased to 3 days) Carbohydrate portion determines renal clearance due to increased sialic acid .High estrogen increase in sialylation of TBG leading to reduced cleasrac and increase concentrations of circulating TBG. TT3 and T$ levels are increased throughout pregnancy. T4 in pregnanct women are generally 1.5x those in nonpregnant. FT3 and FT4 remain in normal range except in late first trimester when they may be high or or highnormal. However no trimester-specific reference ranges for FT4 assays exist and FT4 may over or underestimate FT4 concetnrations in pregnant women.
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Effects of Increased TBG
Increased total T3 and total T4 Free hormone assay are thus preferred FT4I should be done if free hormone determination is not available
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Thyroid Disposal/Clearance
Iodinase Type 1 – liver, kidney, thyroid converts T4 to T3 Type 2 - pituitary, brown fat, brain converts T4 to T3 Type 3 – placenta brain and skin converts T4 to rT3 and T3 to T2 Iodine is recirculated or cleared by kidneys in pregnant, passes to fetus (1 and 2 deiodinase are 5’ deiodinase or outer phenolic ring site of action)type 3 deiodinase is an inner tyrosyl ring site of action
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Increased demand for iodine
Increased GFR Increased iodide clearance by the kidney Siphoning of maternal iodide by the fetus WHO: RDA 200 ug/day during pregnancy
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Increased demand for thyroid hormones
Increased iodide clearance Transplacental transfer of T4 and iodine Placental degradation of T4
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Thyroid stimulation by chorionic gonadotropin
Similarity of TSH and HCG alpha subunit is common to TSH, hCG, FSH and LH Beta subunit is specific but some similarity in TSH and hCG HCG stimulates TSH receptor has weak thyrotropic activity 1/10000 of TSH
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Normal pregnancy TSH suppressed when hCG are highest at 8-12 weeks of gestation Free T3 or T4 were significantly elevated at a time when hCG were maximal TSH suppressed 18% in first trimester 5% in second trimester 2% in third trimester Glinoer J of Clin Invest 1993 A recent study by Spencer 95%confidence interval in first trimester in women without thyroid disease lower limit is 0.03 mU/L.
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Thyroid stimulation by hCG
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Physiologic changes in pregnancy and thyroid function test
Increased TBG First trimester hCG elevation Increased plasma volume Increased plasma type 3 deiodinase Thyroid enlargement Increased iodine clearance Thyroid function test change Elevation of T4 and T3 Elevated FT4 and suppressed TSH Increased T4 and T3 pool size Potential increased T4 and T3 degradation Increased serum Tg Reduced hormone production in iodine insufficient HCG is a weak thyroid stimulator binding to TSH receptor. In first trimester when HCG are highest TSH are often below normal or at the low end of usual normal range. It has been suggest that a conservative uper limit in first tirmest is 2.5 mU/L. A recent study 95% CI for first tirmester in women free of thyroid disease is 0.03 mU/L (Spencer)
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Fetal Ontogeny and Physiology
T3 dependent CNS development Thyroid organogenesis, iodine concentration and hormonogeneiss Dependence on maternal iodothyronines
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Thyroid Hormones and Fetal Brain Development
Nervous system development and brain differentiation synaptogenesis growth of dendrites and axons myelination neuronal migration
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Thyroid Deficiency in the Fetus and Neonate
2 sources of thyroid hormones in fetus Fetal thyroid which begins synthesis at 10 – 12 weeks Maternal thyroid hormones -current evidence shows substantial transfer across the placenta -placenta contains deiodinase that converts T4 to T3
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Thyroid Tests Thyroid Hormones – TT3,TT4, FT3, FT4 FT4I, TSH
Thyroid antibodies TPOAb,TgAb, TSHRAb (TSI,TBII) 5-10% 0f pregnant women without thyroid funciton abnormalities have detectable seum antithyroid antibody levels in first trimester.
