Thyroid Disorders in Pregnancy 2012

8/21/2019 Thyroid Disorders in Pregnancy 2012

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1DEFINITION OF TERMS

2PHYSIOLOGIC CHANGES IN THYROID FUNCTION DURING

PREGNANCY

Thyroid Function and the Fetus

3HYPERTHYROIDISM

Signs and Symptoms

Fetal and Neonatal Effects

Etiology and Differential Diagnosis

4HYPOTHYROIDISM

Signs and Symptoms




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5

CLINICAL CONSIDERATIONS & RECOMMENDATIONS

What laboratory tests are used to diagnose and manage thyroid disorderduring pregnancy?

What medications can be used to treat hyperthyroidism and

hypothyroidism in pregnancy, and how should they be administered and

adjusted during pregnancy?

What changes in thyroid function occur with hyperemesis gravidarum, and

should TFTs be performed routinely in women with hyperemesis?How is thyroid storm diagnosed and treated in pregnancy?

How should a thyroid nodule or thyroid cancer should during pregnancy

be assessed?

How is postpartum thyroiditis diagnosed and treated?

Which pregnant patients should be screened for thyroid dysfunction?

6

SUMMARY OF RECOMMENDATIONS


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Thyroid Gland:


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Thyroid System:


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Second most common endocrinedisease affecting women of

reproductive age

Both HYPERTHYROIDISMandHYPOTHYROIDISMmay INITIALLY

manifest during pregnancy

Obstetric conditions MAYaffectthyroid gland function

gestational trophoblastic disease

hyperemesis


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Thyrotoxicosisa clinical and biochemical state

excess production of and exposure to thyroid hormone

Hyperthyroidismthyrotoxicosis caused by hyperfunctioning of the thyroid

gland

Gravesdiseaseautoimmune disease

production of (TSI) and (TBII) that act on (TSH) receptor

to mediate thyroid stimulation or inhibition respectively


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Thyroid storm

severe, acute exacerbation of the signs and symptoms of

hyperthyroidism

Hypothyroidism

caused by inadequate thyroid hormone productionPostpartum thyroiditis

autoimmune inflammation of the thyroid gland

presents as new-onset, painless hypothyroidism,

transient thyrotoxicosis or thyrotoxicosis followed byhypothyroidism within 1 year postpartum


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PREGNANCY


3HYPERTHYROIDISM

Signs and Symptoms



4HYPOTHYROIDISM

Signs and Symptoms




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Thyroid function test results change in normal

pregnancy, hyperthyroidand hypothyroidstates as

depicted in TABLE 1

Thyroid binding globulin (TBG) concentrations INCREASESinpregnancy

reduced hepatic clearance

estrogenic stimulation of TBG synthesis

TransientINCREASEin (FT4) and (FTI) in 1sttrimesterNote: Elevations NOT beyond the normal non-pregnant range


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Maternal status TSH FT4 FTI TT4 TT3 RT3U

Pregnancy Nochange

Nochange

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

Table 1. Changes in Thyroid Function Test Results in

Normal Pregnancy and in Thyroid Disease


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Plasma iodide levels DECREASEduring

pregnancy

In 15% of women, associated with anINCREASEin thyroid gland size

Thyroid volume, by ultrasonography,

INCREASEDin pregnancy (mean increasesize of 18%)


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At 10-12 weeks

fetal thyroid begins concentrating iodine

At 20 weeks

pituitary TSH controls the fetal thyroid

At 36 wks AOG

Mean adult levels of TSH, TBG, FT4 & FT3 are

reached TSH does NOT cross the placenta

Only small amounts of T4 and T3 cross the

placenta


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Maternal thyroid hormone CROSSES

the placenta

Prevents overt stigmata of

hypothyroidism at birth

Maintain cord blood thyroid hormone

levels at 25-50% of normal

TRH, iodine and TSH receptor

immunoglobulins CROSS the placenta

as do PTU and methimazole


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PREGNANCY


3HYPERTHYROIDISM

Signs and Symptoms



4HYPOTHYROIDISM

Signs and Symptoms




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Occurs in 0.2% of pregnancies

95% of cases are due to Gravesdisease

Distinctive symptoms of Gravesdisease: Ophthalmopathy (lid lag and lid retraction)

Dermopathy (localized or pretibial myxedema)


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Some symptoms of hyperthyroidisimare SIMILAR

to symptoms ofpregnancyor nonthyroid disease,

SERUM TFTS differentiate thyroid disease from

nonthyroid disease.

