Hypothyroidism During pregnancy

1. Prof. Aboubakr Elnashar
Benha University Hospital
Email: elnashar53@hotmail.com
ABOUBAKR ELNASHAR

2. INTRODUCTION
1.CONTROL OF THYROID FUNCTION
2.PHYSIOLOGICAL CHANGES OF THYROID
DURING PREGNANCY
3.FETAL THYROID FUNCTION
4.TO SCREEN OR NOT TO SCREEN?
ABOUBAKR ELNASHAR

3. 1. CONTROL OF THYROID
FUNCTION
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 (T3 and T4) that
regulate metabolism
•TRH and TSH concentrations
are inversely related to T3 and
T4 concentrations. ABOUBAKR ELNASHAR

4. T3 and T4
99% bound to TBG.
1% free
only free forms are biologically active.
ABOUBAKR ELNASHAR

5. 2. 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 2nd & 3rd trimesters.
ABOUBAKR ELNASHAR

6. 4. TSH
decrease in 1st trimester
{increase HCG, HCG has thyrotropin-like activity},
increase in 2nd & 3rd trimester {Increased TBG}
should be < 2.5 mIU/L in 1st trimester
< 3.0 mIU/L after 1st trimester
American Thyroid Association ( 2012, 2014):
Normal
TSH: 0.2 to 3 mIU/L
FT4: 11.84 ± 3.86.
ABOUBAKR ELNASHAR

7. The shaded area represents the normal range in non pregnantABOUBAKR ELNASHAR

8. 5. Pregnancy: relative iodine deficiency
{1. increase mat iodine requirement
{active transport to fetoplacental unit}
2. Increase iodine excretion in urine, 2 fold
{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:
thyroid gland hypertrophies
{trap a sufficient amount of iodine}
ABOUBAKR ELNASHAR

9. 3. FETAL THYROID FUNCTION
During early gestation:
Fetus receives thyroid hormone from the mother. Maternal T4 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 12w
The fetus relies on maternal T4
exclusively before 12 w &
partially thereafter for normal fetal neurologic
development.
ABOUBAKR ELNASHAR

10. Maternal hypothyroidism
±detrimental to fetal development if not detected
and corrected very early in gestation.
Preconceptual optimization of T4 therapy is
important (III)
ABOUBAKR ELNASHAR

11. 4. TO SCREEN OR NOT TO SCREEN?
1.Infertility: Ovulatory disorders
2. Menstrual disorders
Hypothyroidism: mainly oligomenorrhea=
infrequent menstruation
Hyperthyroidism: mainly hypomenorrhea=
scanty menstruation
3. Repeated miscarriage
4. TIDM
ABOUBAKR ELNASHAR

12. 5. Pregnant women:
a.Routine:
Yes
(Mitchell ML, Klein , 2004)
No
(ACOG, 2015)
b. Selective:
(Mestman, 2004)
. S and S of the disorder, goiter
. Family history of autoimmune thyroid disease
. TIDM.
. History of
high-dose neck radiation
thyroid therapy
postpartum thyroiditis
infant born with thyroid diseaseABOUBAKR ELNASHAR

13.  How?:
1. TSH is the first line screening test to assess
thyroid status in pregnancy
(ASRM, 2015)
2. TSH and FT4 should be measured to diagnose
thyroid disease in pregnancy
(ASRM, 2015).
ABOUBAKR ELNASHAR

14. SCREENING FOR THYROID
AUTOANTIBODIES IN PREGNANCY.
universal screening is not recommended.
{Insufficient data to support any benefit of
screening and tt in pregnancy of euthyroid women}
(ASRM, 2015)
ABOUBAKR ELNASHAR

15. HYPOTHYROIDISM
ABOUBAKR ELNASHAR

16. 1.INCIDENCE AND TYPES
2.CAUSES
3.CLINICAL PICTURES
4.LABORATORY TESTS
5.EFFECTS OF PREGNANCY ON
HYPOTHYROIDISM
6.EFFECTS OF HYPOTHYROIDISM ON
PREGNANCY
7.MANAGEMENT
ABOUBAKR ELNASHAR

