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A 28-year-old woman with a history of Graves disease and thyrotoxicosis treated with radioactive iodine 18 months ago is evaluated. She has been taking levothyroxine for 15 months, initially as 0.125 mg/d, but in the past 6 months the dosage has been reduced first to 0.088 mg/d and more recently to 0.050 mg/d because of an apparently reduced requirement.
On physical examination, her pulse rate is 106/min; she has a questionably small goiter or thyroid gland at the upper limit of normal size, brisk deep tendon reflexes, and a 1 + tremor. Laboratory results include a serum free T4 of 2.7 ng/dL, free T3 7.4 pmol/L (normal, 1 .5-6.9 pmol/L), and a serum TSH of
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On physical examination, her pulse rate is 106/min; she has a questionably small goiter or thyroid gland at the upper limit of normal size, brisk deep tendon reflexes, and a 1 + tremor. Laboratory results include a serum free T4 of 2.7 ng/dL, free T3 7.4 pmol/L (normal, 1 .5-6.9 pmol/L), and a serum TSH of
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A 28-year-old woman with a history of Graves disease and thyrotoxicosis treated with radioactive iodine 18 months ago is evaluated. She has been taking levothyroxine for 15 months, initially as 0.125 mg/d, but in the past 6 months the dosage has been reduced first to 0.088 mg/d and more recently to 0.050 mg/d because of an apparently reduced requirement.
On physical examination, her pulse rate is 106/min; she has a questionably small goiter or thyroid gland at the upper limit of normal size, brisk deep tendon reflexes, and a 1 + tremor. Laboratory results include a serum free T4 of 2.7 ng/dL, free T3 7.4 pmol/L (normal, 1 .5-6.9 pmol/L), and a serum TSH of less than0.01 IU/mL. TSH receptor antibodies are positive at 179% (normal, less than 130%). A 24-hour radioiodine uptake is 19.5% (normal, 8% to 30%).
What is the most likely diagnosis?
A. T3 toxicosis
B. Incompletely treated Graves disease
C. Hashitoxicosis
D. Radioiodine-induced thyrotoxicosis
E. Struma ovarii with thyrotoxicosis
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B. Incompletely treated Graves disease
just bcz of antibodies.
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it seems a tired thyroid. isn't? graves?( but not upataking). pt of graves but taking T4.
showman whats happening in this pt.
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This patient has persistent Graves disease with thyrotoxicosis related to either persistence or recurrence of high titers of TSH receptor antibodies stimulating her thyroid remnants. After radioiodine therapy, there commonly occurs a form of radiation thyroiditis with associated thyroid hypofunction leading to the premature diagnosis of permanent postradioiodine hypothyroidism. Levothyroxine therapy is initiated, but the residual thyroid tissue not fully ablated by the treatment will begin to synthesize and release T4 and T3. This does not occur in the absence of TSH-receptor antibodies. The T4 being released from the thyroid gland complements that being taken as presumed replacement dosage, resulting in a total or combined supraphysiologic amount. Thus, the need for the progressively reduction in her dosage of exogenous thyroxine.
This condition is not pure T3 toxicosis because the free T4 is also elevated. Hashitoxicosis is a rare presentation of hyperthyroidism in patients with Hashimoto™s thyroiditis. The latter is marked by high titers of antithyroid peroxidase and anti-thyroglobulin antibodies, but not anti-TSH receptor antibodies. Without evidence of these antibodies and in view of her history of Graves disease, there is no reason to consider a diagnosis of Hashimoto™s disease. Radioiodine-induced thyrotoxicosis occurs within days or weeks of treatment and would not occur spontaneously a year and a half later. Struma ovarii refers to ectopic thyroid tissue in an ovarian teratoma and can rarely cause thyrotoxicosis.
yupp b
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