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Hyperthyroidism Etiologies Clinical presentations Diagnosis
Maternal and fetal consequences Therapeutic options
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Hyperthyroidism Occurs in 1-2/1000 pregnancies
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Causes of hyperthyroidism in pregnancy
Grave’s Disease Gestational Thyrotoxicosis Hydatidiform mole Silent Thyroiditis Multinodular toxic goiter Toxic adenoma Subacute thyroiditis Iatrogenic hyperthyroidism\Iodine induced hyperthyroidism
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Case 1 Leah a 25 year old G1P0 female was confined on her 10th week of gestation because of nausea and vomiting several times daily requiring parenteral fluids. She was referred to you for endocrine evaluation. 2 weeks earlier she was confined for the same problem and gastroscopy was done which was negative.
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Case 1 She has not had any weight gain since start of pregnancy. She had no history of thyroid problem. PE showed no goiter, no tremors nor eye signs. BP was normal. Pulse rate was 92/minute and was afebrile.
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Thyroid Function tests
FT3 RIA pmol/l (4.2-12) FT4 RIA 25 pmol/l (8.8-33) TSH IRMA uIU/ml (0.35 – 5.0)
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Question What is your likely diagnosis? differential diagnosis?
Vs Grave’s hyperthyroidism trophoblastic tumors(molar pregnancy0hCG>100u/ml
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Conditions with suppressed TSH
Increased thyroid hormone production Grave’s Disease Autonomous Thyroid nodule Hyperemesis gravidarum Molar Pregnancy First trimester pregnancy Hyperthyroidism occurs in 1 – 2/1000 pregancies
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Conditions with Suppressed TSH
Normal or Low Thyroid Production Post therapy of hyperthyroidism Pituitary/hypothalamic disease Severe nonthyroidal illness
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Conditions with suppressed TSH
Inflammatory Thyroiditis (usually subacute) Medications high dose L-T4 or T3 dopamine glucocorticoids Acute response to somatostatin and analogs(octreotide)
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Hyperemesis Gravidarum
Severe nausea and vomiting in pregnancy resulting in weight loss and fluid and electrolyte disturbance 60% with suppressed TSH 50% with elevated FT4 (Goodwin 1995;JCEM 75: ) Less than 15% have elevated FT3 or FT3 index (clinical useful test to distinguish from Grave’s) Occurs early 6-9 weeks of gestation
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Gestational Thyrotoxicosis
Spectrum of hCG-induced hyperthyroidism which ranges from an isolated subnormal TSH concentration(up to 18%) to elevation of free thyroid hormone levels in the clinical setting of hyperemesis gravidarum
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Question 2 Will you treat? Treatment is not generally recommended.
Is vomiting related to hyperthyroidism? Not likely Vomiting seen in hypothyroid, euthyroid and hyperthyroid, probably related to hCG induced elevation of estradiol
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Question 3 How will you follow up?
Repeat thyroid function tests after 20th week If persistent hyperemesis and elevated thyroid hormones and suppressed TSH after 20 weeks of gestation consider antithyroid treatment as this may be mild Grave’s disease.
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Gestational Thyrotoxicosis
Transient Symptoms usually resolve within 10 weeks of diagnosis Differs from Grave’s Non-autoimmune etiology (hCG induced) with negative anti thyroid and anti TSH receptor antibody Negative goiter Resolution in almost all patients after 20 weeks of gestation No ophthalmopathy Hyperemesis gravidarum is defined as persistent vomiting, ketonuria and at least 55 weight loss. The severity of nauseas and vomiting has been shoen to correlated with degree of TSh suppression. Hyperemesis gravidarum may be accompanied by gestation thyrodtoxicosis induced by a more bioactive HCG.
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Case 2 Luisa a 30 year old G2P1 female was referred to you on her 12th week of pregnancy because of hypertension, palpitations and weight loss of 5 lbs since start of pregnancy. BP was 145/95 despite bed rest. Cardiologist gave apresoline 10 mg tid. Urinalysis was negative for protein.
