Case Report: Reversible central hypothyroidism-like thyroid dysfunction revealing ACTH-independent cushing syndrome during pregnancy.

Thyroid dysfunction is common during pregnancy, and a reduced free thyroxine (FT4) concentration is often attributed to gestational thyroid disease. However, low FT4 with an inappropriately non-elevated thyroid-stimulating hormone (TSH), particularly when the abnormality persists during levothyroxine treatment, should prompt reassessment and raise suspicion for central hypothyroidism rather than automatic dose escalation. We report a 29-year-old woman referred at 17 weeks of gestation because FT4 remained low (9.18 pmol/L) while TSH was 0.5 μIU/mL during levothyroxine 75 μg/day. This discordant pattern was not typical of primary hypothyroidism. Review of the broader clinical picture revealed rapid weight gain, moon face, buffalo hump, and purple abdominal striae. Cortisol evaluation demonstrated loss of diurnal rhythm, markedly elevated 24-hour urinary free cortisol, and suppressed adrenocorticotropic hormone; magnetic resonance imaging identified a right adrenal mass. ACTH-independent Cushing syndrome caused by an adrenal adenoma was diagnosed. Retroperitoneal laparoscopic adrenalectomy was performed at 18 weeks and 3 days of gestation, followed by hydrocortisone replacement. At the 1-year follow-up, free triiodothyronine (FT3), FT4, and TSH had normalized. Levothyroxine was subsequently tapered and was discontinued at the 2-year follow-up, without recurrence of hypothyroidism. The patient delivered a live-born girl at 39 weeks. This case highlights persistent discordance between FT4 and TSH during levothyroxine treatment as a sentinel clue to occult hypercortisolism in pregnancy. Early recognition can prevent diagnostic delay, avoid unnecessary long-term thyroid hormone replacement, and permit definitive treatment during the optimal gestational window.