Inadequately treated maternal thyrotoxicosis is

associated with a GREATER RISK of preterm

delivery, severe preeclampsia and heart failure

UNTREATED hyperthyroidism is associated with

miscarriage


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Inadequately treated hyperthyroidism is associatedwith an increase in medically indicated

preterm deliveries

low birth weight (LBW)

possible fetal loss

In one study, all of seven fetal losses occurred in

women with persistent hyperthyroidism


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Fetal and neonatal risks associated with Gravesdisease are related to either to:

the disease itself

to thioamide treatment of the disease

The possibility of fetal thyrotoxicosis should beCONSIDERED in ALL WOMEN with a history ofGravesdisease

If FETAL THYROTOXICOSIS is diagnosed, consultationwith a clinician with expertise in such condition iswarranted.


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Thyroid dysfunction in women is mediated by

antibodies that cross the placenta

Gravesdisease

Chronic autoimmune thyroiditis

Risk of immune-mediated hypothyroidism and

hyperthyroidism to develop in the neonate.

In women with Gravesdisease:

TSI and TBII that can STIMULATEor INHIBITthe fetal thyroid

TBII may cause transient hypothyroidism in neonates of

women with Gravesdisease


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1-5% of these neonates have hyperthyroidism or neonatal Graves

disease caused by the transplacental passage of maternal TSI

The incidence is low because of the balance of stimulatory and

inhibitory antibodies with thioamide treatment

Maternal antibodies are cleared less rapidly than thioamides in theneonate, resulting in a sometimes delayed presentation of neonatal

Gravesdisease

The incidence of neonatal Graves disease is unrelated to maternal

thyroid function.

The neonates of women who have been treated surgically or withradioactive iodine prior to pregnancy and require no thioamide

treatment are at higher risk for neonatal Gravesdisease because they

lack suppressive thioamide.14


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The most common cause of hyperthyroidism is Graves

disease.

The other clinical characteristics of Graves disease

also are immune-mediated but they are lessunderstood.

The diagnosis of Gravesdisease is generally made by

documenting elevated levels of FT4 or an elevated FTI,

with suppressed TSH in the absence of a nodular

goiter or thyroid mass.


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Although most patients with Graves disease have

TSH receptor, antimicrosomial, or antithyroid

peroxidise antibodies, measurement of these is

neither required nor recommended to establish thediagnosis

Other etiologies of thyrotoxicosis are excess

production of TSH, gestational trophoblastic

neoplasia, hyperfunctioning thyroid adenoma, toxicmultinodular goiter, subacute thyroiditis, and

extrathyroid source of thyroid hormone.


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PREGNANCY


3HYPERTHYROIDISM

Signs and Symptoms



4HYPOTHYROIDISM

Signs and Symptoms




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Having one autoimmune disease INCREASES

the likelihood of developing another;

5-8% incidence of hypothyroid disease in

patients with type 1 diabetes.

25 % risk of developing postpartum thyroid

dysfunction in women with type 1 DM


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It is unusual for advanced hypothyroidism to

present in pregnancy

Subclinical hypothyroidism is defined as

elevated TSH with normal FTI in an

asymptomatic patient

Untreated hypothyroidism is associated with

an increased risk ofpreeclampsia


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High incidence of LBWin neonates associated

with INADEQUATELY TREATED hypothyroidism

The etiology of LBW in these studies was

preterm delivery, preeclampsia or placental

abruption

Unclear if hypothyroidism is associated with

intrauterine growth restriction


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Women with iodine-deficient hypothyroidism are at

significant risk of having babies with congenital

cretinism

growth failure mental retardation

neuropsychologic deficits

In an iodine deficient population, treatment with

iodine in the first and second trimesters of pregnancysignificantly reduces the incidence of the neurologic

abnormalities of cretinism


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Untreated congenital hypothyroidism also results incretinism.

