Hypothyroidism During pregnancy

Hypothyroidism
During pregnancy

1. Prof. Aboubakr Elnashar
Benha University Hospital
Email: [email protected]

2. Control of thyroid function
by a negative-feedback loop:
•The hypothalamus releases TRH
•TRH acts on the pituitary gland to release TSH
•TSH acts on the thyroid gland to release the thyroid hormones (T
3
and T
4) that regulate metabolism
•TRH and TSH concentrations are inversely related to T
3 and T
4
concentrations.


•99% circulating T
3 and T
4 is bound to TBG.
1% circulate in the free form,
and only the free forms are biologically active.
ABOUBAKR ELNASHAR

3. Management Adverse
effects
T4 T3 TSH %
Eltroxin Yes D D E Overt
Eltroxin if
TPO
Yes N N E Subclinical
No tt No D N N 1.3 Isolated
hypothyroxinemia
ABOUBAKR ELNASHAR

4. Physiological changes of thyroid during pregnancy
1.TBG
Increase {hepatic synthesis is increased}
2. TT4 & TT3
increase to compensate for this rise
3. FT4 & FT3
decrease.
FT4 are altered less by pregnancy, but do fall a little in the
2
nd
& 3
rd
trimesters.
4. TSH
decrease in 1
st
trimester, between 8 & 14 ws {increase
HCG, HCG has thyrotropin-like activity},
increase in 2
nd
& 3
rd
trimester {Increased TBG}
ABOUBAKR ELNASHAR

5. 5. Pregnancy is associated with a state of relative iodine
deficiency
{a. increase maternal iodine requirement because of active
transport to fetoplacental unit
b. Increase iodine excretion in urine, 2 fold, because of
increased GFT & decreased renal tubular reabsorption}
The thyroid gland increases its uptake from the blood 3 fold
{fall of plasma iodine}
If there is already dietary insufficiency of iodine, the thyroid
gland hypertrophies in order to trap a sufficient amount of
iodine
ABOUBAKR ELNASHAR

6. Non-
pregnant
1
st

trimester
2
nd

trimester
3
rd

trimester
TSH
mu/l
0-4 0-1.6 0.1-1.8 0.7-7.3
FT4
pmol/l
11-23 11-22 11-19 7-15
FT3
pmol/l
4-9 4-8 4-7 3-5
The shaded
area
represents
the normal
range in non
pregnant
ABOUBAKR ELNASHAR

7. Thyroid physiology and the impact of pregnancy
ABOUBAKR ELNASHAR

8. Fetal thyroid function
•During early gestation: the fetus receives thyroid hormone from the
mother.

Maternal T
4 crosses the placenta actively, the only hormone
that does so. (T3, TSH)
•The fetus’s need for thyroxine starts to increase as early as 5 ws of
gestation.
Fetal thyroid development does not begin until 10 to 12 ws, and then
continues until term.
The fetus relies on maternal T
4 exclusively before 12 ws & partially
thereafter for normal fetal neurologic development.
•Maternal hypothyroidism could be detrimental to fetal development if
not detected and corrected very early in gestation. Preconceptual
optimization of T4 therapy is important (III)
ABOUBAKR ELNASHAR

9. HYPOTHYROIDISM
ABOUBAKR ELNASHAR

10. Incidence
Much more common in women than men
Common in those with family history
Overt hypothyroidism:
0.3% - 2.5% of pregnancies
active intervention is required to prevent serious damage
to the fetus.
Subclinical disease:
2% to 3% of pregnancies
Current research indicates that intervention may be
indicated.
ABOUBAKR ELNASHAR

11. Causes
•Iodine deficiency:
most common cause in most of the world
•Hashimoto’s thyroiditis (chronic autoimmune thyroiditis):
most common cause in developed countries, where lack of
iodine in the diet is not a problem
characterized by:
antithyroid antibodies (thyroid antimicrosomial and
antithyroglobulin antibodies).
Both iodine deficiency and Hashimoto’s thyroiditis are
associated with goiter.


ABOUBAKR ELNASHAR

12. •Other causes:
radioactive iodine therapy for Graves’ disease;
thyroidectomy
viral thyroiditis
pituitary tumors
Sheehan’s syndrome;
Medications.
Thionamides
Lithium
Drugs that inhibit absorption of thyroid medication
- Ferrous sulfate
- Sucrafate
- Cholestyramine
- Antacids (aluminum hydroxide)

ABOUBAKR ELNASHAR

13. •Iodine and lithium inhibit thyroid function and, along with
dopamine antagonists, increase TSH levels.

•Thioamides, glucocorticoids, dopamine agonists, and
somatostatins decrease TSH levels.

•Ferrous sulfate, sucrafate, cholestyramine, and aluminum
hydroxide antacids all inhibit GIT absorption of thyroid
hormone and therefore should not be taken within 4 hrs of
thyroid medication.
ABOUBAKR ELNASHAR

14. Screening
•Routine screening has been recommended:
infertility
menstrual disorders
Repeated pregnancy loss (RCOG do not recommend)
Type 1 DM,
Pregnant women who have S&S of deficient thyroid function.

•In recent years, some authors have recommended
screening all pregnant women for thyroid dysfunction, but
such recommendations remain controversial.

