SUN-412 - An Overlooked Thyroid Pattern in Pregnancy: A Case of Isolated Maternal Hypothyroxinemia

Introduction:
During pregnancy, physiologic adaptations in thyroid function occur to meet increased maternal and fetal metabolic demands. These changes include elevated placental deiodinase activity, estrogen-mediated increases in thyroxine-binding globulin, and human chorionic gonadotropin-related suppression of thyroid-stimulating hormone (TSH), all of which change the concentrations of thyroid hormones in the blood and require trimester-specific interpretation of thyroid function tests (TFT). We present a case of isolated maternal hypothyroxinemia (IMH), characterized by low free thyroxine (fT4) concentrations in the presence of normal TSH, a biochemical pattern that can be easily overlooked. Although IMH has traditionally been studied mainly in large population-based cohorts, increasing evidence points to clinically significant correlations with maternal adverse outcomes, particularly hypertensive disorders of pregnancy, including preeclampsia. Despite these observational associations, randomized controlled trials evaluating levothyroxine therapy for IMH have not demonstrated clear benefit for maternal outcomes, and current guidelines therefore do not recommend routine treatment. Furthermore, while cohort data provide important population-level insights, detailed case reports describing the individual maternal clinical course and biochemical resolution of IMH remain scarce.
Case report:
A 43-year-old G3P1 female was evaluated at 11 weeks gestation, with TFT demonstrating suppressed TSH (0.01 µIU/mL; ref 0.27–4.5) with elevated fT4 (2.2 ng/dL; ref 0.9–1.8), consistent with gestational transient hyperthyroidism, with negative thyroid autoantibodies. She reported non-specific fatigue attributed to pregnancy and mild nausea, without thyrotoxic symptoms. Subsequently during the second trimester, she developed IMH with low fT4 (0.7 ng/dL) and a normal TSH, while remaining asymptomatic. Serial monitoring showed spontaneous biochemical resolution with normalization of TFT by the third trimester. Pregnancy was complicated by gestational hypertension, with progression to postpartum preeclampsia with severe features. Thyroid function remained normal postpartum, and the patient remained euthyroid at follow-up.

Conclusion:
This case illustrates the transient and evolving nature of IMH during pregnancy, with spontaneous normalization of TFT without therapeutic intervention. Despite biochemical resolution, the subsequent development of gestational hypertension and postpartum preeclampsia highlights that normalization of thyroid parameters does not preclude maternal morbidity. This case highlights the significance of identifying affected patients as a potentially high-risk population requiring careful maternal monitoring and individualized clinical assessment.

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