The incidence of congenital hypothyroidism is 1 in4,000 newborns and

only 5% of neonates are identified by clinicalsymptoms at birth, likely because of the ameliorativeeffects of maternal thyroid hormone.

If identified and treated within the first few weeks oflife, near-normal growth and intelligence can beexpected


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IODINE DEFICIENCY

PRIMARY THYROID ABNORMALITY

HYPOTHALAMIC DYSFUNCTION HASHIMOTOSDISEASE

most common etiology

characterized by production of antithyroidantibodies (thyroid antimicrosomal and

antithyroglobulin antibodies)


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IN PREGNANCY OR POSTPARTUM WOMEN,

Most common etiologies of hypothyroidism

Hashimotosdisease subacute thyroiditis

Thyroidectomy

Radioactive iodine treatment

Iodine deficiency

Associated with goiter Not associated with goiter

Hashimotos disease Subacute thyroiditis

Iodine deficiency


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5

CLINICAL CONSIDERATIONS AND RECOMMENDATIONS

What laboratory tests are used to diagnose and manage thyroid disorderduring pregnancy?

What medications can be used to treat hyperthyroidism and

hypothyroidism in pregnancy, and how should they be administered and

adjusted during pregnancy?

What changes in thyroid function occur with hyperemesis gravidarum, and

should TFTs be performed routinely in women with hyperemesis?How is thyroid storm diagnosed and treated in pregnancy?

How should a thyroid nodule or thyroid cancer should during pregnancy

be assessed?

How is postpartum thyroiditis diagnosed and treated?

Which pregnant patients should be screened for thyroid dysfunction?

6

SUMMARY OF RECOMMENDATIONS


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What laboratory tests are used to

diagnose and manage thyroid

disorder during pregnancy?

What laboratory tests are used to diagnose and


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Mainstay of thyroid function evaluation:

TSH testing

Now performed using monoclonal antibodies

making it more sensitive than the original

radioimmunoassay.


manage thyroid disorder during pregnancy?



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AACE and ATA, recommend TSHas the INITIAL TEST

for screening and evaluation of symptomatic disease

FREE COMPONENT

is the biologically active portion is not subject to change in conditions that alter TBG,

such as pregnancy.

In PREGNANT patients suspected of being

hyperthyroid or hypothyroid, TSH and FT4 or FTI

should be measured.





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FREE THYROXINE assessment by either direct immunoradiometric or chemiluminescent

methods

preferred over the equilibrium dialysis method

FTI calculated as FTI = TT4 x RT3U

if FT4 is not available

FT3

only pursued in patients with thyrotoxicosis with

suppressed TSH but FT4 measurements.

If ELEVATED , T3 thyrotoxicosis (occur before excessive FT4

production develops





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TRH STIMULATION TEST evaluates the secretory ability of the pituitary

ANTIBODY TESTS

TSH RECEPTOR ANTIBODIES either stimulatory (TSI) or inhibitory (TSII)

ANTIMICROSOMAL ANTIBODIES

TSI

Elevated in neonatal Gravesdisease

clinical usefulness is not clear

no practical use for measuring routinely

endocrinologists suggest that its measurement in the third trimester




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What medications can be used to

treat hyperthyroidism and

hypothyroidism in pregnancy?

How should they be administeredand adjusted during pregnancy?

What medications can be used to treat


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Thioamides (PTU and Methimazole)DECREASE thyroid hormone synthesis

by blocking the organification of iodide

PTU also reduces the peripheral

conversion of T4 to T3 quicker suppressant effect than methimazole

PTU is preferred in pregnancy crossed the placenta LESS WELL than methimazole

Methimazole associated with FETAL APLASIA CUTIS


hyperthyroidism and hypothyroidism in pregnancy?



