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Susan, a 44-year-old laboratory technologist, went to a physician because she was concerned that she might be hypothyroid and developing a goiter. The physician palpated Susan’s thyroid and stated that her thyroid seemed a normal size, and ordered an ultrasound of the thyroid. The ultrasound confirmed that Susan’s thyroid was not enlarged and that, if anything, it might be a little smaller than expected. However, the physician noticed that Susan did show symptoms of possible hypothyroidism: her skin was dry with reduced sweating; she appeared to have myxedema, with a puffy face and swelling of the eyelids; and her hair was dry with a tendency to fall out. Susan had only gained a little weight, and the physician stated that it could be due to water retained by her myxedema. She had previously taken a blood test showing normal levels of total T4, but the physician stated that this could be inaccurate, because various factors can affect the binding of T4 to TBG (thyroid binding globulin), and so they need to measure her blood levels of free (unbound) T4. Further, it was important to measure her blood levels of TSH (thyroid- stimulating hormone). Depending on the results of these tests, they would also need to test for the presence of antibodies in her blood directed against thyroid peroxidase (TPO), a useful marker for autoimmune thyroid disease. Susan’s blood test results showed an abnormally elevated TSH level, but a level of free T4 that was at the lower end of the normal range. Further, the test for antibodies against thyroid peroxidase was positive, indicating autoimmune disease affecting the thyroid gland and causing hypothyroidism. The physician explained to Susan that she probably also has antibodies that block the TSH receptor on the thyroid cells, which are different than the kind of antibodies that people with Graves’ disease have, which stimulate the TSH receptors. He said that Susan should start to take levothyroxine, with a goal towards getting TSH levels towards the lower part of the normal range. He advised Susan that it would take a few months for her to feel the full effects of the exogenous levothyroxine. They would continue to monitor TSH levels and the levothyroxine doses needed, and watch the size of the thyroid, which the physician expected would gradually atrophy. 1. How could antibodies that block the TSH receptor affect thyroxine secretion? 2. Why would TSH levels be elevated in a person who is hypothyroid? 3. Why would taking levothyroxine pills cause TSH levels to lower? 4. Why would free T4 be a better indicator of thyroid function than total T4?

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