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Case 2 Prominent eyes were noted so endocrine referral was sought. Further history taking revealed hyperthyroidism 3 years ago with ATD treatment for 1 year. On PE, BP was 140/90 PR 110/minute, with positive lid retraction, diffuse goiter and bruit and fine hand tremors. No leg edema
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Thyroid tests FT3 RIA 15 pmol/l ( 4.2-12) FT4RIA 55 pmol/l (8.8 – 33)
TSH-IRMA uIU/L ( )
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Question 1 What is your likely diagnosis? Chronic hypertension
Grave’s – eye signs, goiter, bruit
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Diagnosis of Grave’s Symptoms of hypermetabolic state
Sometimes goiter with bruit Eye signs Elevated free T3 and freeT4 Suppressed TSH RAIU elevated(not done in pregnant) Elevated TgAb and TPOAb TSH-R Ab positive
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Grave’s Hyperthyroidism
Positive thyroid antibodies TPOAb TgAb TSHRAb (TSI) Unusual to present for the first time in pregnancy Symptoms usually antedate pregnancy for a few months
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Question 2 What are other tests are useful to confirm your diagnosis if available? TPOAb TgAb TSHRAb/TSI – to differentiate from silent thyroiditis
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Question 3 What is your treatment of choice?
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Which ATD is best? PTU favored because:
MMI has been associated with aplasia cutis a congenital scalp defect (Mandel 1994 Thyroid 4: ) PTU is heavily protein bound and believed to cross placenta less 6 women without history of thyroid disease received a single injection of either (35S)MMI or PTU in the first half of pregnancy prior to a therapeutic abortion (Marchant 1977 JCEM 45: )
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Which ATD is best? an in vitro study showed two drugs equally passed placental barrier (Mortimer 1997 JCEM 82:3099) no prospective RCTs compared maternal and fetal outcome; retrospective case series have shown that the rate of fetal hypothyroidism is similar with both drugs (Wing 1994 Am J Obstet Gynecol 170:90)
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What is the dose of ATD in pregnant?
Initial dose may vary according to severity of maternal hypothyroidism Use the lowest dose possible to maintain maternal euthyroidism mg MMI or 300 mg PTU In 30% ATD may be discontinued in last trimester Althoug most studies hav enot foung a clear dose-response relationship between antithroydid drug doses and the risk for neonatal thyroid dysfucntiuon, low doses are recommended to keep FT4 in high normal to slightly thyrotoxic rnage to reduce risk of severe neonatal hypothyroidism and goiter due to transplacental passage. SEveal studies have demonstrated that there are no cognitive delays in the children of mother who took antithyroid medicaitons in pregnancy. If US shows neonatal goiter stop ATD.
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Relation between maternal ATD dose and neonatal function
Direct correlation Lamberg preg CM Mortimer PTU or CM Mitsuda MMI or PTU No dose response Cheron PTU Gardaner PTU Momotani MMI or PTU Momotani MMI or PTU
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PTU vs MMI on fetal thyroid status in maternal Grave’s Momotani1997 JCEM 82:3633
77 pregnant 34 PTU 43 MMI 32 pregnant controls Conclusion: fetal cord blood free T4 levels did not differ among groups Mean fetal cord blood TSH was similar in both ATD treated groups which was higher for each group vs control group Data suggest both groups can safely be used in pregnancy
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No data comparing maternal and cord levels simultaneously for MMI
Correlation of maternal PTU concentrations with cord serum thyroid function test Gardner 1986 JCEM 62: PTU given till term showed PTU concentration in cord higher than maternal levels No data comparing maternal and cord levels simultaneously for MMI
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Effect of ATD overdose on fetus
fetal goiter which may lead to respiratory distress Intrauterine growth retardation 4 studies showed no defects in either cognitive or somatic development of children exposed to maternal ATD in utero but maternal thyroid hormone levels not known
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PTU vs MMI Duration of action short long Potency less more
Placental passage about 1 prob 1 Breast milk less more Toxicity aplasia cutis Other blocks T4 to T3
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Question 4 What are your treatment goals?