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NO SIGNIFICANT DIFFERENCE in mean FT4 or TSH

levels in newborn umbilical cord blood samples

between PTU and methimazole treated mothers

NO RELATIONSHIP between maternal dosage ofthioamide and umbilical cord blood levels of TSH or

FT4

NO SIGNIFICANT DIFFERENCE in incidence of aplasia

cutis between control women without thyroid

disease and women with hyperthyroidismwho were

treated with methimazole





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can suppress Fetal and neonatal thyroid function Transient and rarely requires therapy

Fetal goiter

caused by drug-induced fetal hypothyroidism

Fetal thyrotoxicosis secondary to maternal antibodies (rare)

Monitor ALL fetuses for appropriate growth and normal

heart rate

routine screening for fetal goiter by ultrasonography isUNNECESSARY

Neonatal thyroid dysfunction

- All neonates of women with thyroid disease are at risk





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PTU and Methimazole safe during BREASTFEEDING only small amounts cross into the breastmilk

GOAL OF MANAGEMENT:

To maintain the FT4 or FTI in the high normal range

To use the lowest possible dosage of thioamidestominimize fetal exposure to the drug

MONITORING:

FT4 or FTI every 2-4 weeks

titrate the thioamide until FT4 or FTI are consistently inthe high normal range

In more than 90% of patients, improvement is seenwithin 2-4 weeks after treatment begins





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AGRANULOCYTOSIS Occurs in 0.1-0.4% - Fever and sore throat

CBC should be drawn - Discontinue medication

Cross reaction with other thioamides THROMBOCYTOPENIA

HEPATITIS

VASCULITIS- occur in less than 1% of patients Minor side effectsin 5% of patients

rash, nausea, arthritis, anorexia, fever and loss of taste or smell





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BETA-BLOCKERS

may be used to ameliorate the symptoms of

thyrotoxicosis until thioamides decrease thyroid

hormone levels. Propranolol is the most common -blocker used

for this indication.

THYROIDECTOMY reserved for women in whom thioamide treatment

is unsuccessful.





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IODINE 131

is CONTRAINDICATEDin pregnant womenrisk of fetal

thyroid ablation

Avoid pregnancy for 4 months after I-131 treatment.

IF at less than 10 weeks of gestation when exposed to I-

131, it is unlikely the fetal thyroid was ablated.

If exposure occurred at 10 weeks or later, the woman must

consider the risks of induced congenital hypothyroidism.

Breastfeeding should be avoided for at least 120 days after

treatment with I-131





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SAME as for nonpregnantwomen LEVOTHYROXINE

at sufficient dosages to normalize TSH levels.

4 weeks for thyroxine to alter the TSH level

pregnancy increases maternal thyroid hormone

requirements

TSH levels INCREASED while FTI DECREASED during

pregnancy

INCREASE thyroxine dosage from 0.1mg/day to

0.148mg/day

check TSH levels every trimester




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What changes in thyroid function

occur with hyperemesis

gravidarum?

Should TFTs be performedroutinely in women with

hyperemesis?


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How is thyroid storm diagnosedand treated in pregnancy?


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What changes in thyroid function

occur with hyperemesis

gravidarum?

Should TFTs be performedroutinely in women with

hyperemesis?


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How is thyroid storm diagnosed

and treated in pregnancy?

Treatment of Thyroid Storm in


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Pregnant Women:

1 Propylthiouracil (PTU), 600-800 mg orally stat, then

150-200 mg orally every 4-6 hours. If oral

administration is not possible, use methimazole

rectal suppositories.2 Starting 1-2 hours after PTU administration, saturated solutionof potassium iodide (SSKI), 2-5 drops orally every 8 hours, or

Sodium iodide, 0.5 to 1.0 g/IV every 8 hours, or

Lugols solution, 8 drops every g hours, or Lithium carbonate, 300 mg orally every 6 hours.

3 Dexamethasone, 2mg/IV or IM every 6 hours for 4

doses



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4 Propranolol, 20-80 mg orally every 4-6 hours, or

propranolol, 1-2 mg IV every 5 minutes for a total of 6

mg, then 1-10 mg IV every 4 hours.

If the patient has a history of severe

bronchospasm:

Reserpine, 1-5 mg IM every 4-6 hours

Guanethidine, 1mg/kg orally every 12 hours

Diltiazem, 60 mg orally every 6-8 hours5 Phenobarbital, 30-60 mg orally every 6-8 hours as

needed for extreme restlessness


Pregnant Women:


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How should a thyroid nodule or thyroidcancer during pregnancy be assessed?


