Hyperreactio luteinalis, a rare cause of hyperthyroidism in pregnancy.

This article reports a case of hyperthyroidism in a pregnant woman with hyperreactio luteinalis (HL), which may mimic gestational trophoblastic disease (GTD) and therefore requires a careful differential diagnosis. A nulligravida woman (with an 11-week pregnancy) was referred to endocrinology due to the finding of suppressed TSH with elevated FT4. She had no family or personal history of interest. The patient was in good clinical condition, except for low weight gain and sialorrhea. Examination revealed moderate diffuse goiter, with no signs of Graves’ ophthalmopathy. Laboratory test results included TSH level of 0.01 mU/mL (0.4--4.0) and free thyroxine level >7.77 ng/dL (0.89--1.80). Thyroid antibodies were negative. Thyroid ultrasound examination showed diffuse goiter and no nodules. Laboratory results were confirmed at week 13 of pregnancy. Ultrasonography showed a single pregnancy with a normal amount of amniotic fluid and enlarged ovaries, and multiple thin-walled, anechoic formations consistent with theca-lutein cysts (Fig. 1). Tumor markers (CEA, CA 15.3, CA 19.9, and CA 125) were tested due to the possibility of bilateral mucinous cystadenoma with normal results. The HCG level was 155.562 mU/mL). A chorionic villus biopsy performed at 14 weeks was consistent with a fetus with normal chromosomes. Treatment with methimazole 10 mg/day was prescribed. Polycystic images persisted in ultrasound examination at week 15, but gradually decreased in size in subsequent examinations until they completely disappeared. The patient continued on antithyroid treatment until a live female fetus was delivered by cesarean section at week 38. HCG gradually decreased to a normal level (1.8 mU/mL) in postpartum laboratory tests, which also showed a TSH level of 0.22 mU/mL and a FT4 level of 1.12 ng/mL. A diagnosis of hyperthyroidism in pregnancy is based on suppressed TSH with increased FT4 or FT3 levels. In the first trimester of pregnancy, TSH levels decrease due to stimulation by HCG of the TSH receptor (TSHr), with a peak between 7 and 11 weeks. Thus, TSH levels ranging from 0.03 mU/mL to 2.5 mU/mL are considered normal in the first trimester, while values up to 3.0 mU/mL are considered normal in the second and third trimesters. Therefore, low TSH levels in the first trimester with normal FT4 may be considered ‘‘physiological!’’. As to the etiology of hyperthyroidism, there are conditions caused by pregnancy itself, encompassed under the term of transient gestational thyrotoxicosis (TGT). On the other hand, any other etiology of thyroid hyperfunction occurring outside pregnancy may also develop during pregnancy.