MANAGEMENT OF THYROID DISORDERS IN PREGNANCY

1. THYROID DISORDERS IN
PREGNANCY
Dr G.venkata ramana
HOD Family medicine
RDT hospital Bathalapalli

2. Case scenario 1
• ANC with 8 weeks of gestation came to OPD.
• Her TSH <0.05 micro IU/ml
• Free T4 1.30 ng/dl (0.93-1.70)
• What is the diagnosis?
• What is the management?

3. Case scenario 2
• ANC with 8 weeks of gestation came with
complaints of excessive vomiting
• Her TSH <0.05 micro IU/ml
• Free T4 1.80 ng/dl
• What is the diagnosis?
• What is the management plan?

4. Case scenario 3
• ANC with 10 weeks of gestation came to OPD for
normal check up.No vomiting,no twin gestation.
• O/E thyroid enlarged ,PR 140/min,tremors
present
• Her TSH<0.05 micro IU/ml
• Free T4 2.70 ng/dl
• What is the diagnosis?
• What is the management plan?

5. Case scenario 4
• ANC with 6 weeks of gestation k/c/o Graves
disease on carbimazole came to opd
• Her TSH 2.5 micro IU/ml
• Free T4 1.30 ng/dl
• What is the management plan?

6. Case scenario 5
• ANC with 9 weeks of gestation came to OPD
• Her TSH 7.0 micro IU/ml
• Free T4 1.40 ng/dl
• What is the diagnosis?
• What is the management plan?

7. Case scenario 6
• ANC with 6 weeks of gestation came to opd
• Her TSH >100 micro IU/ml
• Free T4 0.20 ng/dl
• What is the diagnosis?
• What is the management plan?

8. Case scenario 7
• ANC with 8 weeks of gestation came to opd
• Her TSH 3.8 micro IU/ml
• Free T4 1.40 ng/dl TPO antibodies positive
• What is the diagnosis?
• What is the management plan?

9. Case scenario 8
• ANC with 6 weeks of gestation k/c/o
hypothyroidism came to opd
• Her TSH 2.5 micro IU/ml
• Free T4 1.40 ng/dl
• What is the management plan?

10. Functional Anatomy,Physiology of Thyroid

11. Functions of Thyroid hormone
Target Tissue Effect of hormone Mechanism
Heart Chronotropic and
inotropic
Increased number of β-adrenergic receptors
Enhanced responses to circulating catecholamines
Increased proportion of α-myosin heavy chain
(with higher ATPase activity)
Adipose tissue Catabolic Stimulated lipolysis
Muscle Catabolic Increased protein breakdown
Bone Developmental Promote normal growth and skeletal development
Nervous
system
Developmental Promote normal brain development
Gut Metabolic Increased rate of carbohydrate absorption
Lipoprotein Metabolic Formation of LDL receptors
Others Calorigenic Stimulated oxygen consumption by metabolically
active tissues (exceptions: testes, uterus, lymph
nodes, spleen, anterior pituitary) Increased
metabolic rate

12. • Hepatic conversion of carotene to vitamin A, and the accumulation
of carotene in the bloodstream (carotenemia) in hypothyroidism is
responsible for the yellowish tint of the skin.
• Milk secretion is decreased in hypothyroidism and stimulated by
thyroid hormones
• Essential for normal menstrual cycles and fertility
• The skin normally contains a variety of proteins combined with
polysaccharides, hyaluronic acid, and chondroitin sulfuric acid.
• In hypothyroidism, these complexes accumulate, promoting water
retention and the characteristic puffi ness of the skin (myxedema)
• Thyroid hormones also exert effects on reflexes. The reaction time
of stretch reflexes is shortened in hyperthyroidism and prolonged
in hypothyroidism

13. How to interpret thyroid function results?
TSH Free T4 Free T3 interpretation
Undetectable Raised Raised Primary
thyrotoxicosis
Undetectable Normal Raised Primary T3-toxicosis
Undetectable Normal Normal Subclinical
thyrotoxicosis
Elevated high High Secondary
thyrotoxicosis