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Guidelines for clinical management of maternal hyperthyroidism during pregnancy
Use the lowest dose of ATDs to maintain maternal thyroid hormone levels in the upper 1/3 of the normal range to slightly elevated during pregnancy.(FT pmol/l or ng/dl)
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Guidelines for clinical management of maternal hyperthyroidism during pregnancy
Check maternal thyroid hormone levels monthly, using free T4 levels Measure TSI/TBII at weeks Consider fetal ultrasound at weeks if the TSI/TBII levels are elevated or if Doppler detects fetal tachycardia
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Hyperthyroidism guidelines
If either high maintenance ATD doses are required (ie PTU>600 mg/day, MMI . 40 mg/day) or if a patient is non-adherent or allergic to ATD therapy, surgery (ie subtotal thyroidectomy) should be considered.
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Hyperthyroidism guidelines
Low doses of iodides may be used transiently, especially pre-operatively frequent communication between the endocrinologist and obstetrician is essential so that ATD dose titration is performed with monitoring of fetal growth.
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If maternal FT4 levels are decreased, all neonates have decreased FT4
Antithyroid drug therapy for Grave’s disease during pregnancy Momotani 1986 NEJM 316:24-28 If maternal FT4 is either elevated or in upper 1/3 of normal, more than 90% of neonates have normal FT4 If maternal FT4 is in lower 2/3 of normal, 36% of neonates have decrease FT4 If maternal FT4 levels are decreased, all neonates have decreased FT4
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Other forms of treatment
Beta adrenergic blockers –may be used transiently to control adrenergic symptoms ( small series where propranolol was prescribed for 6-12 weeks reported higher rates of miscarriages) Iodides should not be used but may be used if needed to prepare for thyroidectomy Surgery in latter half of second trimester
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Question 5 What are maternal and fetal consequences of hyperthyroidism?
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Pregnancy complications reported in hyperthyroid women
Maternal pre-ecclampsia(14% if untreated vs 6%for treated) Gestational hypertension pregnancy-induced hypertension placental abruption Congestive heart failure(63% if untreated) Preterm labor(88% if untreated; 25% partial treatment 8% if adequate treatment)
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Other potential complications of uncontrolled hyperthyroidism
Maternal Anemia Miscarriage Thyroid storm Fetal prematurity
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Pregnancy complications reported in hyperthyroid women
Fetal Small for gestation age Intrauterine growth retardation Stillbirth (50% if untreated, 16% partial treatment) Fetal/neonatal hyperthyroidism
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ATDs:effect on fetus Maternal factors: Maternal ATD dosage
TSH receptor antibody Maternal thyroid status
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Course of Grave’s in Pregnancy Mestman 1997 Clin Obstet Gynecol 40:45-64
occurs in 1 in 500 pregnancies Fluctuates during gestation Aggravates at weeks Subsequent improvement In third trimester a time of immune tolerance, ATD can be reduced or decreased in 30% Worsens or reactivates in postpartum period
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Case 3 Marissa a 32 year old G5P2 Ab2 female was referred on her 8th weeks of pregnancy because of easy fatigability and hypertension. Her weight gain was 5 lbs in 8 weeks.
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Case 3 Patient had radioactive treatment 3 years ago for Grave’s disease and is on levthyroxine replacement 75 mcg/day. Last thyroid tests were 10 weeks ago and were normal. PE showed BP 145/95 Pulse rate was 70/minute no goiter, DTR were hypoactive.
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Thyroid tests FT3RIA 3.8 pmol/L (4.2 – 12)
TSHIRMA 25 uIU/ml (0.35 – 5.0)
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Question 1 What is your diagnosis? Hypothyroidism in Pregnancy
Hypertension Is this expected? Reason of hypertension not clear but may be due to reduced cardiac output with increased peripheral resistance and increased ympathetic nervous tone an alpha adrenergic response.
