Abstract and Introduction
There has been a substantial increase in the use of radiocontrast-enhanced imaging studies in the past two decades (particularly computed tomography and coronary angiography). Sudden exposure to high levels of iodide may result in thyroid dysfunction (hyperthyroidism and hypothyroidism alike). Although the adverse-event rate is not very high, the condition is notable considering the large number of contrast-enhanced radiographic studies performed. Clinicians often have to decide on the most suitable diagnostic modality and the safest contrast medium when it comes to certain patients. In this study, we stress that the thyroid function of the patients should also be taken into consideration while making such decisions. We discuss in detail the prevalence and types (hypothyroidism and hyperthyroidism) of radiocontrast-induced thyroid dysfunction. We list the subsets of the population that are at a higher risk of radiocontrast-induced thyroid dysfunction and summarize the necessary prophylaxis and possible treatment. The presented principles apply to intravenous, intra-arterial and enteral (endoscopic retrograde cholangiopancreatography) routes of iodinated contrast medium administration.
Iodine is an essential component of thyroid hormones. In healthy individuals, the thyroid gland has intrinsic autoregulatory mechanisms to adapt to excess iodine. In contrast, patients with underlying thyroid disease may fail to adapt to iodine overload resulting in hyperthyroidism or hypothyroidism. Many iodine-containing pharmaceuticals can trigger thyroid dysfunction. In modern medicine, however, the major sources of excess iodine are radiographic contrast media, amiodarone, dietary supplements (kelp, seaweed) and povidone-iodine (PVP-I). Radiocontrast-induced thyroid dysfunction is a clinically relevant and understudied area. The prevalence has not been assessed accurately and varies widely from 0·05% to 5%. It is greater among patients with pre-existing thyroid disease.[2–5] Although infrequent, the condition may bear severe or even life-threatening consequences if unrecognized and untreated. Thyroid dysfunction may be subclinical or overt. The timing of onset may be up to 12 weeks after ICM administration. Thus, physicians and patients should both be aware of the potential thyroid-specific sequelae.
Clin Endocrinol. 2014;80(3):322-327. © 2014 Blackwell Publishing