14. How to interpret thyroid function results?
TSH Free T4 Free T3 interpretation
Mildly elevated 5-
20 mU/l
Low Low Primary
hypothyroidism
Secondary
hypothyroidism
Elevated > 20 mU/l Low Low Primary
hypothyroidism
Mildly elevated 5-
20 mU/l
Normal Normal Subclinical
hypothyroidism
Normal Low Low Secondary
hypothyroidism

15. • Overt hyperthyroidism
• Low thyroid-stimulating hormone [TSH]
• Elevated free thyroxine [T4] and/or triiodothyronine
[T3]
• Subclinical hyperthyroidism
• Low TSH, with
• Normal free T4 and T3

16. THYROID PHYSIOLOGY DURING NORMAL
PREGNANCY
• Major changes in thyroid function during pregnancy:
• An increase in serum thyroxine-binding globulin (TBG)
• estrogen increases TBG production and TBG sialylation,
which results in decreased clearance of TBG
• TBG excess leads to an increase in both serum total,
but not free, T4 and T3 concentrations
• Stimulation of the thyrotropin (TSH)receptor by
human chorionic gonadotropin (hCG)
• There is considerable homology between the beta
subunits of hCG and TSH. As a result, hCG has weak
thyroid-stimulating activity

17. Clinical manifestations

19. Pregnancy complications hyperthyroidism
• Spontaneous abortion
• Premature labor
• Low birth weight
• Stillbirth
• Preeclampsia
• Heart failure

20. Causes of hyperthyroidism
Hyperthyroidism with a normal or
high radioiodine uptake
• Autoimmune thyroid disease
• Graves' disease
• Hashitoxicosis
• Autonomous thyroid tissue
• Toxic adenoma
• Toxic multinodular goiter
• TSH-mediated hyperthyroidism
• TSH-producing pituitary adenoma
• Non-neoplastic TSH-mediated
• Human chorionic gonadotropin-
mediated hyperthyroidism
• Hyperemesis gravidarum
• Trophoblastic disease
Hyperthyroidism with a near absent
radioiodine uptake
• Thyroiditis
• Subacute granulomatous
• Painless thyroiditis
• Amiodarone
• Checkpoint inhibitor-induced
• Radiation thyroiditis
• Palpation thyroiditis
• Exogenous thyroid hormone intake
• Excessive replacement therapy
• Intentional suppressive therapy
• Factitious hyperthyroidism
• Ectopic hyperthyroidism
• Struma ovarii
• Metastatic follicular thyroid cancer

21. Common causes in pregnancy
• Graves' disease (occurring in 0.1 to 1 percent
of all pregnancies)
• human chorionic gonadotropin (hCG)-
mediated hyperthyroidism due to gestational
transient thyrotoxicosis (1 to 3 percent of
pregnancies)

22. Graves' disease
• Hyperthyroidism, goiter, thyroid eye disease
(orbitopathy), and occasionally a dermopathy
referred to as pretibial or localized myxedema.
• Autoimmune disorder
• The presence of TRAbs in serum and thyroid eye
disease on clinical examination distinguishes the
disorder from other causes of hyperthyroidism.
• The thyroid gland is usually, but not always,
diffusely enlarged

23. hCG-mediated hyperthyroidism
• During normal pregnancy, serum human chorionic gonadotropin
(hCG) concentrations rise soon after fertilization and peak at 10 to
12 weeks gestation, after which time the levels decline.
• There is considerable homology between the beta-subunits of hCG
and TSH.
• As a result, hCG has weak thyroid-stimulating activity and may
cause hyperthyroidism during the period of highest serum hCG
concentrations
• Include gestational transient thyrotoxicosis (GTT), hyperemesis
gravidarum, and trophoblastic hyperthyroidism

24. Gestational transient thyrotoxicosis
• During the time of peak hCG concentrations (10 to 12 weeks), total
serum T4 and T3 concentrations increase. Serum free T4 and T3
concentrations increase slightly, usually within the normal range,
and serum TSH concentrations are appropriately reduced.
• Thus, in some women, the high serum concentration of hCG during
early pregnancy can lead to subclinical or mild overt
hyperthyroidism. This phenomenon is called GTT.
• It occurs near the end of the first trimester, and symptoms (if
present) and thyroid hyperfunction subside as hCG production falls
(typically 14 to 18 weeks gestation)

