Management of Decreased T3 and T4 in Pregnancy
Pregnant women with decreased T3 and T4 levels require immediate levothyroxine therapy to prevent irreversible fetal neurodevelopmental damage, as maternal thyroid hormones are critical for fetal brain development, particularly in the first half of pregnancy. 1, 2, 3
Immediate Treatment Initiation
Start levothyroxine immediately without delay when both T3 and T4 are decreased in pregnancy, as this represents overt hypothyroidism requiring urgent intervention. 1
Dosing Strategy Based on Clinical Scenario
For new-onset hypothyroidism with TSH ≥10 mIU/L:
- Start levothyroxine at 1.6 mcg/kg/day 1
- Monitor TSH every 4 weeks until stable and within trimester-specific reference range 1
For new-onset hypothyroidism with TSH <10 mIU/L:
For pre-existing hypothyroidism with TSH above trimester-specific range:
- Increase current levothyroxine dose by 12.5 to 25 mcg per day 1
- Pre-pregnancy dose typically increases by 25-50% during pregnancy 4, 3
- Monitor TSH every 4 weeks until stable 1
Critical Rationale for Urgent Treatment
The urgency stems from the fact that maternal T4 is essential for fetal brain development, especially before fetal thyroid function begins at 17-19 weeks gestation. 2, 5 Maternal T4 crosses the placenta and mitigates T4 and T3 deficiency in fetal tissues, including the brain. 2 In contrast, maternal T3 does not adequately protect the fetal brain from T3 deficiency, even at doses toxic to the mother. 2
Untreated maternal hypothyroidism causes:
- Permanent neurodevelopmental deficits and reduced child IQ 4, 3
- Preeclampsia 4, 3
- Low birth weight 4, 3
- Gestational hypertension and stillbirth 3
- Miscarriage and premature delivery 3
Monitoring Protocol During Pregnancy
Measure serum TSH and free-T4:
- As soon as pregnancy is confirmed 1
- Every 4 weeks after any dose adjustment 1
- At minimum, during each trimester of pregnancy 1
Target TSH in trimester-specific reference range:
- Ideally <2.5 mIU/L in the first trimester 4, 3
- Maintain TSH within trimester-specific normal ranges throughout pregnancy 1
Physiological Context
During normal pregnancy, thyroid function undergoes profound alterations. 6 There is a T4 surge at 12 weeks that declines thereafter, with serum thyroid hormone concentrations falling in the second half of pregnancy. 3 The maternal thyroid must increase hormonal output by approximately 25-50% to meet metabolic demands. 4, 3, 6
Normal pregnancy changes include:
- Marked increase in thyroxine-binding globulin 6
- Marginal decrease in free hormone concentrations (in iodine-sufficient conditions) 6
- Transient TSH suppression near end of first trimester due to hCG stimulation 6
- Increased thyroid hormone turnover due to placental type III deiodinase 6
Critical Safety Considerations
Before initiating or increasing levothyroxine, rule out concurrent adrenal insufficiency, as starting thyroid hormone before corticosteroids can precipitate life-threatening adrenal crisis. 4 If adrenal insufficiency is suspected, start physiologic dose steroids 1 week prior to thyroid hormone replacement. 4
Ensure adequate iodine intake:
- WHO recommends 200 mcg iodine per day for pregnant women 6
- Iodine deficiency amplifies the decrease in free hormone concentrations and causes maternal and fetal goiter 6
- Adequate iodine supplementation early in pregnancy prevents maternal and neonatal goitrogenesis 6
Postpartum Management
Reduce levothyroxine dose to pre-pregnancy levels immediately after delivery. 1
Monitor serum TSH 4 to 8 weeks postpartum to ensure appropriate dosing, as thyroid hormone requirements typically return to pre-pregnancy levels. 1
Common Pitfalls to Avoid
Never use T3 (liothyronine) supplementation during pregnancy, as T3 provides inadequate fetal thyroid hormone delivery and does not protect the fetal brain. 2 Levothyroxine (T4) monotherapy is the only appropriate treatment. 4
Do not delay treatment waiting for repeat testing when both T3 and T4 are decreased, as this represents overt hypothyroidism requiring immediate intervention. 4
Avoid undertreating by targeting TSH >2.5 mIU/L in the first trimester, as even subclinical hypothyroidism is associated with adverse pregnancy outcomes. 4, 3
Do not wait for symptoms to develop before checking TSH, as fetal harm can occur before maternal symptoms appear. 4