A Case Report of Post-Operative J？d-Basedow Phenomennon Following Oral and IV Iodine Contrast Administration

This is a case of thyrotoxicosis, due to the J？d-Basedow phenomenon following administration of oral and IV iodinated contrast in a patient with history of gastrointestinal stromal tumor (GIST) and small bowel obstruction. The patient developed atrial fibrillation and had an extended stay in the intensive care unit. Given the aging population with possible subclinical hyperthyroidism, multinodular goiter, and the rise in contrast administration for routine diagnostic studies, this case serves to raise awareness of the risks of “routine” tests administered to our aging patient population. 1. Introduction Iodine is an essential requirement for thyroid hormone synthesis. For the thyroid gland to synthesize adequate amounts of thyroxine, it must take up approximately 52？mcg of iodide daily [1]. To obtain this amount of iodide, the recommended daily oral intake of iodine is 150？ g for nonpregnant adults, with a tolerable upper level of 1100？ g [2]. The average daily intake in the United States is 150–200？ g, making the US an iodine replete population [3]. In many countries the daily iodine intake is much less, causing those populations to be iodine deficient. Sources of iodine excess can include iodized salt, dietary supplementations, over-the-counter or prescription medications, and radiographic intravenous contrast media (ICM). A typical dose of ICM contains about 13,500？ g of free iodide, of which 15–60？g of bound iodine may be liberated in the body. This infuses the body with an acute iodide load of 90 to several hundred thousand times the recommended daily intake [4]. When large amounts of iodine are encountered in subjects with normal thyroid function, sodium-iodide symporters (NIS) on follicular cells transport an increased amount of iodine intracellularly. The resultant increase in intrathyroidal iodine stores paradoxically blocks thyroid hormone organification. This TSH-independent autoregulatory block is called the Wolff-Chaikoff effect [1]. Within 24 hours of an exposure to iodine excess, the NIS expression is markedly decreased. Intrathyroidal iodine stores normalize, inducing resumption of normal thyroid function (escape from the Wolff-Chaikoff effect) [5]. Defective or absent autoregulatory mechanisms may lead to pathologic consequences of iodine excess. Failure to escape from the Wolff-Chaikoff effect may result in prolonged inhibition of thyroid hormone organification. This results in a rise in TSH and iodine induced hypothyroidism, which can be transitory or permanent in susceptible individuals [5]. Alternatively, some individuals, when