25. Hyperemesis gravidarum
• Women who develop hyperemesis gravidarum
have higher serum hCG and estradiol
concentrations than normal pregnant
women,in addition, their hCG has more
thyroid-stimulating activity .
• Therefore, their serum TSH concentrations are
often lower than those in normal pregnant
women and have high serum free T4
concentrations

26. Features that distinguish the transient hyperthyroidism of
hyperemesis gravidarum from hyperthyroidism of other causes
(Graves)
• vomiting, absence of goiter and ophthalmopathy, and
absence of the common symptoms and signs of
hyperthyroidism (tachycardia greater than 100
beats/minute, hyperdefecation, muscle weakness, tremor).
• serum free T4 concentrations are only minimally elevated
and serum T3 concentrations may not be elevated in
women with hyperemesis gravidarum, whereas both are
usually unequivocally elevated in pregnant women with
true hyperthyroidism from Graves' disease.
• usually does not require treatment, subsides as hCG
production falls

27. Trophoblastic hyperthyroidism
• Hyperthyroidism can also occur with gestational trophoblastic
disease.
• A hydatidiform mole (molar pregnancy) is benign but may give rise
to choriocarcinoma. Both are associated with high serum hCG
concentrations and abnormal hCG isoforms
• Many patients with hyperthyroidism caused by trophoblastic
disease have a normal thyroid gland and few symptoms of thyroid
hormone excess.
• some patients have more typical clinical findings of
hyperthyroidism and a diffuse goiter, but ophthalmopathy is not
present.
• Nausea and vomiting may predominate, as in hyperemesis
gravidarum.
• Treatment is needed

28. Familial gestational hyperthyroidism
• Recurrent gestational hyperthyroidism has
been described in one family due to a mutant
thyrotropin receptor that is hypersensitive to
physiologic concentrations of hCG

29. Determining the etiology of overt hyperthyroidism during
pregnancy or lactation

30. Determining the etiology in non pregnant woman

31. Treatment
• The goal of treatment is to maintain persistent but mild
hyperthyroidism in the mother in an attempt to
prevent fetal hypothyroidism since the fetal thyroid is
more sensitive to the action of antithyroid drugs
• Overtreatment of maternal hyperthyroidism with
thionamide antithyroid drugs can cause fetal goiter and
primary hypothyroidism.
• On the other hand, transient central hypothyroidism
may be seen in infants whose mothers had poorly
controlled hyperthyroidism during pregnancy,
presumably due to suppression of the fetal pituitary-
thyroid axis

32. • To attain the goal of mild hyperthyroidism, the mother's
serum free thyroxine (T4) concentration should be
maintained at or just above the trimester-specific normal
range for pregnancy or the total T4 and triiodothyronine
(T3) should be maintained at 1.5 times above the
nonpregnant reference range.
• The serum thyroid-stimulating hormone (TSH)
concentration should be below the reference range for
pregnancy (eg, goal TSH approximately 0.1 to 0.3 mU/L),
using the lowest possible dose of medication .
• Attaining these goals requires assessment of thyroid
function frequently (ie, at four-week intervals) with
appropriate adjustment of medication

33. Indications for treatment
• Women with symptomatic, moderate to
severe, overt hyperthyroidism due to Graves'
disease, toxic adenoma, toxic multinodular
goiter, or gestational trophoblastic disease
require treatment of hyperthyroidism

34. Treatment of hyperthyroidism is not required in
the following settings
• Transient, subclinical hyperthyroidism (normal serum total or
free T4 and T3 concentrations for pregnancy in the presence
of a subnormal TSH) in the first trimester of pregnancy
• hCG-mediated, overt hyperthyroidism (also called gestational
transient thyrotoxicosis), because it is usually transient and
mild.
• Hyperemesis gravidarum-associated hyperthyroidism,
because it is usually mild and subsides as hCG production falls
(typically by 16 to 18 weeks gestation).
• Subclinical and mild, asymptomatic, overt hyperthyroidism
due to Graves' disease, toxic adenoma, or toxic multinodular
goiter.
• Subclinical hyperthyroidism

35. Therapeutic options
• Most women are treated with thionamides.
• Thyroidectomy in the second trimester is an option for women who are
unable to take thionamides.
• Thionamides They are actively transported into the thyroid gland, where
they inhibit both the organification of iodine to tyrosine residues in
thyroglobulin and the coupling of iodotyrosines.
• Beta blockers – Beta blockers, such as metoprolol or propranolol(but
not atenolol), can be used to treat tachycardia and tremor.
• They are the primary treatment for patients with hydatidiform mole or
gestational trophoblastic neoplasia who generally cannot wait for three to
six week for thionamides to control hyperthyroidism prior to surgery.

