1. 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

2. Outline Thyroid Physiology in Pregnancy Maternal Fetal
Gestational Thyrotoxicosis
Grave’s Disease in Pregnancy
Hypothyroidism
Postpartum thyroiditis

3. 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.

4. H - P Thyroid Axis

5. 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

6. Maternal Physiology Thyroid circulation Thyroxine clearance rate
Dietary iodine requirement
hCG mediated thyroid stimulation

7. 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%)

8. 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.

9. 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

10. 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

11. 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

12. Increased demand for thyroid hormones
Increased iodide clearance
Transplacental transfer of T4 and iodine
Placental degradation of T4

13. 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

14. 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.

15. Thyroid stimulation by hCG

16. 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)

17. Fetal Ontogeny and Physiology
T3 dependent CNS development
Thyroid organogenesis, iodine concentration and hormonogeneiss
Dependence on maternal iodothyronines

18. Thyroid Hormones and Fetal Brain Development
Nervous system development and brain differentiation
synaptogenesis
growth of dendrites and axons
myelination
neuronal migration

19. 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

20. 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.

21. Hyperthyroidism Etiologies Clinical presentations Diagnosis
Maternal and fetal consequences
Therapeutic options

22. Hyperthyroidism
Occurs in 1-2/1000 pregnancies

23. 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

24. 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.

25. 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.

26. 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)

27. Question What is your likely diagnosis? differential diagnosis?
Vs Grave’s hyperthyroidism trophoblastic tumors(molar pregnancy0hCG>100u/ml

28. 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

29. Conditions with Suppressed TSH
Normal or Low Thyroid Production
Post therapy of hyperthyroidism
Pituitary/hypothalamic disease
Severe nonthyroidal illness

30. Conditions with suppressed TSH
Inflammatory
Thyroiditis (usually subacute)
Medications
high dose L-T4 or T3
dopamine
glucocorticoids
Acute response to somatostatin and analogs(octreotide)

31. 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

32. 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

33. 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

34. 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.

35. 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.

36. 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.

37. 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

38. Thyroid tests FT3 RIA 15 pmol/l ( 4.2-12) FT4RIA 55 pmol/l (8.8 – 33)
TSH-IRMA uIU/L ( )

39. Question 1 What is your likely diagnosis? Chronic hypertension
Grave’s – eye signs, goiter, bruit

40. 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

41. 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

42. Question 2
What are other tests are useful to confirm your diagnosis if available?
TPOAb
TgAb
TSHRAb/TSI – to differentiate from silent thyroiditis

43. Question 3
What is your treatment of choice?

44. 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: )

45. 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)

46. 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.

47. 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

48. 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

49. 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

50. 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

51. 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

52. Question 4
What are your treatment goals?

53. 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)

54. 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

55. 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.

56. 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.

57. 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

58. 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

59. Question 5
What are maternal and fetal consequences of hyperthyroidism?

60. 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)

61. Other potential complications of uncontrolled hyperthyroidism
Maternal
Anemia
Miscarriage
Thyroid storm
Fetal
prematurity

62. Pregnancy complications reported in hyperthyroid women
Fetal
Small for gestation age
Intrauterine growth retardation
Stillbirth (50% if untreated, 16% partial treatment)
Fetal/neonatal hyperthyroidism

63. ATDs:effect on fetus Maternal factors: Maternal ATD dosage
TSH receptor antibody
Maternal thyroid status

64. 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

65. 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.

66. 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.

67. Thyroid tests FT3RIA 3.8 pmol/L (4.2 – 12)
TSHIRMA 25 uIU/ml (0.35 – 5.0)

68. 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.

69. Diagnosis of hypothyroidism
Nonspecific signs
fatigue
Weight gain
Constipation
Edema
TSH is first line screening test

70. 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

71. Question 2
How will you adjust your dose?

72. 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

73. 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

74. 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

75. 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

76. 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

77. Question 3
The patient asks you on possible consequences to baby What will you tell her?

78. 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

79. 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:

80. 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

81. 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

82. 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

83. 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

84. 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

85. 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

86. 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

87. 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

88. 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

89. Euthyroidism must be reached in a timely fashion
Surveillance needed throughout pregnancy

90. Screening Insufficient evidence to support population bases screening
However aggressive case finding is appropriate in pregnant women
Surks JAMA 2004;291:228

91. 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.

92. Thyroid tests
FT pmol/l
FT pmol/l
TSH 15 uIU/ml

93. Question 1
What are your considerations?

94. Postpartum thyroid disease
Spectrum of autoimmune thyroid diseases
Postpartum thyroid disease
Subacute thyroiditis
Hashimoto’s thyroiditis
Grave’s (recurrence)

95. 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

96. 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

97. 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

98. 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

99. Subacute Thyroiditis
Granulomatous type
Painful
RAIU – 0
? viral

100. Question 2
What other tests will you request?

101. 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%

102. Question 3
How will you manage this patient?

103. 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

104. 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

105. Thank You!