Our patient is a twenty-four-year-old female with a sixteen-year history of HT-related hypothyroidism on oral levothyroxine 100 mcg once daily. She complained of occasional palpitations, nervousness, weight loss, and irregular menses. Thyrotoxicosis was confirmed with a thyroid function test, and levothyroxine dose was reduced. However, the patient continued to exhibit thyrotoxic symptoms even after completely stopping levothyroxine. On examination, the patient was calm but tachycardic and afebrile, and her blood pressure was 116/90 mmHg, weight was 58 kg, and BMI was 21.8. She was noted to have peripheral tremors. Her thyroid exam revealed the presence of diffuse nontender goiter, with no palpable nodules. Eye examination was only remarkable for mild exophthalmos, and there was no evidence of dermopathy.\nThyroid function revealed depressed TSH <0.01 mIU/L (0.3–4.2) and high T4 26.4 pmol/L (11.6–21.9) (). Based on the persistence of symptoms despite stopping thyroid hormone supplementations and the presence of ophthalmopathy elements, the rare shift to GD was suspected. Autoimmune workup revealed a strong positive Anti-TSH Receptor (Anti-TSHR) titer, in addition to persistent positivity of previously positive thyroid peroxidase antibody (TPO Ab) and an increasing titer of Antithyroglobulin Ab (). Thyroid ultrasound revealed slight enlargement of the right lobe and increased vascularity in both lobes. Radioactive iodine uptake scan (RAIU) showed diffuse radiotracer uptake more prominent in the right thyroid lobe (). Those findings kept with the shift to GD.\nThe patient received suppressive therapy with oral carbimazole 20 mg once daily and propranolol. A subsequent follow-up three months later showed normalization of thyroid function and improvement in clinical status.
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.