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).
A 32-year-old female presented with symptoms of low energy level, weight gain, cold intolerance, increased bowel movements, flaking, and itchy scalp in the year 2014. On examination, she was found to have a palpable goiter. Her family history was significant for thyroid disease affecting her sibling. Neck ultrasound demonstrated diffusely enlarged thyroid with mild heterogeneous echotexture and left hypoechoic solid nodule measuring 0.75 cm []. Thyroid function test (TFT) was within the normal limits (TSH: 3.4 μIU/mL and FT4: 1.1 ng/dL; normal laboratory values of TSH 0.350–4.940 uIU/mL and FT4: 0.7–1.5 ng/dL respectively) however, antithyroid peroxidase (1446.0 IU/ml; reference range 0.0–5.6 IU/ml) and Tg antibodies (95.4 IU/ml; reference range 0.0–4.1 IU/ml) were high. A diagnosis of euthyroid Hashimoto's disease was made, and the patient was followed up on ultrasound and TFT.\nIn the year 2016, the patient presented with irritability and anxiety. Repeat ultrasound showed status quo. However, there was a surge in thyroid antibodies and an increase in TSH levels (7.2 μIU/mL). The clinical impression was consistent with Hashimoto's thyroiditis and the patient was started on low-dose thyroxine, which she tolerated well for 3 years. On yearly follow-up, there was a downtrend in thyroid antibodies, TSH returned to normal range, and findings on ultrasound remained stable.\nIn October 2019, the patient presented with syncopal episode. Evaluation of TFT demonstrated low TSH of 0.003 μIU/mL and raised FT4 of 2.4 ng/dL. The patient was asked to stop thyroxine tablets and to repeat TFTs in 4 weeks. Repeat TSH was <0.002 μIU/mL and FT4 of 2.6 ng/dL. I-123 thyroid uptake and the scan was performed, which demonstrated findings consistent with Graves' disease [] with 24 h uptake of 63.6% (normal range 10%–25%). The patient was subsequently treated with 15.9 mCi of radioiodine (I-131). Follow-up in 6 weeks of radioiodine therapy, the patient was clinically stable.