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How is postpartum thyroiditis

diagnosed and treated?


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Which pregnant patients

should be screened for thyroid

dysfunction?


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.

Level A Recommendation

Levels of TSH or FT4/FTI should be

monitored to manage thyroid

disease in pregnancy


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.

Level B Recommendation

The following recommendations arebased on limited or inconsistentscientific evidence

Either PTU or Methimazole can be usedto treat pregnant women withhyperthyroidism

Thyroid function tests are not indicatedin asymptomatic pregnant women withslightly enlarged thyroid glands.


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.

Level C Recommendation

There is no need to measure TFTs

routinely in women with

hyperemesis.

There are insufficient data to

warrant routine screening of

asymptomatic pregnant women for

hypothyroidism.


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.

Level C Recommendation

Indicated testing of thyroid functionmay be performed in women with apersonal history of thyroid disease or

symptoms of thyroid disease. The presence of maternal thyroid

disease is important information to thepaediatrician to have at the time ofdelivery.

Thyroid nodules should be investigatedto rule out malignancy


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What changes in thyroid function occur with hyperemesis gravidarum


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What changes in thyroid function occur with hyperemesis gravidarum,

and should TFTs be performed routinely in women with

hyperemesis?

Nausea and vomiting of pregnancy have been attributed to thehigh HCG levels in the first trimester, and women with hyperemesis

gravidarum have been assumed to have particularly high HCG levels

and to be at risk for hyperthyroidism. Complete resolution of

biochemical and clinical hyperthyroidism also has been reported in

other studies. 37,38 These studies have reported that some

women with hyperemesis gravidarum required a short course of

thioamides; however, most had resolution of their signs and

symptoms without treatment. 38,39 Women who required

treatment throughout pregnancy had other symptoms of thyroiddisease, including thyroid enlargement, persistent tachycardia

despite fluid replacement and abnormal response to TRH

stimulation. 39


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In a study comparing pregnant women with hyperemesis andthose without hyperemesis, there was no difference in mean

TSH or FT3 levels. 40 Levels of FT4 and HCG were significantly

higher in women with hyperemesis but HCG levels correlated

significantly and positively with FT4 levels and negatively withTSH levels only in the hyperemesis group. Hyperemesis

gravidarum is associated with biochemical hyperthyroidism

but rarely with clinical hyperthyroidism and is largely

transitory, requiring no treatment. Routine measurements of

thyroid function are not recommended in patients with

hyperemesis gravidarum unless other overt signs of

hyperthyroidism are evident.

How is thyroid storm diagnosed and


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How is thyroid storm diagnosed and

treated in pregnancy?

Thyroid storm is a medical emergency characterized byan extreme hypermetabolic state. It is rare, about 1%, but has

a high risk of maternal heart failure. 9 Older literature

described a maternal mortality of 25% but this has not been

substantiated by more recent data. 9,41 It is diagnosed by acombination of the following: fever, tachycardia out of

proportion to the fever, changed mental status, vomiting,

diarrhea and cardiac arrhythmia. 42 Often there is an inciting

event such as infection, surgery, labor or delivery. Diagnosis

can be difficult to make and requires expedient treatment to

avoid the severe consequences of untreated thyroid storm,

which include shock, stupor and coma


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. If thyroid storm is suspected, serum FT4, FT3 and TSH levelsshould be evaluated to help confirm the diagnosis, buttherapy should not be withheld pending the results.

Therapy for thyroid storm consists of a standard series ofdrugs (see Box). PTU or methimazole blocks additionalsynthesis of thyroid hormone, and PTU also inhibits peripheralconversion of T4 to T3. Saturated solution of potassiumiodide and sodium iodide block the release of thyroidhormone from the gland. Dexamethasone decreases thyroid

hormone release and peripheral conversion of T4 to T3, andpropranolol inhibits the adrenergic effects of excessive thyroidhormone.


