THE PATHOLOGY OF THYROID IN PREGNANCY

SCRIPT

Mentor :
dr. H Dadan Susandi SpOG

Co-ass:
Cindy May McGuire / 12100118032

OBGYN SECTOR
RSUD DR. SLAMET GARUT
MEDICAL DOCTOR STUDY PROGRAM
MEDICAL SCHOOL
UNIVERSITAS ISLAM BANDUNG
2019
 MENTOR APPROVAL SHEET

APPROVAL

Script

Title:
THE PATHOLOGY OF THYROID IN PREGNANCY

Co-ass:
Cindy May McGuire / 12100118032

Has been agreed to be presented in:

9 December 2019

Mentor

dr. H Dadan Susandi SpOG

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 ACKNOWLEDGEMENT

The writer would like to acknowledge her countless thanks to the most gracious
and the most merciful, ALLAH SWT who always give all the best of this life and
there is no doubt about it. Shalawat and salaam to the prophet Muhammad SAW
and his family. This script is presented to fulfill one of the requirements in
accomplishing the assignment papers study of Medical Faculty in the Islamic
University of Bandung.
The writer would like to take her opportunity to express her deep and
sincere gratitude to dr. H Dadan Susandi SpOG as a preceptor and a mentor in this
Obgyn sector who patiently taught me about medical knowledge.
This paper contains some of the medical journals that contains Information
about diseases that often are around us. I realized this assignment is not perfect. I
hope this paper is usefull for us.

Garut, 5 December 2019

Writer

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 CONTENTS

Mentor Approval Sheet.........................................................................................i

Acknowledgement.................................................................................................ii
Contents.................................................................................................................iii

CHAPTER I Introduction……………………………………………………......1
CHAPTER II Review of the Literature.................................................................2
2.1 Embryology of thyroid.............................................................................2
2.2 Anatomy and Histology of thyroid...........................................................2
2.3 Physiology of thyroid...............................................................................2
CHAPTER III Discussion.....................................................................................8
3.1 Definition..................................................................................................8
3.2 Etiology and epidemiology......................................................................8
3.3 Risk Factor...............................................................................................10
3.4 Pathophysiology.......................................................................................11
3.5 Classification and symptoms................................................................... 14
3.6 Diagnosis..................................................................................................15
3.7 Treatment..................................................................................................24
3.8 Complication............................................................................................31
3.9 Prognosis..................................................................................................32
CHAPTER IV Conclusion..................................................................................26

References...........................................................................................................27

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 CHAPTER I

INTRODUCTION

Thyroid disorders affect a substantial proportion of the general population, but

most have a remarkably higher incidence in women. Worldwide, the most
common cause of thyroid disorders is iodine deficiency. Although eradicated in
many parts of the world, it is still a major health problem affecting almost a third
of the world's population. About twenty million people are believed to be
significantly mentally handicapped as a result of iodine deficiency. In iodine-
sufficient regions, the autoimmune thyroid diseases, Hashimoto's thyroiditis and
Graves’ disease, are the most common clinical entities affecting the thyroid. The
prevalence of thyroid disorders depends on the diagnostic criteria used and the
surveyed population's age and sex. The prevalence of overt hypothyroidism is ∼
3–20 per 1000 females and ∼ 1–7 per 1000 males. The most common cause of
hypothyroidism is Hashimoto's thyroiditis. The prevalence of hyperthyroidism is
∼ 2–19 per 1000 females and ∼ 1–2 per 1000 males. Graves’ disease is its most
frequent cause. The differences in the prevalences of hypo- and hyperthyroidism
in men and women are most commonly explained by influences of sex steroids on
immunoregulatory mechanisms. Thyroid carcinomas are relatively rare neoplasms
that account for 0.6–1.6% of all malignancies. The annual incidence of papillary,
follicular, and differentiated thyroid carcinomas cancer is 1–10 per 100,000
people. They are about three times more common in women than men.
In addition to the striking gender differences in the frequency of
autoimmune thyroid diseases and thyroid cancer, several other aspects of thyroid
physiology and disease are distinct in women. Pregnancy is characterized by
intricate physiological changes in iodine balance, thyroid activity, thyroid
hormone transport, and peripheral metabolism. Pregnancy also has modulating
influences on autoimmune thyroid disorders and can be complicated by a distinct
form of hyperthyroidism, gestational hyperthyroidism, which is caused by the
secretion of the placental hormone human chorionic gonadotropin (hCG). The
hCG-induced rise in thyroid hormone levels has also been implicated in the
pathogenesis of hyperemesis gravidarum (nausea and vomiting of pregnancy).
After delivery, postpartum thyroiditis may result in either hyper- or
hypothyroidism.

