SAT-587 Rapid Induction of Thyrotoxicosis from Iodinated Contrast Medium (ICM)

Abstract

ICM used in computerized tomography (CT) is well known to induce thyrotoxicosis occasionally in patients with latent disorders prone to thyrotoxicosis (e.g. autonomous multinodular goiter and Graves’ disease) and even in patients without known thyroid disease. This phenomenon is thought to be due to the inability to regulate thyroid hormone synthesis in the presence of a supra-physiological availability of iodine. The onset of thyrotoxicosis in such cases is generally 2-12 weeks after iodine exposure. Less well known is the induction of a destructive thyroiditis created by thyroidal exposure to large concentrations of iodine. The onset of thyrotoxicosis from the latter cause is thought to be within a few days. Several cases exhibit an onset within a day of iodine exposure. We describe a case in which suppressed TSH and elevated FT4 levels were observed only 13 hours after exposure to ICM in a CT-Chest Angiogram. The patient was a 75 y/o man with no recognized hx of a thyroid disorder, admitted to the ICU on Day-1 with shortness of breath thought secondary to COPD or to a PE. Though tachycardic (85-100/min), he did not appear clinically thyrotoxic on the basis of other symptoms and physical findings. The thyroid exam was normal. His most recent TSH and Free T4 (FT4) levels, only 2 mo prior to admission, were normal [TSH-3.27, NL=0.358-3.74 mU/L], [FT4-1.13, NL=0.76-1.46 ng/dl]. On Day-1 at 16:05 the patient received 100 ml of iopamidol (755 mg/ml) IV, which ruled out a PE. TSH and FT4 levels drawn at 06:50 on Day-2 were 0.011 and 5.81, respectively. The Free T3 (FT3) level was mid-normal at 3.01 [NL=2.18-3.98 pg/ml]. Reverse T3 was elevated at 149 [NL=8-25 ng/dl]. Anti-Peroxidase and Anti-Thyroglobulin antibodies were not elevated but Thyroid Stimulating Immunoglobulins (TSI) were elevated at 503% [NL <140%]. At 10:58 on the same morning he received another 100 ml of iopamidol for a CT-Abdominal Angiogram, which ruled out rupture of his chronic abdominal aortic aneurysm. A thyroid ultrasound documented a normal size gland with only an inhomogeneous parenchyma and a 0.5 cm cyst. On Day-7 the plasma iodine level was 778 [NL=52-109 mcg/L]. After review of the above data, the patient was thought to be moderately thyrotoxic and started on prednisone 60 mg QD for 5 days and methimazole 5 mg BID for 6 days, decreased to 2.5 mg BID for 12 days, then discontinued. The FT4 normalized within 6 days of starting methimazole. The TSH level normalized within 8 weeks. Over this period, the heart rate normalized and the dyspnea improved considerably. The plasma Iodine level 2 mo after admission was normal at 76 mcg/L. This case documents an unusually rapid induction of thyrotoxicosis (13 hours) in a patient with latent Graves’ disease and normal TSH and FT4 levels only 60 days prior to iodine exposure. After starting treatment with methimazole the FT4 normalized in only 6 days.