36. Therapeutic options
• Thyroidectomy – Thyroidectomy during
pregnancy is rarely necessary but is an option
for women who cannot tolerate thionamides
because of allergy or agranulocytosis.
• Plasmapheresis has also been used to rapidly
control hyperthyroidism in women with
trophoblastic disease and severe
hyperthyroidism

37. MEDICAL MANAGEMENT
• Control of symptoms — In pregnant women with
symptomatic, moderate to severe hyperthyroidism, beta
blockers may be given to ameliorate symptoms.
• start with metoprolol 25 to 50 mg daily. Propranolol, 20 mg
every six to eight hours, is an alternative option. The dose
can be increased as needed to control symptoms.
• However, if possible, beta blockers should be weaned as
soon as the hyperthyroidism is controlled by thionamides
because occasional cases of neonatal growth restriction,
hypoglycemia, respiratory depression, and bradycardia
have been reported after maternal administration

38. • Decrease thyroid hormone synthesis
• Pretreatment evaluation — Prior to initiating
thionamides, obtain baseline blood tests, including a
complete blood count (white count with differential)
and a liver profile (bilirubin and transaminases).
• do not use thionamides in patients with a baseline
absolute neutrophil count <1000 cells/microL or
elevated liver transaminases (more than fivefold the
upper limit of normal) except in selected patients after
careful assessment of alternatives and risks.

39. • Choice of thionamide — The choice of
thionamide depends upon which trimester
the drug is being initiated. Methimazole is
preferred to PTU except during the first
trimester of pregnancy

40. Mechanism of action of
antithyroid drugs
Thyroid-stimulating
hormone (TSH) activates
steps 1, 2, 3, 4, and 5
Ionic inhibitors blockstep 1
Excess iodide interferes
with steps 1, 2, 3 and 5 with
primary action on step 3
and 5
Propylthiouracil inhibits
steps 2 and 6
Carbimazole inhibits step 2
only

41. Diagnosed prior to pregnancy
• Women diagnosed with Graves' disease prior to pregnancy who are
taking methimazole could :Elect to have definitive therapy with
surgery or radioiodine prior to pregnancy.
• Women should then postpone pregnancy until they have become
euthyroid following definitive treatment and on replacement
therapy. This option is recommended for women who are requiring
high doses of methimazole to maintain a euthyroid state.
• Switch to PTU before trying to conceive. This option is most
reasonable in younger women with normal periods who are
expected to conceive within one to three months.
• Switch to PTU as soon as the pregnancy test is confirmed. This
option is more reasonable for older individuals having difficulty
conceiving. It is recommended that a pregnancy test be obtained
weekly.

42. • Diagnosed during the first trimester
• Women diagnosed with symptomatic, moderate
to severe hyperthyroidism during the first
trimester of pregnancy should take PTU.
• Patients may continue PTU for the remainder of
pregnancy or switch back
to methimazole/carbimazole at 16 weeks.
• Diagnosed after the first trimester
• Women diagnosed with symptomatic, moderate
to severe hyperthyroidism after the first trimester
should take methimazole/carbimazole.

43. Teratogenic effects of antithyroid drugs
• All three antithyroid drugs have been associated with possible
teratogenic effects, but teratogenic effects are more severe
with methimazole and carbimazole compared with PTU.
• There are numerous case series of aplasia cutis, a scalp defect, in
newborns exposed to methimazole in utero.
• More serious congenital malformations, such as tracheoesophageal
fistulas, patent vitellointestinal duct, choanal atresia, omphalocele,
and omphalomesenteric duct anomaly, have also been observed
with maternal use of methimazole and carbimazole but not PTU .
• However, mild congenital anomalies, including preauricular sinuses
and cysts and urinary tract abnormalities, have been observed after
PTU.