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 Among the multiple peripheral actions of thyroid hormones, the effects on
the cardiovascular system, lipid metabolism, and bone are particularly prominent.
It is well recognized that cardiovascular disease and osteoporosis have distinct
characteristics in women, and thyroid hormone excess or deficiency may further
modulate these important health problems.
Hence, thyroid diseases continue to present challenges to researchers and
clinicians, and many of these disorders are particularly relevant to the health of
women.

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 CHAPTER II

REVIEW OF THE LITERATURE

2.1. Embryology of Thyroid

The thyroid is the first endocrine gland to develop in the embryo. It begins
to form about 24 days after fertilization from a median endodermal
thickening in the floor of the primordial pharynx. This thickening soon
forms a small out-pouching – ‘the thyroid primordium’. As the embryo
and tongue grow, the developing thyroid gland descends in the neck,
passing ventral to the developing hyoid bone and laryngeal cartilages. For
a short time the thyroid gland is connected to the tongue by a narrow tube,
the thyroglossal duct. At first the thyroid primordium is hollow but it soon
becomes solid and divides into right and left lobes connected by the
isthmus of the thyroid gland which lies anterior to the developing 2nd and
3rd tracheal rings.

By seven weeks the thyroid assumes its definitive shape and

reaches its final site in the neck. The thyroglossal duct by this time has
normally degenerated and disappeared. The proximal opening of the
thyroglossal duct persists as a small pit in the tongue-‘the foramen cecum’.
A pyramidal lobe extends superiorly from the isthmus in about 50% of
people. The pyramidal lobe may be attached to the hyoid bone by fibrous
tissue and /or smooth muscle‘the levator of thyroid gland’. A pyramidal
lobe and the associated smooth muscle represent a persistent part of the
distal end of the thyroglossal duct.

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Summary table:

Event Week Day

Specification of the thyroid domain in the ventral
endoderm week 3 E20 - 22
Thyroid bud (medial anlage) formation weeks 3 - 4 E20 - 24
Thyroid bud begins migration week 4 E24 - 28
Formation of the lateral anlagen (ultimobranchial
bodies) weeks 4 - 7  
Migration of lateral anlagen weeks 5 - 7  
Thyroglossal duct disappears weeks 5 - 6 E30 - 40
Thyroid migration is complete weeks 7 - 8 E45 - 50
Fusion with ultimobranchial bodies weeks 7 - 9 E44 - 60
Onset of folliculogenesis week 10 E70
Release of thyroid hormone weeks 10 - 12 E80

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2.2. Anatomy and Histology of Thyroid

The thyroid gland is situated low down at the front of neck weighing about
25 g. The gland has two lobes, each pear shaped hugging anterolateral
aspects of cervical trachea from oblique line of thyroid cartilage to 5th or
6th tracheal ring. The right lobe is often larger than left and isthmus joins
them anteriorly at the level of 2nd and 3rd tracheal rings. Isthmus is
plastered quite firmly to the anterior surface of trachea. A small portion of
gland substance, pyramidal lobe often projects upwards from isthmus,
generally to the left of midline. The gland has its own capsule and is also
enclosed by an envelope of pretracheal fascia which is thickened
posteriorly and attached to the cricoid cartilage and upper tracheal rings
(suspensory ligament of Berry). This fixation and investment of gland by
pretracheal fascia are responsible for the gland moving up and down with
larynx during swallowing.

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 Measurements: Each lobe: Vertical – 5 cm, Anteroposterior – 2
cm, Transverse – 3 cm Isthmus: Vertical and Transverse – 1.25 cm.

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 Vascular supply of thyroid gland has rich blood supply. Each
thyroid lobe is supplied by a superior and an inferior thyroid artery and
drained by three veins. The superior vascular pedicle contains superior
thyroid artery, which is the 1st branch of the external carotid, and its
accompanying vein, which drains into the internal jugular vein. These
enter upper pole of gland at its apex and branches to the front and back of
the gland. These vessels are easily dealt with surgically, because the loose
space between the two capsules is developed at the upper pole of the
thyroid lobe and a ligature is placed close to the upper pole, to include
both vessels and exclude the external laryngeal nerves. The inferior
thyroid arteries arises from thyrocervical trunk, passes behind the carotid
sheath and then runs transversly across the space between this and the
thyroid gland to enter the deep surface of the gland as several separate
branches close to tracheothyroid groove. These are close to recurrent
laryngeal nerve and inferior parathyroid gland and hence inferior thyroid
artery should be ligated in its transverse portion medial to the carotid
sheath.

