Autoimmune Thyroid Disease with Fluctuating Thyroid Function

A 38-y-old East Asian woman presented in 1985 with weight gain and cold intolerance. She was found to have a small goiter and an elevated thyroidstimulating hormone (TSH) level of 58 mU/l (normal range, 0.5–5). She was diagnosed with primary hypothyroidism and was treated with levothyroxine (L-T4) 0.1 mg/d. Her symptoms promptly improved. Between 1985 and 1993, she felt generally well. Her adherence to treatment was variable, and when she was reviewed her TSH levels were raised on several occasions (in the range of 15–38 mU/l). In her past medical history, she had an ectopic pregnancy in 1990 and bilateral oophorectomy in 2000 for benign cystadenomas. There was no family history of thyroid or autoimmune diseases. While the patient was on vacation in the summer of 1993, she stopped taking L-T4 altogether. Upon her return, thyroid function tests (TFTs) showed a TSH level of 0.46 mU/l, free thyroxine (FT4) at 15 pmol/l (normal range, 11–24), and thyroid hormone T3 at 1.9 nmol/l (normal range, 1.0–2.5). Antimicrosomal antibody titer was 1:400. Between June 1994 and November 1998, she continued to feel well on no treatment. TSH was measured annually and remained normal (range, 0.8– 1.6 mU/l). On 3 June 1999, the patient presented with palpitations, heat intolerance, excessive sweating, and anxiety. She also reported eye staring but no diplopia, proptosis (bulging eyes), or eye pain. She had no neck pain, dysphagia, or change in voice. She was clinically thyrotoxic with tachycardia, tremor, lid lag, and retraction. She had a symmetrical goiter, 40 g in size, that was firm, non-tender, and mobile with no distinct nodules or bruits. Hertel exophthalmometric measurements were 18 mm in both eyes (normal is up to 18 mm). The rest of the examination was unremarkable. TSH was less than 0.06 mU/l and FT4 was 31 pmol/l (Figure 1). Liver enzymes were normal. Radioiodine uptake was 41% (normal range, 25%–35%) at 24 h with homogeneous distribution of the tracer. On 8 June 1999, the patient was started on methimazole 20 mg/d. By 2 July 1999, she was feeling well, and TFTs showed FT4 at 24 pmol/l, T3 at 2.2 nmol/l, and TSH at less than 0.06 mU/l. On 25 July 1999, she was treated with 14 mCi of I. On 2 September 1999, the patient presented with severe symptoms of palpitations, heat intolerance, tremor, headache, nausea, and vomiting. Clinically, she was severely thyrotoxic, with a regular pulse of 110/min, and an oral temperature of 37.4 8C. She was irritable but fully conscious and oriented. She had lid lag and retraction and mild proptosis of the left eye (20 mm). The goiter was the same size (40 g) and consistency as during her presentation on 3 June1999, but it was now moderately tender. TFTs showed FT4 at more than 77 pmol/l, T3 at 6.4 nmol/l, and TSH at less than 0.06 mU/l. Methimazole was increased to 15 mg three times a day. Because of the severity of her hyperthyroidism, Lugol’s solution was added at five drops, three times a day, for 14 d. The patient declined corticosteroids. After a few days, she felt better and repeat FT4 was 42 pmol/l and TSH was less than 0.06 mU/l. Liver enzymes, however, were now raised: AST at 95 U/l, ALP at 372 U/l, and total bilirubin at 10 lmol/l. The methimazole was discontinued and replaced 2 wk later with propylthiouracil at a dose of 100 mg twice daily. The patient continued to improve over the following several weeks. Liver enzymes slowly normalized after about 2.5 mo. On 3 November 1999, the propylthiouracil was discontinued. TFTs done 2 and 4 wk later showed FT4 at 6 and 5 pmol/l and TSH at 18 and 30 mU/l, respectively. It was thought that this might be a transient hypothyroidism after I therapy or a permanent postablation hypothyroidism. The latter was considered more likely, and therefore the patient was started on L-T4. Five weeks later, she was doing well, and was clinically euthyroid with FT4 of 16 pmol/l and TSH of 0.8 mU/l.