Clinical Case: A 27 year-old primigravida was referred for gynaecology assessment after her 12 week booking ultrasound scan showed a multiloculated cystic mass in the Pouch of Douglas. She reported fatigue, dry skin and constipation for several months. She had no past medical history and took no regular medications. She had conceived naturally, and her periods were previously regular. There was a family history of hypothyroidism in her sister. She emigrated from India 3 years earlier with her husband.
Investigations and management: Pelvic MRI at 14 weeks gestation revealed bilateral multicystic ovarian masses (measuring 9.2×5.6 cm and 7.8×5.1 cm). Ca125 was mildly elevated, a non-specific finding in pregnancy. A serial MRI, performed at 20 weeks gestation, showed enlargement of both masses (14.4×6.4 cm and 15.6×7.5 cm), suggestive of spontaneous ovarian hyperstimulation syndrome. Thyroid function tests were performed and revealed severe primary hypothyroidism (free T4 <5, NR 9-21 pmol/L; TSH >200, NR 0.355 mU/L]. Anti-TPO antibodies were strongly positive (1597.1, NR <6 U/mL). TSH receptor antibodies were in the normal range (1.1, NR 0.01.9 U/L). Following assessment at the endocrine antenatal clinic, levothyroxine 100mcg daily was commenced. The patient returned to India for the remainder of her pregnancy, therefore her remaining clinical course is unknown.
Discussion: Rapidly enlarging ovarian cysts are a rare consequence of severe hypothyroidism and represent a form of spontaneous ovarian hyperstimulation syndrome. This has been reported previously in the context of pregnancy. The mechanisms of cyst enlargement include TSH stimulation of ovarian FSH receptors, and, in some cases, activating mutations of the FSH receptor. Cyst shrinkage and resolution is reported with successful treatment of hypothyroidism. The impact of untreated maternal hypothyroidism on fetal development is not well defined however impaired neurocognitive development has been reported in offspring.