The inferior thyroid veins leave lower border of gland and pass
through the loose fascial space to join the left brachiocephalic vein. They
are fragile and require to be ligated singly. The middle thyroid vein is
short, thin walled vessel, leaving the middle of the gland and directly
courses laterally to pass in front of or behind the carotid artery and enter
the internal jugular vein. It is the 1st vessel encountered in thyroidectomy.

The thyroidea ima artery runs from brachiocephalic trunk in

front of trachea and it is small and surgically irrelevant. Blood supply of
retrosternal extension comes from neck and hence its operative removal
can always be conducted by cervical approach.

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 Lymphatic drainage: Major: Middle and Lower jugular, Posterior
triangle nodes. Lesser: Pretracheal and para tracheal, Superior mediastinal
nodes. Because of wide distribution of nodes, standard radical neck
dissection has been abandoned in favor of ‘regional’ node removal in
cases of management of thyroid neoplasms.

Innervation of the thyroid gland receives its innervation from the

superior, middle and inferior cervical sympathetic ganglia. They are
vasomotor in function. The important close surgical relations of nerves of
the thyroid gland: These are the recurrent laryngeal nerves, the external
laryngeal nerves and the parathyroid glands. These should be recognized
and cared for during thyroid surgery.

The External laryngeal nerve is a branch of superior laryngeal

nerve, descends on the fascia of the inferior pharyngeal constrictor is
closely related to superior vascular pedicle of thyroid and leaves this at a
variable height above the gland to travel medially to cricothyroid muscle.
It is important for pitch of voice and its damage alters the voice.

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 The Recurrent laryngeal nerve innervates laryngeal musculature
and provides sensory innervation to the glottic larynx. The RLN arises
from the vagus at the level of subclavian artery on the right and at the level
of aortic arch on the left. They are taken caudally during embryonal
growth and thus run an upward course to reach vocal cords. They lie in TE
groove and then bear a variable relationship to the branches of inferior
thyroid artery before entering the larynx. In majority, the nerve is found
easily in TE groove just below thyroid gland but its course may vary and it
may be much more lateral. In 0.3% to 0.8% of cases, a non recurrent nerve
has been reported, which arises from cervical portion of vagus at the level
of larynx or thyroid gland. Vast majority of these occur on right side in
conjunction with an anomalous retroesophageal subclavian artery Rare
cases of left non recurrent laryngeal nerve have been reported.

The parathyroid glands, most commonly 4 in number arise from

3rd branchial pouch (Inferior parathyroids) and 4th branchial pouch
(Superior parathyroids). The superior parathyroids most consistently

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 located (80%) within 1 cm superior to the intersection of the RLN and the
ITA near the crico thyroid joint.

The histology of thyroid consists of large number of closed follicles

(200-300 microm in diameter) lined by a single layer of epithelial cells.
The follicles contain colloid. Colloid is made up of proteins, especially the
iodinated glycoprotein, thyroglobulin, a 19S protein to which tyrosine
residues is bound and in which thyroid hormone synthesis and storage
takes place. The follicles are bound together in groups to form lobules
each supplied by an end artery. There are para follicular cells constituting
< 2% of total cells which are scattered on outer aspects of the follicles and
secrete calcitonin. The thyroid gland is highly vascular and is the only
endocrine gland to store its secretion outside the cells.

2.3. Physiology of Thyroid

In synthesis and release of the hormones are produced in the colloid when atoms
of the mineral iodine attach to a glycoprotein, called thyroglobulin, that is secreted
into the colloid by the follicle cells. The following steps outline the hormones’
assembly:

1. Binding of TSH to its receptors in the follicle cells of the thyroid gland
causes the cells to actively transport iodide ions (I–) across their cell membrane,
from the bloodstream into the cytosol. As a result, the concentration of iodide ions
“trapped” in the follicular cells is many times higher than the concentration in the
bloodstream.
2. Iodide ions then move to the lumen of the follicle cells that border the
colloid. There, the ions undergo oxidation (their negatively charged electrons are
removed). The oxidation of two iodide ions (2 I–) results in iodine (I2), which
passes through the follicle cell membrane into the colloid.
3. In the colloid, peroxidase enzymes link the iodine to the tyrosine amino
acids in thyroglobulin to produce two intermediaries: a tyrosine attached to one

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iodine and a tyrosine attached to two iodines. When one of each of these
intermediaries is linked by covalent bonds, the resulting compound is
triiodothyronine (T3), a thyroid hormone with three iodines. Much more
commonly, two copies of the second intermediary bond, forming
tetraiodothyronine, also known as thyroxine (T4), a thyroid hormone with four
iodines.

