Management of hyperthyroidism in pregnancy.

Abstract

Hyperthyroidism in pregnancy most commonly results from gestational transient thyrotoxicosis (GTT), though Graves' disease, and less frequently, toxic nodular disease also occurs. Differentiating these conditions requires integration of clinical findings, trimester-specific thyroid function tests thresholds, and thyroid-stimulating immunoglobulin measurement when autoimmune etiology is suspected. Untreated or inadequately managed maternal overt hyperthyroidism that is not due to GTT is associated with significant maternal and fetal complications, including preeclampsia, thyroid storm, growth restriction, and fetal or neonatal thyrotoxicosis. Graves' disease management requires a delicate balance between achieving maternal euthyroidism and minimizing fetal drug exposure. Propylthiouracil is preferred during the first trimester to reduce teratogenic risk. If antithyroid drug (ATD) therapy is still required beyond 16 weeks of gestation, the decision to continue on propylthiouracil or switch to methimazole should be guided by shared decision-making between the patient and clinician. The use of the lowest effective ATD dose and close biochemical monitoring remain fundamental principles. Beta-adrenergic blockade may provide short-term symptomatic relief, whereas iodides are reserved for selected cases intolerant to ATDs. Thyroidectomy is typically reserved for patients with refractory hyperthyroidism or contraindications to ATDs and is preferably performed during the second trimester of pregnancy. Postpartum relapse of Graves' disease is common. Methimazole is considered safe during lactation at low doses, with no adverse effects on infant growth or neurodevelopment, while radioactive iodine therapy remains contraindicated. Collectively, contemporary evidence emphasizes early diagnosis, individualized therapy, and multidisciplinary care as central to optimizing maternal and fetal outcomes in hyperthyroidism during the reproductive years.