A 60-year-old man originally from China with no prior history of thyroid or autoimmune disease received a standard course of 48-week pegylated IFN-α and ribavirin therapy for chronic HCV (genotype 1b) with achievement of sustained virological response. He had compensated chronic liver disease with cirrhosis (Child-Pugh A) without other complications and no other reported medical problems. He denied previous use of amiodarone, lithium, medications, or supplements containing iodine or exposure to contrast. He was a nonsmoker and did not drink alcohol. Six months after commencing treatment, he reported fatigue, weight gain of 3 kg, and slowed cognition at a routine clinical visit. He denied changes to his skin, hair, or bowel habits. On examination, his vital signs were normal. His weight was 78 kg with a body mass index (BMI) of 26.8 kg/m2. There was no goitre and there were no signs of oedema, dermopathy, ophthalmopathy, or lymphadenopathy. Cardiac, respiratory, and gastrointestinal examinations were normal and in particular no stigmata of chronic liver disease was present. A peripheral neurological examination including reflexes was normal.\nSerum biochemistry including electrolytes, renal function, and full blood count were within normal limits, with no biochemical or serological evidence of decompensated liver disease. Alpha-fetoprotein (AFP) was normal at 3.5 kIU/L [normal, 0.0–6.0]. Pretreatment HCV quantitative RNA was >3,000,000 IU/mL and was undetectable 6 months after commencing treatment. A recent abdominal ultrasound revealed a radiologically normal liver with no signs of portal hypertension or hepatic lesions. His serum thyroid stimulating hormone (TSH) prior to therapy was 1.65 mIU/L [normal, 0.27–4.2] with a normal free T4 (fT4) of 14.5 pmol/L [normal, 12–25]. The TSH at the time of review (i.e., 6 months later) was 58.8 mIU/L, free T4 was 11.1 pmol/L, and free T3 was 4.2 pmol/L [normal, 2.5–6.0] (). Anti-TPO (983 IU/mL, normal <35) and anti-TG (733 U/mL, normal <80) antibodies were elevated ().\nGiven his symptoms and biochemical evidence of autoimmune hypothyroidism, the patient was commenced on standard adult thyroxine replacement therapy at 100 mcg daily. His symptoms improved and there was full clinical and biochemical resolution of his hypothyroid state. Fourteen months later, he returned for follow-up reporting symptoms of hyperthyroidism with weight loss, tremor, and palpitations. He had lost 5 kg of weight. At the time of review, serum TSH was suppressed at <0.02 mIU/L with elevated fT4 of 54.3 pmol/L, fT3 of 20.2 pmol/L, and an elevated TRAb of 4.0 U/L (normal <1.0), with anti-TPO (1,163 IU/mL) and anti-TG (114 U/mL) antibodies. Technetium scan revealed bilateral diffuse increased tracer uptake (5.9%, normal 0.5–3.5%), consistent with Graves' Disease ().\nThe patient's thyroxine was ceased and he was placed on antithyroid treatment with carbimazole 5 mg TDS. He self-ceased therapy 6 months later, with serendipitous clinical and biochemical remission. His serum TSH was 3.84 mIU/L, fT4 17 pmol/L, and fT3 4.5 pmol/L, but with persistently elevated anti-TPO at 383 IU/mL. Anti-TG 23 U/mL and TRAb < 1 U/L were normal. At the time of writing, the patient remained clinically and biochemically euthyroid.
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.