These hormones remain in the colloid center of the thyroid follicles until
TSH stimulates endocytosis of colloid back into the follicle cells. There,
lysosomal enzymes break apart the thyroglobulin colloid, releasing free T3 and T4,
which diffuse across the follicle cell membrane and enter the bloodstream.

In the bloodstream, less than one percent of the circulating T 3 and T4

remains unbound. This free T3 and T4 can cross the lipid bilayer of cell
membranes and be taken up by cells. The remaining 99 percent of circulating T 3
and T4 is bound to specialized transport proteins called thyroxine-binding
globulins (TBGs), to albumin, or to other plasma proteins. This “packaging”
prevents their free diffusion into body cells. When blood levels of T3 and T4 begin
to decline, bound T3 and T4 are released from these plasma proteins and readily
cross the membrane of target cells. T3 is more potent than T4, and many cells
convert T4 to T3 through the removal of an iodine atom.

Iodine is a raw material essential for thyroid hormone synthesis. Minimum

daily required intake to maintain normal thyroid function is 150 µg. Normal
plasma Iodine level is 0.3 µg/dl. Normal diet contains about 500mcg Iodine.
Thyroid hormones normal levels are T3 - 70-190ng/dl (1.1 – 2.9 nmol/L), T4 - 5-
12 mcg/dl (64 –154 nmol/L) and for normal daily secretion: T3 - 4 µg (7 nmol),
T4 - 80 µg (103 nmol).

Regulation of thyroid hormone synthesis, the release of T3 and T4 from the

thyroid gland is regulated by thyroid-stimulating hormone (TSH). As shown in the
picture below, low blood levels of T3 and T4 stimulate the release of thyrotropin-

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releasing hormone (TRH) from the hypothalamus, which triggers secretion of
TSH from the anterior pituitary. In turn, TSH stimulates the thyroid gland to
secrete T3 and T4. The levels of TRH, TSH, T3, and T4 are regulated by a negative
feedback system in which increasing levels of T3 and T4 decrease the production
and secretion of TSH.

Functions of the thyroid hormones, T3 and T4, are often referred to as

metabolic hormones because their levels influence the body’s basal metabolic
rate, the amount of energy used by the body at rest. When T 3 and T4 bind to
intracellular receptors located on the mitochondria, they cause an increase in
nutrient breakdown and the use of oxygen to produce ATP. In addition, T 3 and T4
initiate the transcription of genes involved in glucose oxidation. Although these
mechanisms prompt cells to produce more ATP, the process is inefficient, and an

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abnormally increased level of heat is released as a byproduct of these reactions.
This so-called calorigenic effect (calor- = “heat”) raises body temperature.

Adequate levels of thyroid hormones are also required for protein

synthesis and for fetal and childhood tissue development and growth. They are
especially critical for normal development of the nervous system both in utero and
in early childhood, and they continue to support neurological function in adults.
As noted earlier, these thyroid hormones have a complex interrelationship with
reproductive hormones, and deficiencies can influence libido, fertility, and other
aspects of reproductive function. Finally, thyroid hormones increase the body’s
sensitivity to catecholamines (epinephrine and norepinephrine) from the adrenal
medulla by upregulation of receptors in the blood vessels. When levels of T 3 and
T4 hormones are excessive, this effect accelerates the heart rate, strengthens the
heartbeat, and increases blood pressure. Because thyroid hormones regulate
metabolism, heat production, protein synthesis, and many other body functions,
thyroid disorders can have severe and widespread consequences.

The thyroid gland undergoes definite physiological changes during

pregnancy. Moderate thyroid enlargement and increased vascularity occurs as a
result of pregnancy hormone-induced glandular hyperplasia. Thyroid stimulation
starts as early as the first trimester by human chorionic gonadotropin hormone

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(beta-HCG), which shares some structural homology with thyroid-stimulating
hormone (TSH). There is also an estrogen-mediated increase in circulating levels
of thyroid-binding globulin (TBG). Furthermore, there is a relative decline in the
availability of iodide, secondary to the increased renal clearance and overall losses
to fetus and placenta.1 Circulating TBG is known to increase 2–3-fold during
pregnancy. Serum TBG increases a few weeks after conception and reaches a
plateau during mid-gestation. The mechanism behind this increase involves
increased hepatic synthesis and estrogenmediated prolongation of TBG half-life
from 15 minutes to 3 days.

Total thyroxine (T4) and total triiodothyronine (T3) concentrations

increase sharply in early pregnancy and plateau early in the second trimester at
concentrations 30%–100% greater than prepregnancy values, primarily following
the rise in TBG. However changes in free T4 and T3 concentrations during
pregnancy are controversial. Some authors have reported a decrease in free
hormones, whereas others have reported no change or even an increase. Pregnant
women in general have lower free-hormone concentrations at term than
nonpregnant women.3–5 Beta-HCG has a mild thyrotropic activity and shares
85% sequence homology with TSH beta subunit. During the first trimester of
pregnancy, beta-HCG is at its greatest concentration, while serum TSH drops.
Thyroglobulin frequently increases during pregnancy reflecting an increased
activity of the thyroid gland.

