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 36 years old female presented with a 3 months history of easy fatigability, cold intolerance, polymenorrhagia, constipation and weight gain in the beginning of year 2005. On examination she had bradycardia and dry skin. The thyroid gland was palpable, non-tender mostly diffuse but some nodular feeling at upper pole of left lobe. Clinical suspicion of primary hypothyroidism was made and it was confirmed by TSH value of greater than 50 uIU/ml with FT4 of less than 0.30 ng/dl and positive thyroid antibodies. Thyroxine was started at a dose of 100 mcg/day. Gradually the requirement of thyroxine decreased and by the end of 2005 onwards she maintained her TSH within normal range on 50 mcg/day of thyroxine. In the beginning of 2008 the dose was further reduced to 25 mcg/day but again towards the end of 2009 thyroxine dose was increased to 50 mcg/day because of slightly increased TSH of 8.86 uIU/ml. Slightly more than a year later in the beginning of 2011, she presented with weight loss of 3 kg with a feeling of anxiety and associated tremors of hands. TSH at this time was less than 0.005 uIU/ml with a FT4 of 2.4 ng/dl, confirming the state of thyrotoxicosis. Thyroxine was stopped and patient was observed intermittently over a period of 6 months. She remained clinically and biochemically hyperthyroid with a repeat TSH of <0.005 uIU/ml and an FT4 of 2.66 ng/dl. Thyroid scintigraphy with technetium 99 was done and it showed an increased homogenous tracer uptake. Finally she was started on Neomercazole in mid of 2011and remains on it till to date.