44. • Initial dosing — To minimize the risk of hypothyroidism in the fetus,
give the lowest dose of thionamide necessary to control thyroid
function:
• PTU 50 mg two to three times daily
• Methimazole 5 to 10 mg daily
• Carbimazole 5 to 15 mg daily
• However, in patients with severe hyperthyroidism, full initial doses
of PTU (100 mg three times per day) or methimazole (10 to 30 mg
daily) may be required to control hyperthyroidism.
• For patients switching between PTU and methimazole, the closest
dose approximation should be made.300 mg of PTU would be
roughly equivalent to 10 or 15 mg of methimazole.

45. • Monitoring and dose adjustments — Graves' disease
frequently ameliorates in the third trimester.
Whenever possible, based on thyroid function tests
and assessment of TRAb measurements, thionamides
should be tapered and potentially discontinued during
the third trimester.
• Toxic adenoma and toxic multinodular goiter are
unlikely to remit during pregnancy, and therefore,
women with hyperthyroidism due to these disorders
are usually maintained on thionamides throughout
pregnancy.

46. Monitoring and dose adjustments
• Thyroid function tests should be obtained every four weeks throughout
pregnancy
• The thionamide dose should be adjusted based on the results of the
thyroid function tests to maintain serum free T4 concentrations at or just
above the upper limit of normal, using a trimester-specific reference
range, or the total T4 and T3 should be maintained at approximately 1.5
times the upper limit of normal for nonpregnant adults. Serum TSH
concentrations should be maintained below the reference range for
pregnancy.
• with the recommended therapeutic target being TT4: 12-18 μg/dL (or fT4, 2-2.5
ng/dL). The recommended range for TSH in patients on ATDs has been suggested
to be 0.1-0.4 mIU/L.

47. • TRAb – For women diagnosed with hyperthyroidism during
pregnancy who will be taking thionamides, serum TRAb should be
measured at diagnosis and, if elevated, again at 18 to 22 weeks and
at 30 to 34 weeks of gestation.
• Disappearance of TRAb indicates potential remission of Graves'
disease, and the dose of thionamides can be reduced and
potentially discontinued.
• High TRAb levels in late pregnancy are associated with an increased
risk of fetal and neonatal hyperthyroidism
• Adverse effects – PTU-associated liver failure, which can occur at
any time during the course of treatment, has a sudden onset and a
rapidly progressive course.
• Patients should be advised to stop their medication and contact
their clinician if they develop weakness, malaise, nausea and
vomiting, jaundice, dark urine, or light-colored stools

48. • Thionamide intolerance — For women with Graves' disease who
cannot tolerate thionamides because of allergy or agranulocytosis,
thyroidectomy during pregnancy may be necessary.
• The indications for surgery are similar to those in nonpregnant
individuals. Surgery during pregnancy, however, is associated with
an increased risk of spontaneous abortion or premature delivery
and significantly higher rates of surgical complications than
nonpregnant women . These risks are minimized by operating
during the second trimester.
• Prior to thyroidectomy, pregnant women with intolerance to
thionamides should be pretreated with beta blockers
(metoprololor propranolol) and a short course (ie, 7 to 10 days) of
potassium iodine solution (35 to 50 mg iodine per drop, 1 to 3
drops daily). Iodine lowers serum thyroid hormone concentrations
acutely and, in addition, decreases thyroid gland vascularity

49. • History of treated hyperthyroidism
• Euthyroid women with a history of remission after prior treatment of
Graves' disease with thionamides have a small risk of recurrence when
they become pregnant or postpartum. In such women, thyroid function
tests (TSH and free or total T4) should be measured in early pregnancy,
again if hyperthyroid symptoms appear, and postpartum. Abnormal tests
require confirmation and treatment depending on the underlying
abnormality.
• Euthyroid women taking thyroid hormone after definitive therapy with
radioiodine or surgery have a small risk of fetal hyperthyroidism from
transplacental transfer of TRAb . TRAb should be measured during the first
trimester and, if elevated, at 18 to 22 weeks of gestation.
• Measurement of TRAb is not necessary for women in remission after
stopping a course of thionamides, as thyroid function tests that confirm
euthyroidism indicate the absence of elevated TRAb levels.
• If TRAb levels are elevated, the fetus should be monitored for
hyperthyroidism.