The fetal thyroid gland begins concentrating iodine and synthesizing

thyroid hormones after 12 weeks of gestation. Any requirement for thyroid
hormones before this time is solely supplied by the mother. It is during the first
trimester of pregnancy that the thyroid hormones are most important to fetal brain
development. Still, significant fetal brain development continues considerably
beyond the first trimester, making thyroid hormones important also later in
gestation. Overt maternal thyroid failure during the first half of pregnancy has
been associated with several pregnancy complications and intellectual impairment

14
in the offspring. It is currently less clear whether milder forms of thyroid
dysfunction have similar effects on pregnancy and infant outcomes

Gestation Thyroid stimulating hormone (mIU/L)

First trimester 0.1–2.5
Second trimester 0.2–3.0
Third trimester 0.3–3.0
Note that individual laboratories may have slightly different pregnancy-specific
ranges and it is important to confirm ranges with local pathologist.

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 CHAPTER III

DISCUSSION

3.1 DEFINITION

Thyroid disease is a medical condition that affects the function of the thyroid
gland. The thyroid gland is located at the front of the neck and produces thyroid
hormones that travel through the blood to help regulate many other organs,
meaning that it is an endocrine organ.

Thyroid dysfunction changes in how well your thyroid gland works, can
start during or after pregnancy in women who never had thyroid problems before.
This occurs because pregnancy causes major changes in the levels of hormones
made in the thyroid gland.

3.2 ETIOLOGI AND EPIDEMIOLOGY

Hyperthyroidism in pregnancy is usually caused by Graves’ disease and occurs in

1 to 4 of every 1,000 pregnancies in the United States.1 Graves’ disease is an
autoimmune disorder. With this disease, your immune system makes antibodies
that cause the thyroid to make too much thyroid hormone. This antibody is called
thyroid stimulating immunoglobulin, or TSI.
Hypothyroidism in pregnancy is usually caused by Hashimoto’s disease
and occurs in 2 to 3 out of every 100 pregnancies. 1 Hashimoto’s disease is an
autoimmune disorder. In Hashimoto’s disease, the immune system makes
antibodies that attack the thyroid, causing inflammation and damage that make it
less able to make thyroid hormones. Postpartum thyroiditis is an autoimmune
condition similar to Hashimoto’s disease.
Overt hypothyroidism is estimated to occur in 0.3-0.5% of pregnancies.
Subclinical hypothyroidism appears to occur in 2-3%, and hyperthyroidism is
present in 0.1-0.4%.

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 3.3 RISK FACTOR

Women are at increased risk of an under active thyroid during or after pregnancy
if they are over age 30 or have:

 Past infertility or preterm delivery

 A family history of thyroid or autoimmune disease
 Type 1 diabetes or other autoimmune disease
 Prior radiation treatment of the head or neck
 Past thyroid surgery
 Thyroid antibodies, mainly thyroid peroxidase (TPO) antibodies, which
are often present in Hashimoto’s disease
 A goiter (enlargement of the thyroid gland)
 Current treatment with levothyroxine, a thyroid hormone drug, unless the
dose is adjusted before or soon after conception.

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 3.4 PATHOPHYSIOLOGY

3.5 CLASSIFICATION AND SYMPTOMS

a. Hyperthyroidism

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 When the thyroid makes too much of the thyroid hormones
T3 and T4, it is called overactive thyroid or hyperthyroidism. This
problem also causes very low levels of thyroid stimulating hormone
(TSH), a hormone that tells the thyroid to make T3 and T4. This is because
too much T3 and T4 in the body causes TSH production to shut down. An
overactive thyroid greatly increases metabolism (how your body uses
energy). It most often affects women ages 20 to 40, in their childbearing
years. Symptoms of hyperthyroidism include feeling too hot when others
are comfortable, rapid heartbeat, trembling hands, weight loss even though
you eat enough, tiredness and/or trouble sleeping, feeling irritable and
anxious

b. Autoimmune thyroid disease

Autoimmune thyroid diseases, including Graves’ disease and

autoimmune thyroiditis, are common in women of childbearing age.

