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.
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.