Thyroid disease in pregnancy
Pregnancy shifts the thyroid axis through hCG-driven TSH suppression and rising thyroxine-binding globulin, so interpreting thyroid tests requires trimester-specific reference ranges rather than nonpregnant cutoffs. The two decisions that matter most antepartum are distinguishing self-limited gestational transient thyrotoxicosis from Graves disease, and treating maternal hypothyroidism promptly, since undertreatment of either drives preeclampsia, preterm birth, and impaired fetal neurodevelopment.
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What this article covers
- Overview
This article covers antepartum thyroid disease only: physiologic thyroid changes of pregnancy, gestational transient thyrotoxicosis, Graves disease in pregnancy, and hypothyroidism in pregnancy.
- Epidemiology
Gestational transient thyrotoxicosis affects 1%-3% of pregnancies, the most common cause of a suppressed early-pregnancy TSH, far more common than Graves disease.
- Risk factors
Preexisting Hashimoto thyroiditis or positive TPO antibodies: the leading cause of gestational hypothyroidism, and a marker for closer TSH surveillance even if euthyroid at conception.
- Pathophysiology
hCG cross-reacts with the TSH receptor via a shared alpha subunit: rising first-trimester hCG binds the TSH receptor indiscriminately, stimulating hormone secretion and suppressing pituitary TSH by…
- Clinical features
Gestational transient thyrotoxicosis: mild, often asymptomatic or nonspecific (palpitations, heat intolerance, tachycardia overlapping normal pregnancy), onset in the first trimester tracking the hCG…
- Differential diagnosis
Gestational trophoblastic disease (molar pregnancy): markedly elevated hCG causes more severe thyrotoxicosis, plus vaginal bleeding before 16 weeks and no fetal heart tones; confirmed by ultrasound and a strikingly high beta-hCG.
- Diagnosis
Diagnosis rests on trimester-specific TSH reference ranges, not the nonpregnant range: in the late first trimester (weeks 7-12), hCG lowers both TSH limits (lower limit down about 0.4 mIU/L, upper…
- Management
First, confirm whether treatment is needed.
- Complications
Maternal heart failure or thyroid storm: poorly controlled hyperthyroidism can progress to high-output failure; labor, delivery, and surgery are recognized precipitants of storm (up to 30% mortality) in uncontrolled Graves disease.
- Prognosis
Gestational transient thyrotoxicosis is self-limited and resolves by mid-pregnancy as hCG falls after its peak, with no long-term sequelae.
- Prevention
Counsel every pregnant and lactating patient to take a daily iodine supplement of 150 mcg, since iodine requirements rise up to 50% and not all prenatal vitamins include it.
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Related articles
- Graves disease
Graves disease is an autoimmune disorder in which thyrotropin receptor antibodies stimulate the thyroid, causing hyperthyroidism, and is the most common cause of thyrotoxicosis in iodine-sufficient regions. Diagnosis rests on a suppressed thyroid-stimulating hormone with elevated free thyroxine and positive thyrotropin receptor antibodies, and first-line treatment is a thionamide, most often methimazole, with radioactive iodine or thyroidectomy reserved for recurrence or patient preference.
- Hyperthyroidism
Hyperthyroidism is the clinical syndrome of thyroid hormone excess, produced by a range of causes from Graves disease and autonomously functioning nodules to destructive thyroiditis and exogenous hormone ingestion. Diagnosis begins with a suppressed thyroid-stimulating hormone and elevated free thyroxine, followed by radioactive iodine uptake testing or antibody measurement to identify the cause, and first-line treatment is a beta blocker for symptom control while the underlying cause directs thionamide, radioactive iodine ablation, or thyroidectomy therapy.
- Hypothyroidism
Hypothyroidism is thyroid hormone deficiency, most commonly caused by autoimmune (Hashimoto) thyroid failure in iodine-sufficient countries, diagnosed by an elevated thyroid-stimulating hormone with a low or normal free thyroxine. First-line treatment is levothyroxine dosed at 1.6 mcg/kg lean body weight orally once daily, titrated using thyroid-stimulating hormone rechecked no sooner than 6 weeks after any dose change.
- Thyroid storm
Thyroid storm is a rare, life-threatening exaggeration of thyrotoxicosis with multiorgan dysfunction and mortality up to 30%, most often precipitated by discontinuation of antithyroid drugs, infection, surgery, or trauma in a patient with underlying hyperthyroidism. It is a clinical diagnosis treated emergently in the ICU with intravenous beta-blockade, a thionamide (propylthiouracil transitioning to methimazole), potassium iodide given only after the thionamide, and high-dose glucocorticoids.
- Postpartum thyroiditis
Postpartum thyroiditis is a destructive, painless thyroiditis that occurs in the first year after delivery, typically following the same thyrotoxic-then-hypothyroid-then-recovery course as painless thyroiditis, and permanently affects thyroid function in about 20% of cases. Treatment is symptomatic, with a beta-blocker for thyrotoxic symptoms and levothyroxine for a symptomatic or persistent hypothyroid phase, since thionamides and radioactive iodine are not indicated.
- Gestational diabetes mellitus
Gestational diabetes mellitus is carbohydrate intolerance first identified in the second or third trimester, diagnosed with a 50-g glucose challenge test followed by a confirmatory 100-g oral glucose tolerance test. Insulin is first-line pharmacologic therapy when glycemic targets are not met with diet and exercise, and untreated hyperglycemia drives fetal macrosomia, shoulder dystocia, neonatal hypoglycemia, and later maternal type 2 diabetes.
- Preeclampsia
New-onset hypertension after 20 weeks of gestation with proteinuria or end-organ dysfunction, driven by abnormal placental spiral artery remodeling and widespread endothelial dysfunction. Eclampsia is preeclampsia complicated by seizures; magnesium sulfate treats and prevents seizures, and prompt delivery is the only definitive cure for both.