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Diagnosis of hypothyroidism
Nonspecific signs fatigue Weight gain Constipation Edema TSH is first line screening test
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Thyroid hormone therapy during pregnancy
Increased requirement during pregnancy By about 45% in one study (12 patients)Mandel et al NEJM 1990 By 67 ug/day in another study Appeared early in first trimester and throughout pregnancy Need to saturated TBG binding sites, increased T4 clearanceand decreased T4 absorption late pregnancy
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Question 2 How will you adjust your dose?
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Treatment of hypothyroidism in pregnancy
Initial dosage 150 mcg/day or 2 mcg/kg actual body weight Readjustment TSH high but <10mU/ml add mcg/day TSH>10<20 add75mcg/day TSH>20 add 100 mcg/day
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Hypothyroidism Start with a daily dose of 2 mcg/kg per day
If TSH is minimally elevated(ie 10 mU/L in pregnancy, a mg of levothyroixine per day often is adequate
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guidelines for clinical management of maternal hypothyroidism
Check serum TSH early in pregnancy Adjust levothyroxine dosage to maintain a normal serum TSH. Increment in dosage may depend on etiology of hypothyrodism. Athyreosis(Grave’s after I-131 therapy) – 45% increment
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guidelines for clinical management of maternal hypothyroidism
Hashimoto’s thyroiditis – 25% increment Subclinical hypothyroidism may not require increment TSH should be monitored every 8-10 weeks or if a dose adjustment is made, should be checked 4 weeks later. 25% of those with initial normal serum TSH levels in the first trimester and 37% of those with initial normal serum TSH in second trimester will later require dosage increases
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Hypothyroidism Patients should be instructed to separate levothyroxine ingestion and prenatal vitamin containing iron or iron supplements by at least 6 hours After delivery, the levothyroxine dose should be reduced to prepregnancy dosage and the serum TSH level should be rechecked at 6 weeks postpartum
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Question 3 The patient asks you on possible consequences to baby What will you tell her?
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Complications in Pregnant Hypothyroidism
Maternal Gestational hypertension- 22% in overt, 15% in subclinical,7.6% in general population Pre-ecclampsia Pregnancy induced hypertension Postpartum hemorrhage Anemia- 31% in overt, 0% in subclinical Placenta abruption 18% in overt, 0% in subclinical
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Maternal consequence of Hypothyroidism
25756 singleton pregnancies 2.3% had subclinical hypothyroidism Placental abruption occurred more often (RR 3.9, 95% CI Preterm birth (<34 weeks) more common (RR 1.8, 95% CI ) Casey Obstetric Gynecol 2005;105:
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Complications In Pregnant Hypothyroidism
Fetal Small for gestational age – 22% in overt, 9% in subclinical, 6-8% in general population Stillbirth – 56% in overt, 6% in subclinical Transient congenital hypothyroidism due to transplacental passage of maternal blocking antibodies Possible impairment in cognitive function Impaired somatic development Not confirmed in other studies
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Implications of hypothyroidism in pregnancy
11 pregnancies T4 2.3 ug/dl TSH 105 mU/L 8 treated: no complication but 1 Trisomy 21 in 41 year old mother 3 untreated:1 IUFD 2 normal births all infants normal at 3 years old Montoro Ann of Int Medicine In papers over the last 15 years better outcome Previously, report of successful pregnancy even in untreated. Placental passage of T4 even at low levels in mother
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Hypothyroidism in pregnancy
9403 singleton pregnancies TSH >6mU/L in 2% Fetal death OR 4.4 CI Allan WC J Med Screening 2000;7:127
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Maternal hypothyroidism during early pregnancy and intellectual development in progeny
8 children exposed to hypothyroidism in early pregnancy (4-10 years) 9 control siblings 4-15 years Conclusion no difference in IQ Liu 1994 Arch Int Medicine
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Consequence of hypothryoidism in pregnancy
TSH measured in pregancnt women 47 women TSH >99.7th tile 15 with TSH 98-99th tile + low T4 124 matched women with normal TSH At 7-9 y/o had 15 test for intelligence, attention, language, reading abililty, school performance and visual motor performance Haddow NEJM 1999:341;549
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Haddow study in 62 children born to women with
TSH mean 13.4 vs 1.4 in control on 17th week of gestation FT4 0.7 vs 1 ng/dl Lower performance on all 15 tests, IQ average 4 points lower More had IQ <85 (15% vs 5%) Children of 48 mothers untreated for hypothyroidism had IQ average 7 points lower (p0.005) with 19 scoring <85
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Haddow study Conclusions
Decreased intellectual and school performance in children exposed to mild asymptomatic hypothyroidism intellectual and school performance was not affected if hypothyroidism was treated with thyroxine replacement even if not adequate
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Maternal thyroid peroxidase antibodies during pregnancy: a marker of impaired child development?
