Thyroid Disease in Pregnancy

Abdelrahman Al-daqqa

Physiologic Changes in Thyroid

Function During Pregnancy

Thyroid binding globulin (TBG) increases

due to reduced hepatic clearance and
estrogenic stimulation of TBG synthesis
The test results that change in pregnancy
are influenced by changes in TBG
concentration
Plasma iodide levels decrease due to fetal
iodide use and increased maternal
clearance -> leads to notable increase in
gland size in 15% of women (without
abnormal TFTs)

Physiologic Changes in Thyroid

Function During Pregnancy
Maternal
Status

TSH

Free T4

Free
Thyroxine
Index
(FTI)

Total T4

Total T3

Resin
Triiodothyronine
Uptake
(RT3U)

**initial
screening
test**

Pregnancy

No
change

No
change

No
change

Increase

Increase

Decrease

Hyperthyroidism

Decrease

Increase

Increase

Increase

Increase
or no
change

Increase

Hypothyroidism

Increase

Decrease

Decrease

Decrease

Decrease
or no
change

Decrease

The Fetal Thyroid

Begins concentrating iodine at 1012 weeks

Controlled by pituitary TSH by
approximately 20 weeks

Hyperthyroidism

Occurs in 0.2% of
pregnancies; Graves
disease accounts for
95% of cases

Look for:
-Nervousness
-Tremor
-Tachycardia
-Frequent stools
-Sweating
-Heat intolerance
-Weight loss
-Goiter
-Insomnia
-Palpitations
-Hypertension
-Lid lag/lid retraction
-Pretibial myxedema

Fetal & Neonatal Effects of

Hyperthyroidism

Associated with preterm delivery, low birth

weight, fetal loss
Fetal thyrotoxicosis (related to disease itself or
treatment)
Risk of immune-mediated
hypo/hyperthyroidism (due to antibodies
crossing the placenta, esp. in Graves or chronic
autoimmune thyroiditis)

Antibodies in Graves disease can be either

stimulatory or inhibitory
Neonates of women with Graves who have been
surgically/radioactively treated are at higher risk, b/c
not taking suppression

Causes & Diagnosis of

Hyperthyroidism

Most common cause of hyperthyroidism is

Graves disease

Document elevated FT4 or elevated FTI with

suppressed TSH, in absence of goiter/mass
Most patients have antibodies to TSH receptor,
antimicrosomal, or antithyroid peroxidase antibodies,
but measurement of these is not required (though
some endocrinologists recommend measuring TSI,
which are stimulatory antibodies to TSH receptor)

Other causes:

Excess TSH production, gestational trophoplastic

disease, hyperfunctioning thyroid adenoma, toxic
goiter, subacute thyroiditis, extrathyroid source of TH

Treatment of Hyperthyroidism

Goal is to maintain FT4/FTI in high normal

range using lowest possible dose (minimize
fetal exposure)
Measure FT4/FTI q2-4 weeks and titrate
Thioamides (PTU/methimazole) -> decrease
thyroid hormone synthesis by blocking
organification of iodide

PTU also reduces T4->T3 and may work more

quickly
PTU traditionally preferred (older studies found that
methimazole crossed placenta more readily and was
associated with fetal aplasia cutis; newer studies
refute this)

Treatment of Hyperthyroidism

Effect of treatment on fetal thyroid

function:

Possible transient suppression of thyroid

function
Fetal goiter associated with Graves (usually
drug-induced fetal hypothyroidism)
Fetal thyrotoxicosis due to maternal antibodies
is rare -> screen for growth and normal FHR
Neonate at risk for thyroid dysfunction; notify
pediatrician

Breastfeeding safe when taking

PTU/methimazole

Treatment of Hyperthyroidism

Beta-blockers can be used for

symptomatic relief (usually Propanolol)
Reserve thyroidectomy for women in
whom thioamide treatment unsuccessful
Iodine 131 contraindicated (risk of fetal
thyroid ablation especially if exposed after
10 weeks); avoid
pregnancy/breastfeeding for 4 months
after radioactive ablation

Hypothyroidism

Symptoms: fatigue, constipation, cold

intolerance, muscle cramps, hair loss, dry
skin, slow reflexes, weight gain,
intellectual slowness, voice changes,
insomnia
Can progress to myxedema and coma
Subclinical hypothyroidism: elevated TSH,
normal FTI in asymptomatic patient
Associated with other autoimmune
disorders

Type 1 DM -> 5-8% risk of hypothyroidism;

25% postpartum thyroid dysfunction

Hypothyroidism: Fetal & Neonatal

Effects

Higher incidence of LBW (due to

medically indicated preterm
delivery, pre-eclampsia, abruption)
Iodine deficient hypothyroidism ->
congenital cretinism (growth failure,
mental retardation, other
neuropsychological deficits)

Causes & Diagnosis of

Hypothyroidism

Causes:

Hashimotos (chronic thyroiditis; most common

in developed countries) & iodine deficiency ->
both associated with goiter
Subacute thyroiditis -> not associated with
goiter
Thyroidectomy, radioactive iodine treatment
Iodine deficiency (most common worldwide;
rare in US)

Treatment of Hypothyroidism

Treat with Levothyroxine in

sufficient dose to return TSH to
normal
Adjust dosage every 4 weeks
Check TSH every trimester

ACOG Recommendations

Screening of all pregnant women

with a personal history, physical
examination, or symptoms of a
thyroid disorder.

