A 28-year-old woman in her 24th week of pregnancy visited our hospital experiencing febrile sensation and palpitation. The woman was diagnosed with hyperthyroidism 10 years earlier and had taken thionamide periodically. She had not taken any medication recently because she did not display any signs or symptoms of hyperthyroidism. At the 20th week of gestation, she had a relapse of hyperthyroidism and resumed taking the thionamide (propylthiouracil 300 mg) that she had received at a local clinic. At that time, her blood count was within the normal range.
At her initial visit to the hospital, her blood pressure was 110/70 mmHg, pulse rate 110/min,respiratory rate 23/min and body temperature 39C. Her height and body weight were 163 cm and 55 kg. On physical examination, the patient was alert, her heart rhythm was regular and there was no sign of a murmur. She had a diffuse goiter and mild ophthalmopathy, and there was no evidence of any upper respiratory tract infection.
Her full blood count showed total WBCs at 1,600/mm3 with neutrophils 213/mm3 and lymphocytes 963/mm3, platelets 233x103/mm3 and hemoglobin 9.1 g/dL. Level of free T4 was 5.7 ng/mL (0.7~1.9), total T3 was 6.51 ng/mL (0.6~1.7), and TSH was<0.005 mU/mL (0~4.7). TBII (TSH-binding inhibitory immunoglobulin) was 61% (< 14.9%). AST/ALT were 49/47 IU/L and BUN/Creatinine were 12/1.0 mg/dL. An EKG showed sinus tachycardia and chest X-rays were normal. A fetal ultrasound examination revealed a normal sized fetus for the gestation period. The fetal heart rate was 160 beats/min and a non-stress test showed a reactive response.
Following the discontinuation of propylthiouracil, we began intravenous antibiotics (cephalosporin) and hydration (5% sodium dextrose fluid). Due to the possibility of teratogenecity, we excluded the use of G-CSF (granulocyte-colony stimulating factor). The patient's neutrophil count recovered to normal range with supportive care and her fever resolved after 10 days, yet her symptoms of hyperthyroidism were aggravated. At this point it was difficult to choose the optimal treatment method which would save both the mother and fetus. After considering all treatment options, it was decided that a total thyroidectomy rather than a subtotal thyroidectomy was the better option in this case, in order to prevent any future relapse. We also prescribed a beta-adrenergic blocker (propranolol 80 mg/day) and a Lugol solution (5% Lugol solution 1.2 mL/day) because a thyroidectomy without preoperative management was viewed to be too risky due to the high risk of thyrotoxic crisis. The treatment consisting of the beta-adrenergic blocker and the Lugol solution led to a rapid decline ofserum free T4 and total T3 concentration back to their normal ranges within 2 week (Figure 1). At 28 weeks of gestation, the patient underwent a total thyroidectomy without complications. Thyroxine replacement began on the first day following the operation and the patient's thyroid hormone levels were normalized after levothyroxine (synthyroid) 0.2 mg replacement.
The maternal TBII level at 38 weeks of gestation decreased to 23% and labor was induced at 40 weeks. A 3,370 g healthy male infant was born without any clinical features of thyrotoxicosis.