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Finally, Phenobarbital can be used to reduce extreme agitation orrestlessness and may increase the catabolism of thyroid hormone. 42

General supportive measures should also be undertaken, including

administration of oxygen, maintenance of intravascular volume and

electrolytes, use of antipyretics, use of a cooling blanket, and appropriate

maternal and fetal monitoring; invasive central monitoring and continuousmaternal cardiac monitoring in an ICU setting may be indicated. The

perceived underlying cause of the storm should also be treated. As with

other acute maternal illnesses, fetal well-being should be appropriately

evaluated with ultrasonography, biophysical profile or non-stress test

depending on the gestational age of the fetus. In general, it is prudent toavoid delivery in the presence thyroid storm unless fetal indications for

delivery outweigh the risks to the woman.


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Treatment of Thyroid Storm in Pregnant Women:

1Propylthiouracil (PTU), 600-800 mg orally stat, then 150-200 mg orally every 4-6 hours. If oral

administration is not possible, use methimazole rectal suppositories.

2Starting 1-2 hours after PTU administration, saturated solution of potassium iodide (SSKI), 2-5 drops orally

every 8 hours, orSodium iodide, 0.5 to 1.0 g/IV every 8 hours, or

Lugols solution, 8 drops every g hours, or

Lithium carbonate, 300 mg orally every 6 hours.

3Dexamethasone, 2mg/IV or IM every 6 hours for 4 doses

4Propranolol, 20-80 mg orally every 4-6 hours, or propranolol, 1-2 mg IV every 5 minutes for a total of 6

mg, then 1-10 mg IV every 4 hours.

If the patient has a history of severe bronchospasm:

Reserpine, 1-5 mg IM every 4-6 hours

Guanethidine, 1mg/kg orally every 12 hours

Diltiazem, 60 mg orally every 6-8 hours5Phenobarbital, 30-60 mg orally every 6-8 hours as needed for extreme restlessness

H h ld th id d l th id h ld


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How should a thyroid nodule or thyroid cancer should

during pregnancy be assessed?

The incidence of thyroid cancer in pregnancy is 1 per1,000. 43 Any thyroid nodule discovered during

pregnancy should be diagnostically evaluated,

because malignancy will be found in up to 40% of

these nodules. 34,44 Pregnancy itself does not

appear to alter the course of thyroid cancer. 43,45

Whether pregnancy increases the risk that a thyroid

nodule becomes cancerous is less clear. 34


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In a cohort study comparing thyroid cancer in pregnant orpostpartum women with nonpregnant women, there were no

differences in the presenting physical findings, tumor type, rumor

size, presence of metastases, time between diagnosis and

treatment, recurrence rates of death rates. 43 Women in this study

were monitored for a median of 20 years. These data strongly

suggest that pregnancy does not affect the outcome of thyroid

cancer. In addition, except for the time between diagnosis and

surgery, there was no difference in outcome between those women

who had thyroidectomy during pregnancy and those who had theprocedure after pregnancy. Significantly more pregnant women

had no symptoms, emphasizing the importance of the physical

examination during pregnancy.


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Another study compared pregnancy outcomes among womenwith thyoid cancer who fell into 1 of 3 categories: a.) before

treatment b.) after thyroidectomy but before I-131 treatment

c.) after treatment with both thyroidectomy and I-131. 46

The study found no differences in stillbirths, LBW, ormalformations among the three groups. The incidence of

spontaneous abortion was significantly higher in women who

had any treatment for thyoid cancer but was not different

between those women who had surgery only and those who

had surgery an I-131 treatment.


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If the diagnosis of cancer is made, a multidisciplinarytreatement plan should be determined. The options are

pregnancy termination, treatment during pregnacy and

preterm or term delivery with treatment after pregnancy.

This decision will be affected by the gestational age atdaignosis and the tumor characteristics. Definitive treatment

for thyroid cancer is thyroidectomy and radiation.

Thyroidectomy can be performed during pregnancy,

preferably in the second trimester, but radiation should be

deferred until after pregnancy. Breastfeeidng should be

avoided for at least 120 days after I-131 treatment. 34

How is postpartum thyroiditis diagnosed and


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How is postpartum thyroiditis diagnosed and

treated?