Poorly controlled Graves’ disease is associated with an increased risk of

fetal loss, premature birth, pre-eclampsia, intra-uterine growth retardation,

and thyroid storm.

c. Hypothyroidism

Hypothyroidism is a condition that is caused by an underactive

thyroid gland. It may happen during pregnancy. Many symptoms of the
condition are similar to pregnancy symptoms. For example, they can both
cause fatigue, weight gain, and changes in menstruation. Having low
thyroid hormone levels can also cause problems with becoming pregnant.
It can also be a cause of miscarriage. 

The most common symptoms include:

 Feeling tired

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  Inability to stand cold temperatures

 Hoarse voice

 Swelling of the face

 Weight gain

 Constipation

 Skin and hair changes, including dry skin and loss of eyebrows

 Brittle nails

 Carpal tunnel syndrome (hand tingling or pain)

 Slow heart rate

 Shortness of breath with activity

 Muscle cramps, weakness, joint pain

 Trouble concentrating

 Irregular menstrual periods

d. Subclinical hypothyroidism

Subclinical hypothyroidism in pregnancy is associated with an

increased risk of recurrent miscarriage, intrauterine growth restriction,
preterm birth, low birth weight, perinatal mortality and pre-eclampsia.
Thyroxine may reduce associated risks. Recent studies support thyroxine
replacement in women with subclinical hypothyroidism undergoing
assisted reproduction technologies, to improve pregnancy outcome. The
aim of treatment is to achieve a TSH less than 2.5 mIU/L.
Women with subclinical hypothyroidism should be tested for
antithyroid antibodies as this impacts on the effects in pregnancy and may
also be associated with other autoimmune conditions such as type 1
diabetes. At present there are no data to support treating pregnant women
who have subclinical hypothyroidism if they do not have antibodies.

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 The American Thyroid Association in 2017 updated its guidelines
for the management of thyroid disease in pregnancy following new
research. Thyroxine should be given if there are antithyroid antibodies and
the initial TSH is 2.5–4 mIU/L. If the initial TSH is 4 mIU/L or more, start
thyroxine irrespective of antibody status. If a decision is made to treat
subclinical hypothyroidism, the suggested starting dose of thyroxine is 50
micrograms per day. Thyroid function tests are checked within four weeks
of starting therapy.
In the postpartum period the ongoing need for thyroxine needs to
be reassessed. The concentrations of thyroid hormones that prompted
treatment during pregnancy may be satisfactory in a non-pregnant woman.
If the woman had antithyroid antibodies but the initial TSH was less than 4
mIU/L, cease thyroxine and recheck thyroid function at six weeks. If the
TSH was greater than 4 mIU/L continue thyroxine. In women who did not
have antithyroid antibodies but had TSH greater than 4 mIU/L, cease
thyroxine and check thyroid function in six weeks.
Targeted screening is reported to miss up to 30% of cases of
thyroid dysfunction. A recent study reported 9.6% of cases of subclinical
hypothyroidism would have been missed by targeted screening. If
prospective trials find that treating subclinical hypothyroidism in
pregnancy is beneficial, this would support universal screening in future.

e. Postpartum thyroiditis

Postpartum thyroiditis is defined as the development of hypothyroidism,

thyrotoxicosis or both in the year following delivery, in any woman who
did not have clinical evidence of thyroid disease before pregnancy. It
occurs in 7–10% of postpartum women, although this varies depending on
iodine intake and genetic factors.
Investigation for postpartum thyroiditis is recommended if there is
a clinical suspicion and it should be considered as a differential diagnosis

21
 in women presenting with depressive symptoms in the postpartum period.
Almost 50% of women with antithyroid peroxidase antibodies in early
pregnancy will develop postpartum thyroiditis, therefore it is the most
useful marker identifying those at risk. Thyroid function tests are indicated
at three and six months postpartum in these women and those with known
autoimmune disease, previous postpartum thyroiditis or chronic viral
hepatitis.
Annual TSH tests for 5–10 years are recommended for women
with a history of postpartum thyroiditis. They have an increased risk of
developing permanent overt hypothyroidism.

3.6 DIAGNOSIS

- History and Physical examination

- TSH test

Health care professionals usually check the amount of TSH in your blood first.
TSH is a hormone made in the pituitary gland that tells the thyroid how much T4
and T3 to make.

A high TSH level most often means you have hypothyroidism, or an underactive
thyroid. This means that your thyroid isn’t making enough hormone. As a result,
the pituitary keeps making and releasing TSH into your blood.

A low TSH level usually means you have hyperthyroidism, or an overactive

thyroid. This means that your thyroid is making too much hormone, so the
pituitary stops making and releasing TSH into your blood.

If the TSH test results are not normal, you will need at least one other test to help
find the cause of the problem.

- T4 tests

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A high blood level of T4 may mean you have hyperthyroidism. A low level of T 4
may mean you have hypothyroidism.