17. 1. INCIDENCE AND TYPES
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
{prevent serious damage to the fetus}.
Subclinical hypothyroidism :
2% to 3% of pregnancies
Intervention may be indicated.
ABOUBAKR ELNASHAR

18. TTAdverse
effects
T3FT4TSH
EltroxinYesDDEOvert
Eltroxin if
TPO
±NNESub
clinical
No ttNoNDNIsolated
hypothyroxinemia
ABOUBAKR ELNASHAR

19. 2. 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

20. •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

21. •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: should not be taken
within 4 h of thyroid medication.
ABOUBAKR ELNASHAR

22. 3. CLINICAL PICTURES
Fatigue, weight gain, constipation, cold
intolerance
muscle cramps
hair loss, dry skin, brittle nails
intellectual slowness, depression, insomnia
bradycardia
periorbital edema, myxedema, and myxedema
coma
ABOUBAKR ELNASHAR

23. 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•
Many features are common in normal pregnancy:
ABOUBAKR ELNASHAR

24. ABOUBAKR ELNASHAR

25. 4. LABORATORY TESTS
The standard for diagnosis.
{1. screening is controversial
2. symptomatology does not reliably distinguish
hypothyroidism from normal pregnancy}
Overt hypothyroidism:
Symptomatic patient
Elevated TSH level
low levels of FT4 and FT3.
Subclinical hypothyroidism:
Asymptomatic patient.
Elevated TSH
Normal FT4 and FT3
ABOUBAKR ELNASHAR

26. American Thyroid Association (2014):
1. Clinical hypothyroidism:
TSH (> 3 mIU/L) in conjunction with a low FT4. OR
TSH ≥ 10 mIU/L, irrespective of their FT4 level
2. Subclinical hypothyroidism
TSH: 3 -10 mIU/L with a normal FT4.
ABOUBAKR ELNASHAR

27. 5. EFFECT OF PREGNANCY ON
HYPOTHYROIDISM
 Pregnancy increase T4 dose in one-fourth of
women
 Dose increases should be in response to
abnormal TFTs interpreted with reference to normal
ranges for pregnancy.
 Dose increased in early pregnancy
{±inadequate replacement prior to pregnancy}
and most do not need to decrease their dose again
postpartum.
ABOUBAKR ELNASHAR

28. 6. EFFECTS OF HYPOTHYROIDISM ON
PREGNANCY
Depends on the severity of the condition.
A. Uncontrolled hypothyroidism.
PET
Anaemia
Miscarriage
IUFD and SB
PTL
SFGA
Developmental anomalies including reduced IQ.
ABOUBAKR ELNASHAR

29. ABOUBAKR ELNASHAR

30. •Congenital hypothyroidism
{severe iodine deficiency}:
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

31. B. Subclinical hypothyroidism.
•Low IQs of the children
(Mitchell and Klein, 2004).
•Placental abruption
•PTL
(Casey, 2005).
ABOUBAKR ELNASHAR

32. 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

33. 7. TREATMENT
Treat overt hypothyroid disease in pregnancy with
adequate thyroid hormone to minimize risk of adverse
outcomes
(ASRM, 2015).
Non pregnant:
1.7 μg/kg/d or
25 μg/d adjusted by 25 μg/d every 2 to 4 ws until
euthyroid state is achieved.
ABOUBAKR ELNASHAR

34. •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)
ABOUBAKR ELNASHAR

35. •Monitoring:
TSH should be monitored /4 ws
•Once euthyroid state has been achieved:
TSH should be monitored /trimester until delivery.
The following upper-normal reference ranges are
recommended:
1st T: 2.5 mIU/L
2nd T: 3.0 mIU/L
3rd T: 3.5 mIU/L.
(American Association of Clinical Endocrinologists and the American
Thyroid Association, 2013)
ABOUBAKR ELNASHAR

36. ABOUBAKR ELNASHAR

37. Benha University Hospital, Egypt
E-mail:elnashar53@hotmail.com
ABOUBAKR ELNASHAR