50. POSTPARTUM ISSUES
• BREAST FEEDING
• Given the concerns about propylthiouracil (PTU)-
associated hepatotoxicity,
methimazole/carbimazole is preferred rather
than PTU for nursing mothers.
• Methimazole should be administered following a
feeding in divided doses.
• When the maternal dose of methimazole is >20
mg daily, infants should have thyroid function
tests assessed after one and three months.

51. • Relapse-Postpartum hyperthyroidism may be due to a relapse of
Graves' disease or to postpartum thyroiditis.
• The disorders can be differentiated from one another based upon
the clinical presentation, the number of months postpartum (earlier
onset favors thyroiditis), thyrotropin receptor antibody (TRAb)
measurement, and evaluation of serum T3-to-T4 ratio.
• Women with Graves' disease who have been treated during
pregnancy need careful monitoring during the postpartum period
as they may experience an exacerbation.
• One approach is to measure thyroid function tests (TSH, free T4) six
weeks postpartum, then every six weeks if an adjustment in
thionamide dose is needed or every four months if thyroid tests
remain normal .
• In addition, women with Graves' disease who have been in
remission are at risk for having a relapse during this period.

52. Hypothyroidism in pregnancy
• Overt hypothyroidism (elevated TSH, reduced
free T4)
• Subclinical hypothyroidism (elevated TSH,
normal free T4)

53. Screening for hypothyroidism
• It is recommended that all pregnant women
should be screened at 1st antenatal visit by
measuring TSH levels. TSH cut off should be
lower rather than keeping it on 4.0 mIU/L.
However, the trimester specific TSH cut off
recommended are:
• 1st trimester 2.5 mIU/L
• 2nd trimester 3.0 mIU/L
• 3rd trimester 3.0 mIU/L

54. Clinical manifestations

55. Causes
Primary hypothyroidism
Chronic autoimmune thyroiditis
Iatrogenic-Thyroidectomy,Radioiodine therapy or external irradiation
Iodine deficiency or excess
Drugs - thionamides, lithium, amiodarone, interferon alfa, interleukin-
2, tyrosine kinase inhibitors, checkpoint inhibitor immunotherapy
Infiltrative diseases - fibrous thyroiditis, hemochromatosis, sarcoidosis
Transient hypothyroidism Painless (silent, lymphocytic) thyroiditis
Subacute granulomatous thyroiditis
Postpartum thyroiditis
Subtotal thyroidectomy
Following radioiodine therapy for Graves' hyperthyroidism
Congenital thyroid agenesis, dysgenesis, or defects in hormone synthesis
Central hypothyroidism
TSH deficiency,TRH deficiency
Generalized thyroid hormone resistance (some patients)

56. Pregnancy complications
• Overt hypothyroidism
• Overt hypothyroidism complicating pregnancy is unusual
• Two factors contribute to this finding; some hypothyroid women are
anovulatory , and hypothyroidism complicating pregnancy is associated
with an increased rate of first trimester spontaneous abortion .
• In continuing pregnancies, hypothyroidism has been associated with
an increased risk of several complications, including :
• Preeclampsia and gestational hypertension
• Placental abruption
• Nonreassuring fetal heart rate tracing
• Preterm delivery, including very preterm delivery (before 32 weeks)
• Low birth weight
• Increased rate of cesarean section
• Postpartum hemorrhage
• Perinatal morbidity and mortality
• Neuropsychological and cognitive impairment in the child

57. Pregnancy complications
• Subclinical hypothyroidism
• The risk of complications during pregnancy is lower in women with
subclinical, rather than overt, hypothyroidism.
• However, in some , women with subclinical hypothyroidism were
also reported to be at increased risk for severe preeclampsia,
preterm delivery, placental abruption, neonatal respiratory distress
syndrome, and/or pregnancy loss compared with euthyroid women.
• Assessment of antibody status is important because women with
subclinical hypothyroidism and positive anti-thyroid peroxidase
(TPO) antibodies tend to have the highest risk of adverse pregnancy
outcomes, and adverse outcomes occur at a lower TSH than in
women without TPO antibodies