In some cases, high or low T4 levels may not mean you have thyroid problems. If
you are pregnant or are taking oral contraceptives NIH external link, your thyroid
hormone levels will be higher. Severe illness or using corticosteroids—medicines
to treat asthma, arthritis, skin conditions, and other health problems—can lower T4
levels. These conditions and medicines change the amount of proteins in your
blood that “bind,” or attach, to T4. Bound T4 is kept in reserve in the blood until
it’s needed. “Free” T4 is not bound to these proteins and is available to enter body
tissues. Because changes in binding protein levels don’t affect free T4 levels,
many healthcare professionals prefer to measure free T4.

- T3 test

If your health care professional thinks you may have hyperthyroidism even
though your T4 level is normal, you may have a T3 test to confirm the diagnosis.
Sometimes T4 is normal yet T3 is high, so measuring both T4 and T3 levels can be
useful in diagnosing hyperthyroidism.

- Thyroid antibody tests

Measuring levels of thyroid antibodies may help diagnose an autoimmune thyroid

disorder such as Graves’ disease—the most common cause of hyperthyroidism
and Hashimoto’s disease—the most common cause of hypothyroidism. Thyroid
antibodies are made when your immune system attacks the thyroid gland by
mistake. Your health care professional may order thyroid antibody tests if the
results of other blood tests suggest thyroid disease.

- Ultrasound

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 Ultrasound of the thyroid is most often used to look for, or more closely at,
thyroid nodules. Thyroid nodules are lumps in your neck. Ultrasound can help
your doctor tell if the nodules are more likely to be cancerous.

- Thyroid scan

Health care professionals use a thyroid scan to look at the size, shape, and position
of the thyroid gland. This test uses a small amount of radioactive iodine to help
find the cause of hyperthyroidism and check for thyroid nodules. Your health care
professional may ask you to avoid foods high in iodine, such as kelp, or medicines
containing iodine for a week before the test.

- Radioactive iodine uptake test

A radioactive iodine uptake test, also called a thyroid uptake test, can help
check thyroid function and find the cause of hyperthyroidism. The thyroid
“takes up” iodine from the blood to make thyroid hormones, which is why this
is called an uptake test. Your health care professional may ask you to avoid
foods high in iodine, such as kelp, or medicines containing iodine for a week
before the test.

For this test, you will swallow a small amount of radioactive iodine in
liquid or capsule form. During the test, you will sit in a chair while a technician
places a device called a gamma probe in front of your neck, near your thyroid
gland. The probe measures how much radioactive iodine your thyroid takes up
from your blood. Measurements are often taken 4 to 6 hours after you swallow
the radioactive iodine and again at 24 hours. The test takes only a few minutes.

3.7 TREATMENT

Pregnant women that has hypothyroidism should be initiated to do the

treatment as soon as the diagnosis of overt hypothyroidism is made. The

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starting dose of levothyroxine is 0.10–0.15 mg/day (1–2 µg/kg/day) and
should be adjusted every 4 weeks to keep the TSH at the lower end of normal.
Women who are on levothyroxine at the beginning of pregnancy should have
their dose increased by approximately 30% as soon as pregnancy is confirmed
and have their TSH and free T4 levels checked every 8 weeks. Levothyroxine
replacement requirements most likely will increase as the pregnancy
progresses. This increase can be secondary to the increased demand for T4
with the progression of pregnancy as well as its inadequate intestinal
absorption caused by accompanied ferrous sulfate replacement in most
pregnant ladies. Thus levothyroxine and ferrous sulfate dosages should be
spaced at least 4 hours apart.

The goal of treatment of hyperthyroidism during pregnancy is to keep the

patient euthyroid, with the FT4 level in the upper limit of normal range so as
not to cause fetal or neonatal hypothyroidism. Propylthiouracil (PTU) is the
drug of choice, but methimazole is also frequently used. Both are thionamides,
which act by inhibiting the iodination of thyroglobulin and preventing
thyroglobulin synthesis by competing with iodine for the enzyme peroxidase.
PTU is given in a dose of 100–150 mg/8 hours (300–450 mg/day). It may take
2–4 weeks from the start of treatment to see a clinical change. Free T4 levels
should be monitored monthly. After achieving an euthyroid state, the dosage
of PTU should be tapered to minimize fetal exposure to thionamides. If PTU
or methimazole are contraindicated, beta blockers may be used to control the
adrenergic symptoms of thyrotoxicosis, particularly tachycardia. In addition,
beta blockers block the peripheral conversion of T4 to T3. Propranolol in a
dose of 20–40 mg 2–3 times a day is commonly used. In acute cases,
intravenous esmolol (up to 200 g/kg/minute) may be used to maintain a heart
rate of less than 90 beats/min. Surgery should be reserved for the most severe
cases. Radioactive iodine is an absolute contraindication in pregnancy. It is
also important to continue medications throughout the postpartum period, as

25
exacerbation of Graves’ disease is common during this time. PTU and
methimazole are considered compatible with breastfeeding.