Postpartum thyroiditis occus in 5% of womenwho do not have a history of thyroid disease. 47Studies have found that approximately 44% ofwomen with postpartum thyroiditis have

hypothyroidism, while the remaining women areevenly split between thyrotoxicosis andthyrotoxicosis followed by hypothyroidism. 47,48 Inone study, goiter was present in 51% of women with

postpartum thyroiditis. 48 Postpartum thyroiditisalso may occur after pregnancy loss and has a 70%risk of recurrence. 49,50


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The diagnosis of postpartum thyroiditis is made by documentingnew-onset abnormal levels of TSH or FT$ or both. If the diagnosis isin doubt, measuring antimicrosomal or thyroperoxidase antithyroidperoxidase antibodies may be useful to confirm the diagnosis.

The need for treatment in women with postpartum thyroiditis

is less clear. In a prospective study of 605 asymptomatic pregnantand postpartum women, only 5 or 11% diagnosed with postpatumthyroiditis developed permanent hypothyroidism. 48 Furthermore,none of the women with thyrotoxicosis required treatment. 48Those who were treated received T4 for extremely high levels of

TSH with suppressed T4 or increasing goiter size. Because of thelow incidence postpartum thyroiditis and the low likelihood ofrequireing treatment, screening with TFTs and antimicrosomalantibodies in asymptomatic women is not warranted.47,51


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Women who develop a goiter in pregnancy or postpartum orwho developed postpartum hypothyroid or hyperthyroid

symptoms (including excessive fatigue, weight gain, dry skin,

dry hair, cold intolerance, persistent amenorrhea, difficulty

concentrating, depression, nervousness or palpitations)should have their TSH and FT4 levels evaluated. 47,48,51 As

noted previously, thyroid antimicrosomal or antithyroid

peroxidase antibodies may also be useful. If the patient has

hypothyroidism the decision to treat depends on the serverity

of abnormality and symptoms. Women with the highest

levels of TSH and antithyroid peroxidase antibodies have the

highest risk for developing permanent hypothyroidism. 48

Which pregnant patients should be screened for


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Which pregnant patients should be screened for

thyroid dysfunction?

It is appropriate to perform indicatedtesting of thyroid function in women with a

personal history of thyroid disease or

symptoms of thyroid disease. Theperformance of TFTs in asymptomatic

pregnant nwomen who have a mildly enlarged

thyroid is not warranted. Development of asignificant goiter or distinct nodules should be

evaluated as in any patient.


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An observational study has drawn considerable attention to the suject ofmaternal subclinical hypothyroidism and resulte in calls from someprofessional organizations for universal screening for maternalhypothyroidism. 20 Investigators screened maternalserum samplesobtained in the second trimester for purposes of maternal sermalphafetoprotein screening for neural tube defectsfor elevated TSHlevels. 20 Out of 25,216 samples, only 75 had TSH levels above the 99.7thpercentile. The investigators then compared the results ofneuropsychologic testing for 62 children of hypothyroid women with thoseof 124 children of matched women with normal thyroid glands when thechildren were approximately 8 years of age. They found no significantdifference in mean IQ scores between the chidlren of hypothyroid womenand controls (p = 0.06). There was a significant difference in mean IQ

scores when the children of untreated hypothyroid women werecompared with controls but not between children of ountreated andtreated hypothyroid women, Among the children of the untreatedwomen, 19% had full scale IQ scores of 85% or lower, compared with only5% of the children of women with normal thyroid glands.


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It is important to achknowledge the lmitations of the currentunderstanding of this issue. The datea availabot areobservational. There have been no interveition trials todemonstrate the efficacy of screening and treatement toimprove neuropsychologic performance in the offspring of

hypothyroid women. The avilable data are consitetn with thepossibilit that maternal hypothyroidism is associated with adecrement in some neuropsychologic testing. However, theassociateion needs furhter testing to document its validityand, if confirmed, evidence that treatment ameliorates theeffect. For all of these reasons, it would be premature torecommend universal screening for hypothyroidism duringpregnancy.


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Thyroid Disorders in Pregnancy 2012

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