A 44-year-old woman with 5-year history of Basedow’s disease had a total thyroidectomy. She had no past and family history and had no drug allergy. She was diagnosed as Basedow’s disease at 39 years old and after then she started taking 30 mg of thiamazole (MMI). In physical examination, she had no remarkable symptom such as palpitation, general fatigue and insomnia and did not have a goiter. Her height and body weight were 158.0 cm and 63.6 kg. Her vital signs were: heart rate 112 beats/min, blood pressure 132/86 mmHg. Laboratory data were as follows: white blood cell count, 4580 /μL (neutrophil 57.7%); red blood cell count, 476 × 104 /μL; hemoglobin, 12.7 g/dL; platelet, 26.5 × 104 /μL; Na, 142 mmol/L; K, 5.2 mmol/L. Renal and liver function was within normal range (creatinine (CRE), 0.38 mg/dL; blood urea nitrogen (BUN), asparate aminotransferase (AST), 25 U/L; alanine transaminase (ALT), 26 U/L; alkaline phosphatase (ALP), 231 U/L; γ-glutamyltranspeptidase (γ-GTP), 17 U/L; lactate dehydrogenase (LDH), 174 U/L). Thyroid-associated data were as follows: thyroid-stimulating hormone (TSH), < 0.010 μIU/mL; free triiodothyronine (FT3), 19.05 pg/mL; free thyroxine (FT4) 4.88 ng/dL; TRAb, 10.6 IU/L (electro chemiluminescence immunoassay (ECLIA), SRL Inc., Tokyo); TPOAb, 216.9 IU/mL (ECLIA, SRL Inc., Tokyo); TgAb antibody, 428.9 IU/mL (ECLIA, SRL Inc., Tokyo). Ultrasound examination revealed that the thyroid gland was hypervascular although it was not enlarged (Fig. ). Based on such findings, we finally diagnosed her as Basedow’s disease. Two weeks after starting MMI therapy, she had liver dysfunction (AST, 420 U/L; ALT, 368 U/L; ALP, 565 U/L; γ-GTP, 178 U/L; LDH, 337 U/L), and we changed the treatment of MMI to 300 mg of propylthiouracil (PTU) although her thyroid hormone levels were decreased (TSH, < 0.010 μIU/mL; FT3, 7.2 4 pg/mL; F T4 1.97 ng/dL). After then, her liver function was improved, and we tapered PTU. About 2 years later, her thyroid hormone levels were within normal range with 50 mg of PTU every other day, and her TRAb became negative. After then, we stopped PTU therapy.\nAbout 1.5 years later, she had low grade fever and palpitation and visited our office again. Her body weight was 70.9 kg. Her vital signs were: heart rate 116 beats/min, blood pressure 140/98 mmHg. Laboratory data were as follows: white blood cell count, 3710 /μL (neutrophil 58.3%); red blood cell count, 535 × 104 /μL; hemoglobin, 12.2 g/dL; platelet, 22.4 × 104 /μL; Na, 142 mmol/L; K, 4.2 mmol/L. Renal and liver function was within normal range (CRE, 0.52 mg/dL; BUN 9 mg/dL; AST, 25 U/L; ALT, 17 U/L; ALP, 218 U/L; γ-GTP, 19 U/L; LDH, 206 U/L). Thyroid-associated data were as follows: TSH, < 0.010 μIU/mL; FT3, 5.22 pg/mL; FT4, 1.85 ng/dL; TRAb, 4.6 IU/L; TPOAb, 147.4 IU/mL; TgAb, 591.2 IU/mL. Ultrasound examination revealed that the thyroid gland was not hypervascular compared to that at the onset of Basedow’s disease (Fig. ). Based on such findings, we finally diagnosed her as the relapse of Basedow’s disease. We started again 300 mg of PTU and tapered PTU dose. About 4 months later, her thyroid hormone levels became within normal range by taking 50 mg of PTU every other day. During the PTU therapy, her WBC levels were slightly lower and CRP levels were slightly higher, although she had no symptom in the whole body including in skin. We checked various autoimmune antibodies. Anti-double stranded DNA IgG antibody, anti-SS-A/Ro antibody and anti-SS-B/La antibody were all negative. However, anti-nuclear antibody (ANA), myeloperoxidase-anti-neutrophil cytoplasmic antibody (MPO-ANCA) and proteinase3-anti-neutrophil cytoplasmic antibody (PR3-ANCA) were all positive (ANA, 37.8 (+); MPO-ANCA, 35.0 U/mL; PR3-ANCA, 36.9 U/mL).