Lower IQ in children of euthyroid mothers with elevated TPO-ab vs negative TPO ab titers Pop et al JCEM 1995
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No congenital anomalies in most studies
In humans, it is still still poorly understood why some very hypothyroid women even if untreated may deliver seemingly normal children It is unknown if there is a critical threshold of maternal thyroid hormone level or if in some cases T4 may be inactivated to a greater extent by placental deiodinases
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Euthyroidism must be reached in a timely fashion
Surveillance needed throughout pregnancy
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Screening Insufficient evidence to support population bases screening
However aggressive case finding is appropriate in pregnant women Surks JAMA 2004;291:228
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Case 4 Isabel a 40 year old G7P7 female was referred to you 3 months after delivery because of sluggishness and depression. Upon further history you elicited sore throat and neck pain accompanied by palpitations 1 month after delivery which lasted for 2 weeks. ENT consult was done and was given antibiotics. PE showed a diffuse non tender goiter, no cervical lymphadenopathy.
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Thyroid tests FT pmol/l FT pmol/l TSH 15 uIU/ml
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Question 1 What are your considerations?
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Postpartum thyroid disease
Spectrum of autoimmune thyroid diseases Postpartum thyroid disease Subacute thyroiditis Hashimoto’s thyroiditis Grave’s (recurrence)
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Postpartum thyroiditis vs subacute (de Quervain’s)
PPT SAT painless painful TPOab high neg or low Tgab high neg or low ESR slightly high very high
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Risks for postpartum thyroid disease
High risk: Prior episode of PPTD History of Hashimoto’s or Grave’s disease Type 1 diabetes mellitus Recurrent miscarriages Moderate risk Goiter Family history of thyroid disease
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Three phases of PPTD Transient hyperthyroidism due to leakage of hormone low RAIU, not pain, ESR normal or slightly elevated lymphocytic thyroiditis 2-3months up to 6 months post partum Transient hypothyroidism euthyroidism
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Postpartum thyroiditis
8-10% of women Temporary period of hyperthyroidism of 6 weeks to 3 months postpartum No treatment for hyperthyroid phase but beta blockers may be used to relieve symptoms 6-12 months of LT4 in hypothyroid phase; some long term
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Subacute Thyroiditis Granulomatous type Painful RAIU – 0 ? viral
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Question 2 What other tests will you request?
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Diagnostic tests RAIU - 2hrs, 5% (NV = 5-12%) 24 hrs, 15% (NV = %) ESR mml/hr TGAb IU/ml (NV = ) TPOAb IU/ml (NV = 0-100) Antibodies present in 75%
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Question 3 How will you manage this patient?
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Treatment for PPTD Levothyroxine if hypothyroidism is symptomatic
hypothyroidism may occur up to one year postpartum Persistent or new hypothyroidism occurs in about 25% after one year.. May be a transition to Hashimotos’s thyroiditis
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Summary Slide Thyroid disorders should be considered in pregnancy in patients at risk. Signs and symptoms may be misleading so there should be a high index of suspicion. Thyroid tests should be used and interpreted in the light of physiologic changes during pregnancy. Judicious treatment is critical to assure success in pregnancy outcome
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Thank You!
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