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CASE STUDY
JP is a 33-year-old woman who presents with complaints of fatigue requiring daytime naps, weight gain, cold intolerance, and muscle weakness for the last few months. These complaints are new since she used to always feel “hot,” noted difficulty sleeping, and could eat anything that she wanted without gaining weight. She also would like to become pregnant in the near future. Because of poor medication adherence to methimazole and propranolol, she received radioactive iodine (RAI) therapy, developed hypothyroidism, and was started on levothyroxine 100 mcg daily. Other medications include calcium carbonate three times daily to “protect her bones” and omeprazole for “heartburn.” On physical examination, her blood pressure is 130/89 mm Hg with a pulse of 50 bpm. Her weight is 136 lb (61.8 kg), an increase of 10 lb (4.5 kg) in the last year. Her thyroid gland is not palpable and her reflexes are delayed. Laboratory findings include a thyroid-stimulating hormone (TSH) level of 24.9 μIU/mL (normal 0.45–4.12 μIU/mL) and a free thyroxine level of 8 pmol/L (normal 10–18 pmol/L). Evaluate the management of her past history of hyperthyroidism and assess her current thyroid status. Identify your treatment recommendations to maximize control of her current thyroid status.
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The normal thyroid gland secretes sufficient amounts of the thyroid hormones—triiodothyronine (T3) and tetraiodothyronine (T4, thyroxine)—to normalize growth and development, body temperature, and energy levels*. These hormones contain 59% and 65% (respectively) of iodine as an essential part of the molecule. Calcitonin, the second type of thyroid hormone, is important in the regulation of calcium metabolism and is discussed in Chapter 42.
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The recommended daily adult iodide (I−)† intake is 150 mcg (200 mcg during pregnancy and lactation and up to 250 mcg for children).
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Iodide, ingested from food, water, or medication, is rapidly absorbed and enters an extracellular fluid pool. The thyroid gland removes about 75 mcg a day from this pool for hormone synthesis, and the balance is excreted in the urine. If iodide intake is increased, the fractional iodine uptake by the thyroid is diminished.
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Biosynthesis of Thyroid Hormones
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Once taken up by the thyroid gland, iodide undergoes a series of enzymatic reactions that incorporate it into active thyroid hormone (Figure 38–1). The first step is the transport of iodide into the thyroid gland by an intrinsic follicle cell basement membrane protein called the sodium/iodide symporter (NIS). This can be inhibited by large doses of iodides as well as anions (eg, thiocyanate (SCN−), pertechnetate (TcO4−), and perchlorate (CIO4−). At the apical cell membrane a second I− transport enzyme called pendrin controls the flow of iodide across the membrane. Pendrin is also found ...