•Routine screening is not endorsed by the ACOG
ABOUBAKR ELNASHAR

15. Clinical pictures
• Similar to physiologic conditions seen in most pregnancies.
•Fatigue, constipation, cold intolerance, muscle cramps, hair loss, dry
skin, brittle nails, weight gain, intellectual slowness, bradycardia,
depression, insomnia, periorbital edema, myxedema, and myxedema
coma

SYMPTOM
HYPOTHYROIDISM PREGNANCY
Fatigue o o•
Constipation •0 •o
Hair loss o•
Dry skin •o
Brittle nails •o
Weight gain •o o•
Fluid retention •o •o
Bradycardia •o •
Goiter •o o
Carpal tunnel
syndrome
•o o•
ABOUBAKR ELNASHAR

16. ABOUBAKR ELNASHAR

17. laboratory tests
Because screening is controversial and symptomatology
does not reliably distinguish hypothyroidism from normal
pregnancy, laboratory tests are the standard for diagnosis.
Overt hypothyroidism:
symptomatic patient
elevated TSH level
low levels of FT
4 and FT
3.
Subclinical hypothyroidism:
asymptomatic patient.
elevated TSH
normal FT
4 and FT
3
ABOUBAKR ELNASHAR

18. Effects of hypothyroidism on pregnancy
The impact of maternal hypothyroidism on the fetus depends
on the severity of the condition.
A. Uncontrolled hypothyroidism.
Miscarriage
Anaemia
Intrauterine fetal demise and stillbirth
preterm delivery,
low birth weight,
preeclampsia,
developmental anomalies including reduced IQ.

ABOUBAKR ELNASHAR

19. •Maternal and congenital hypothyroidism resulting from
severe iodine deficiency:
profound neurologic impairment & mental retardation.

•If the condition is left untreated.
Congenital cretinism:
Growth failure, mental retardation, and other
neuropsychologic deficits including deaf-mutism.

•If cretinism is identified & treated in the first 3 months of life:
near-normal growth and intelligence can be expected.

•For this reason, newborn screening for congenital
hypothyroidism.

ABOUBAKR ELNASHAR

20. B. Asymptomatic overt hypothyroidism.
Women who had previously been diagnosed with hypothyroidism,
(abnormal TSH and FT
4 levels), but who do not have symptoms.
1. Impaired psychomotor development at 10 months in infants born to
mothers who had low T
4 during the first 12 ws of gestation (Pop et
al,1999)
2. low IQ scores in the offspring at 7 to 9 yrs of age was correlated
with elevated maternal TSH levels at less than 17 weeks’ gestation
(Haddow et al, 1999).
An inverse correlation between a woman’s TSH level during
pregnancy and the IQ of her offspring (Klein et al, 1991).
and colleagues confirmed that maternal hypothyroxinemia is a risk for
neurodevelopmental abnormalities that can be identified as early as 3
weeks of age (Kooistra et al, 2006)
ABOUBAKR ELNASHAR

21. C. Subclinical hypothyroidism.
•Low IQs of the children whose mothers were not treated
(Mitchell and Klein, 2004).
•Undiagnosed subclinical hypothyroidism were more likely
to be complicated by
placental abruption
preterm birth (Casey, 2005).
ABOUBAKR ELNASHAR

22. Overt
Hypothyroidism
Subclinical
Hypothyroidism
No. of Patients* 60 (%) 57 (%)
PIH 13 (21) 9 (15)
Placental
abruption
3 (5) 0
PPH 4 (6.6) 2 (3.5)
Stillbirths 4 (6.6) 1 (1.7)
Congenital
malformations
2 (3.3) 0
LBW 10 (16.6) 5 (8.7)


Maternal and Neonatal Complications of
Hypothyroidism in Pregnancy
ABOUBAKR ELNASHAR

23. Treatment
The treatment of choice is synthetic T
4, or levothyroxine
(Levothyroid, Levoxyl, Synthroid, and Unithroid).
Non pregnant:
1.7 μg/kg/day or
12.5 to 25 μg/day adjusted by 25 μg/day every 2 to 4 ws
until euthyroid state is achieved.




ABOUBAKR ELNASHAR

24. •Pregnant:
Safe in pregnancy and lactation [II]. {Very little thyroxin
crosses the placenta and the fetus is not at risk of
thyrotoxicosis}
•Patients who were on thyroxine therapy before pregnancy
should increase the dose by 30% once pregnancy is
confirmed (Bombrys et al, 2008)

•Monitoring:
TSH should be monitored /4 ws
to maintain a TSH level between 1 and 2 mU/L and FT
4 in
upper third of normal.
•Once euthyroid state has been achieved, TSH should be
monitored /trimester until delivery.
ABOUBAKR ELNASHAR

25. The following upper-normal reference ranges are
recommended:
1
st
T: 2.5 mIU/L
2
nd
T3.0 mIU/L
3
rd
T: 3.5 mIU/L.
American Association of Clinical Endocrinologists and the American Thyroid
Association, 2013

ABOUBAKR ELNASHAR

26. During pregnancy,
thyroid function
merits regular
monitoring, fine-
tuning of treatment
ABOUBAKR ELNASHAR

27. Benha University Hospital, Egypt
E-mail:[email protected]

28. ABOUBAKR ELNASHAR