During pregnancy. The preferred treatment for pregnant women with

hyperthyroidism due to Graves’ disease is antithyroid medication. These
drugs prevent the thyroid from making too much thyroid hormone.
Temporary (gestational) hyperthyroidism does not need this treatment.

Pregnant women with Graves hyperthyroidism or thyroid nodules should

start antithyroid drug treatment or, if already taking this medication, see their
doctor about the dose. Hyperthyroidism due to Graves disease most often
improves as pregnancy advances but may worsen during the first six months
after birth. Therefore, your doctor may need to change your dose of
antithyroid medicine both during and after pregnancy.

In the first trimester of pregnancy, the preferred drug to treat

hyperthyroidism is propylthiouracil (PTU). Another antithyroid drug,
methimazole, may cause birth defects if taken during early in pregnancy.
Women may need to take methimazole in the first three months of pregnancy
if they cannot tolerate PTU.

After the first trimester, experts recommend switching from PTU to

methimazole. This is because in rare cases PTU can cause severe liver injury.
Both drugs are equally effective. Talk to your doctor about the benefits and
risks of these medicines, and which is the best choice for you.

Antithyroid medication can treat most cases of Graves disease in

pregnancy. Rarely, some women may need surgery to remove part of the
thyroid. The best time for this surgery during pregnancy is the second
trimester (months 4 through 6).

Women who are or may be pregnant should not receive treatment with
radioactive iodine. This radioactive drug usually destroys the patient’s thyroid

26
 gland to stop it from being overactive and can harm the unborn baby’s
thyroid.

While breastfeeding. Women who are breastfeeding should not get

radioactive iodine treatment. They may continue antithyroid drug therapy if
they take their medicine as prescribed.

For thyroid cancer, the first way to treat thyroid cancer is usually by
removing either the cancerous tissue or the whole thyroid gland, a surgical
procedure known as a thyroidectomy.

3.8 COMPLICATION

- Hyperthyroidism and pregnancy complications

Hyperthyroidism an overactive thyroid during pregnancy is associated with

increased risk of:

 Severe morning sickness (hyperemesis)

 Miscarriage

 Preeclampsia

 Hypertension in pregnancy

 Stillbirth/fetal death

 Preterm birth

 Maternal heart failure

 The need for an induced labor

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  Fetal growth restriction and low fetal birth weight

 Fetal tachycardia (high heart rate)

 Fetal hypothyroidism

 Fetal hyperthyroidism

- Hypothyroidism and pregnancy complications

Official guidelines of the American Thyroid Association and research studies

have found that untreated hypothyroidism and inadequately treated
hypothyroidism are associated with an increased risk of many pregnancy
complications, including:

 Miscarriage, also known as spontaneous pregnancy loss

 Placental abruption, which is the separation of the placenta from the

uterus, causing bleeding, contractions, prematurity, fetal distress, and even
death to the mother and/or the unborn baby.

 Gestational hypertension (high blood pressure) and preeclampsia, which

occurs at twice the normal rate in women with hypothyroidism

 Gestational diabetes — a temporary form of diabetes in pregnant women

 Stillbirth/fetal death

 Premature rupture of membranes (PROM) and preterm birth at less than

37 weeks of gestation

 The need for an induced labor

 Breech presentation, which usually requires surgical cesarean section (C-

section) delivery

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  Need for C-section delivery

 Maternal hemorrhage

 Heart rhythm irregularities in the fetus, including elevated heart rate

(tachycardia) and low heart rate (bradycardia)

 Lower APGAR score— an assessment of the newborn’s appearance,

pulse, grimace, activity, and respiration

 Low milk supply in the mother, known as hypogalactia

 Post-partum depression

3.9 PROGNOSIS

Untreated thyroid diseases during pregnancy has a prognosis of dubia ad

bonam, but may lead to premature birth, preeclampsia (a severe increase in
blood pressure), miscarriage, and low birth weight among other problems.
Therefore, it is important to talk to your doctor if you have had a history of
hypothyroidism or hyperthyroidism so you can be monitored before and during
your pregnancy, and to be sure that your medication is properly adjusted, if
necessary.  

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 CHAPTER IV

CONCLUSION

It is well documented that thyroid disorders are associated with maternal and fetal
complications during gestation. This present paper has discussed the possible
ways to prevent and manage these outcomes to assure a safe and proper ending to
pregnancy.

30
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