Rheumatoid Arthritis

Rheumatoid Arthritis in Pregnancy

Affects 1-2% of the general population
More common in women
RA in pregnancy is a common challenge
Sex hormones have effects on disease
activity
70-80% of cases improve during pregnancy
Post-partum flare common

Effect of Pregnancy on RA

Minimal effects on fetal morbidity and

mortality
Steroids may increase risk of IUGR and
PPROM
Active disease correlates with lower birth
weights

Treatment of RA in Pregnancy

Avoid NSAIDS and high dose aspirin

Low-dose aspirin safe
Use lowest doses of prednisone
Sulfasalazine, hydroxychloroquine in
refractory cases

RA Medications and Breast-feeding

Avoid:

Aspirin
Azathioprine
Cyclosporin
Cyclophosphamide
Methotrexate
Chlorambucil
High dose prednisone

Immune Thrombocytopenic
Purpura
ITP

Immune thrombocytopenic purpura

(ITP)

is a clinical syndrome in which a decreased

number of circulating platelets
(thrombocytopenia) manifests as a
bleeding tendency,
easy bruising (purpura), or extravasation of blood
from capillaries into skin and mucous membranes
(petechiae). Although most cases of acute ITP,
particularly in children, are mild and self-limited,
intracranial hemorrhage may occur when the
platelet count drops below 10 109/L (< 10
103/L);[1] this occurs in 0.5-1% of children, and
half of these cases are fatal.[2]

ITP Diagnostic Criteria:

Isolated thrombocytopenia
No drugs or other conditions that
may
affect platelet count
Exclude HIV, Hep C, SLE

ITP Pathology:

Increased platelet destruction

Inhibition of platelet production at
megakaryocyte level
Mediated by IgG Abs against platelet
membrane glycoproteins
Usually a chronic condition

ITP Clinical Features:

Petechiae, purpura, easy bruising

Epistaxis, menorrhagia, bleeding from gums
GIT bleeding, hematuria: rare
Intracranial hemorrhage very rare

ITP and Pregnancy

May affect fetus in up to 15% of cases

Neonatal count may drop sharply several days after
birth
Difficult to differentiate from gestational
thrombocytopenia
Epidurals safe if count > 50000
Prednisone +/- IVIG if count < 50000
Manage delivery according to standard obstetric
practice
Avoid NSAIDS post-partum

Gestational Thrombocytopenia

Incidence about 5%
Occurs late in pregnancy
Mild (>70 000)
No fetal neonatal
thrombocytopenia
Postpartum resolution

Myasthenia Gravis

Myasthenia Gravis:

Typically presents with fluctuating skeletal

muscular weakness
May be ocular or generalised
May have antibodies to the AChR
10-15% have a thymoma
Respiratory muscle involvement may lead
to respiratory failure

Myasthenia Gravis in Pregnancy:

Pregnancy has a variable effect on the

course of MG
Post-partum exacerbations in 30%
Infections can trigger exacerbations
Steroids can cause transient worsening
MgSO4 is contraindicated

Myasthenia Gravis Effect on the Fetus

Transplacental passage of IgG anti-AChR

Neuromuscular junction disorders
Transient neonatal MG in 10-20%
Decreased FMs and breathing
Polyhydramnios
Arthrogryposis multiplex congenita

Myasthenia Gravis Labour & Delivery

First stage of labour not affected

Second stage: expulsive efforts may
weaken
Assisted vaginal delivery may be indicated
Pre-labour anaesthetic assessment
indicated

Systemic Lupus Erythematosus

SLE features associated with high maternal and fetal risks

pregnancy relatively contraindicated

Severe pulmonary hypertension

Restrictive lung disease
Heart failure
History of severe HELLP or PET
Stroke within previous 6/12
Lupus flare within previous 6/12

SLE complications in pregnancy:

Disease exacerbation
Miscarriage, stillbirth
IUGR, preterm labour
Neonatal lupus
Drugs and breast-feeding

Neonatal Lupus:

of

Occurs in up to 2% of mothers with SLE

Targets skin and cardiac tissue,rarely other tissues
Congenital partial or complete heart block
Heart block detected in utero
Complete heart block: PNM of 44%
Rash: erythematous annular lesions
Rash clears within 6/12
Maternal dexamethasone may prevent progression
heart block
Neonatal pacemaker if HR<55