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Endocrine Care |
Endocrine-Metabolic Service, Department of Medicine (H.B.B.), Department of Clinical Investigation (B.L.S., R.H.), and Nuclear Medicine Service, Department of Radiology (P.F.), Walter Reed Army Medical Center, Washington, D.C. 20307-5001; and Endocrinology Division, Department of Medicine, Sinai Hospital (D.S.C., N.W.), Baltimore, Maryland 20010
Address all correspondence and requests for reprints to: Dr. Henry B. Burch, Chief, Endocrine-Metabolic Service, Department of Medicine, Walter Reed Army Medical Center, Washington, D.C. 20307-5001. E-mail: henry.burch{at}na.amedd.army.mil
Abstract
Acute changes in thyroid hormone levels before and after radioiodine therapy for Graves’ disease were compared in 42 patients randomized to receive either antithyroid drug pretreatment or no pretreatment. Five patients (11.9%), including 3 in the pretreatment arm and 2 in the no pretreatment arm experienced a late exacerbation of thyrotoxicosis after radioiodine therapy. The majority (19 of 21, 90.5%) of pretreated patients experienced a transient increase in free T4 and free T3 after discontinuation of antithyroid drugs, with little further elevation after radioiodine therapy. After stopping antithyroid drugs and before radioiodine administration, mean serum free T4 values rose from 14.7 ± 6.9 to 21.6 ± 12.1 pmol/L, representing a 46.9% increase, whereas serum free T3 levels rose from 4.9 ± 1.7 to 8.1 ± 6.3 pmol/L, representing a 65.3% increase. The average pretreated patient experienced a 52.4% increase [95% confidence interval (CI), +26.4% to +78.5%] in free T4 and a 61.8% increase (95% CI, +23.5% to +100.0%) in free T3. Conversely, the majority (19 of 21, 90.5%) of nonpretreated patients experienced a rapid decline in thyroid hormone levels after radioiodine treatment. Over the 14 days after radioiodine therapy mean free T4 values in nonpretreated patients fell from 85.8 ± 60.4 to 58.0 ± 76.5 pmol/L, representing a 32.4% decrease, whereas mean free T3 levels fell from 16.1 ± 8.0 to 10.8 ± 11.1 pmol/L, representing a 32.9% decrease. The average nonpretreated patient experienced a 20.6% decrease (95% CI, -47.3% to +7.0%) in free T4 and a 24.3% decrease (95% CI, -1.2% to -47.4%) in free T3 during this time period. Excluding 2 patients with a late exacerbation after radioiodine, 19 nonpretreated patients experienced a decrease in mean free T4 values from 76.8 ± 46.6 to 36.6 ± 19.8 pmol/L, representing a 52.3% decrease, whereas mean free T3 levels fell from 15.5 ± 7.7 to 7.8 ± 3.6 pmol/L, representing a 49.7% decrease. The average decrease in free T4 levels among this subgroup of patients was 30.1% (95% CI, -4.6% to -55.6%), whereas the average decrease in free T3 was 34.4% (95% CI, -13.7% to -55.1%). High levels of TSH receptor autoantibodies at diagnosis were associated with an acute worsening of thyrotoxicosis after stopping antithyroid drug pretreatment. We conclude that pretreatment with antithyroid drugs does not protect against worsening thyrotoxicosis after radioiodine, but may allow such patients to start from a lower baseline level should an aggravation in thyrotoxicosis occur. The findings support the recommendation that most patients with Graves’ disease do not require antithyroid drug pretreatment before receiving radioiodine.
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