58. Patients not currently taking thyroid hormone
• Indications for treatment
• TSH >4 mU/L
• •Free T4 below the reference range, TPO
antibodies positive or negative – should be
treated with thyroid hormone
• •Free T4 within the reference range, TPO
antibodies positive or negative – Because
maternal euthyroidism is potentially important
for normal fetal cognitive development, suggest
treatment

59. • TSH 2.6 to 4 mU/L TPO antibodies positive and a history of recurrent
miscarriage, many experts offer treatment with T4 (50 mcg daily)
• In the absence of a history of recurrent miscarriage, some experts also
offer T4 (50 mcg daily) (based on weak evidence).
• If a decision is made not to treat, TSH should be reassessed every four
weeks during the first trimester and once each in the second and third
trimester to monitor for the development of hypothyroidism.
• If TSH rises above the population and trimester-specific upper limit of
normal (approximately 4 mU/L), begin treatment with T4.
• TSH 2.6 to 4 mU/L TPO antibodies negative – do not treat with T4.
• TSH between the trimester-specific lower limit of normal and 2.5
mU/L – do not require T4 treatment.
• Low free T4, normal TSH (maternal hypothyroxinemia) – do not treat
treat with T4

60. Levothyroxine initial dosing
• The goal of T4 replacement in pregnancy is to restore
euthyroidism as soon as possible. General dosing guidance is as
follows:
• TSH >4 mU/L (or above population and trimester-specific upper
limit of normal), with low free T4 (using assay method and
trimester-specific reference range) – Close to full replacement dose
(approximately 1.6-2.0mcg/kg body weight per day)
• TSH >4 mU/L, with normal free T4 – Intermediate dose
(approximately 1 mcg/kg per day)
• TSH 2.6 to 4 mU/L – If a decision has been made to treat euthyroid
women with TPO antibodies, low dose (typically 50 mcg daily)
• T4 should be taken on an empty stomach, ideally an hour before
breakfast, but few patients are able to wait a full hour.

61. Monitoring and dose adjustments
• After initiation of T4 therapy, the patient should be reevaluated
and serum TSH measured in four weeks.
• The goal is to maintain TSH in the lower half of the trimester-
specific reference range. If not available, a goal TSH of <2.5 mU/L is
reasonable.
• If the TSH remains above the normal trimester-specific reference
range, the dose of T4 can be increased by 12 to 25 mcg/day. TSH
should be measured every four weeks during the first half of
pregnancy because dose adjustments are often required. TSH can
be monitored less often (at least once each trimester) in the latter
half of pregnancy, as long as the dose is unchanged.
• Overtreatment should be avoided.
• Overtreatment with levothyroxine during pregnancy has been
associated with an increase in preterm delivery and behavioral
difficulties in the children

62. • Postpregnancy adjustments— Since the criteria
for treating pregnant women differ from the
criteria from treating nonpregnant women, it is
not always necessary to continue levothyroxine
after delivery.
• Unless another pregnancy is imminent, however,
the majority of women who were started on
levothyroxine for TSH between 2.5 and 4.0 mU/L
do not need to continue levothyroxine treatment.

63. Management of pregnant women with or at risk for
hypothyroidism

64. Preexisting treated hypothyroidism
• Goal preconception TSH — Women with
preexisting hypothyroidism who are planning to
become pregnant should optimize their thyroid
hormone dose preconception.
• The goal preconception serum TSH level is
between the lower reference limit and 2.5 mU/L.
• Approximately 50 to 85 percent of women with
preexisting hypothyroidism need more T4 during
pregnancy

65. • Early dose adjustments — hypothyroid women who
are newly pregnant should preemptively increase
their levothyroxine dose by approximately 30 percent .
Further dose changes are made based upon serum TSH
concentrations measured every four weeks until the
TSH becomes normal
• Another approach is to measure serum TSH as soon as
pregnancy is confirmed, then again four weeks later,
four weeks after any change in the dose of T4, and at
least once each trimester . The dose should be
adjusted as needed every four weeks to achieve a
normal TSH level.

66. • Monitoring — The T4 dose should be reduced
to prepregnancy levels after delivery, but
serum TSH should be measured four to six
weeks later to confirm that the reduction was
appropriate

67. Thank you