\nWe performed a total thyroidectomy. Table shows laboratory data before a total thyroidectomy in this subject taking 50 mg of PTU every other day. In general, the thyroid gland in subjects with Basedow’s disease shows diffuse goiter due to chronic stimulation. However, her thyroid was flat and atrophic although diffuse hyperplasia of the thyroid gland was observed in histopathological macroscopic findings (Fig. ). Furthermore, hyperplasia of the thyroid gland was shown in part and hyperplastic thyroid follicles with papillary infoldings was observed in histopathological microscopic examination. Tall follicular cells with papillae usually lacked fibrovascular cores and peripheral scalloping was present (Fig. ). On the other hand, a part of the thyroid area showed a dense lymphoplasmacytic infiltrate, accompanied by follicles containing germinal centers. In addition, a destroyed pattern of lymphoid follicle was observed (Fig. ).\nOne year later, thyroid-associated autoimmune antibodies were all decreased (TRAb, 2.2 IU/L; TSAb, 130% (enzyme immunoassay, SRL Inc., Tokyo); TPOAb, 98. 3 IU/mL; TgAb, 151.0 IU/mL), and 2 years later thyroid-associated autoimmune antibodies were further improved (TRAb, 1.1 IU/L; TSAb, 90%; TPOAb, 24.0 IU/mL; TgAb, 12.8 IU/mL). White blood cell count became within normal range (about 5000–7000 /μL (neutrophil 58–68%) and CRP level became almost normal (0.15–0.20 mg/dL).
46 years old female, mother of 3 children diagnosed as having primary hypothyroidism on the basis of clinical symptoms of easy fatigability, weight gain and increase sleep and a serum TSH level of >75 uIU/ml, FT4: 0.25 ng/dl and strongly positive thyroid antibodies in December 2002. Thyroxine 50 mcg/day was started which she continued. After 2 years she presented to us with complain of weight loss. Her serum TSH level was 0.035 uIU/ml and a T4: 7.84 ng/dl so thyroxine was stopped. She came for follow up after 5 months with serum TSH: 0.010 uIU/ml off thyroxine. After another 6 months her serum TSH remained suppressed with a value of 0.018 uIU/ml and an FT4 of 1.18 ng/dl and she remained off thyroxine. After further 2 years her TSH was 0.837 uIU/ml, FT4 0.922 ng/dl and FT3 3.06. And after 1 year she presented with a TSH level of <0.005 uIU/ml, raised FT4 and positive thyroid microsomal antibodies (1: 1600). Techniteum 99 thyroid scan showed diffusely increased homogenous tracer uptake. Neomercazole was started at the dose of 5 mg/day which was gradually increased to 10 mg/day. She followed up after 4 months with TSH: 0.01 uIU/ml, T4: 5.84 ng/dl, T3: 1.99 ng/dl. Neomercazole was continued. Then she came for follow up after 1 year, at this time she was clinically euthyroid but biochemically hypothyroid with serum TSH: 14.89 uIU/ml, FT4:0.65 ng/dl. Neomercazole was stopped and advised to repeat TFT’s after 8 weeks. She came after 4 months with TSH: 3.98 uIU/ml, so no treatment was advised. After a period of 1 year she again came with complains of weight loss and palpitations. At this time her TSH: < 0.005 uIU/ml, FT4: 2.25 ng/dl. Neomercazole was restarted and Radioactive iodine 131 ablation planned.