Iodinated contrast–induced thyrotoxicosis

Abstract

A 72-year-old man presented to the emergency department with shortness of breath. He had a history of left ventricular failure, hypertension, treated esophageal carcinoma and recurrent deep vein thromboses. His medications included warfarin, bumetanide, spironolactone, ramipril, bisoprolol, acetylsalicylic acid and simvastatin. Clinical examination, chest radiography and echocardiography confirmed worsening of congestive cardiac failure. The doses of the diuretics he was taking were adjusted and his symptoms improved.Thyroid function tests done during the admission showed elevated serum free thyroxine at 54.0 (normal 12.0-22.0) pmol/L and total triiodothyronine at 3.3 (normal 1.3-2.6) nmol/L, and suppressed thyroid-stimulating hormone (TSH) at less than 0.02 (normal 0.27-4.20) mIU/L. He had never taken amiodarone and had not received iodinated contrast before his presentation. Clinical assessment showed no stigmata of Graves disease, but nodularity of the thyroid gland was noted. Ultrasonography of the thyroid confirmed enlargement of both thyroid lobes with multiple nodules bilaterally. Thyroid peroxidase antibody titre was 207 (normal < 35) IU/L, and TSH receptor antibodies were not measured.A clinical diagnosis of toxic multinodular goitre was made. This was based on confirmation of multinodular goitre on ultrasonography, as well as the regional prevalence of thyroid disease, types of thyroid disease common in the patient's age group, absence of pathognomonic features of Graves disease and poor specificity of thyroid peroxidase antibody testing for Graves disease in this population. The patient was given carbimazole and became euthyroid; 15 months later, he underwent definitive treatment with radioiodine. Carbimazole was stopped 2 weeks after radioiodine treatment. He subsequently remained clinically and biochemically euthyroid.Three months after radioiodine therapy, at another centre, the patient underwent elective coronary angioplasty with 2 drug-eluting stents to the proximal left anterior descending artery, with no immediate complications. At the time of the angioplasty, he was clinically euthyroid. A total of 260 mL of iodinated contrast (iodixanol, iodine content 320 mg/mL) was infused intravenously during the procedure. A few days later, he reported shortness of breath and symptoms similar to his first presentation. On examination, his chest was clear, and an electrocardiogram showed no ischemic changes. An echocardiogram excluded pericardial effusion, and his left ventricular function, although moderately impaired, was no worse than previously. The doses of the diuretics he was taking were increased, but his symptoms did not improve.Eleven days after the angioplasty, thyroid function tests done in anticipation of a follow-up appointment in the endocrinology clinic showed a free thyroxine level of 73.6 pmol/L with a suppressed TSH of less than 0.02 mIU/L (Figure 1). Anti-thyroid peroxidase antibody titre was 754 IU/L, and TSH receptor antibody titre was not measured. On examination, the patient had no ...

Clinical diagnosis of Graves’ or non-Graves’ hyperthyroidism compared to TSH receptor antibody test

“…Thyrotoxicosis, a clinical state resulting from inappropriately high thyroid hormone levels, is a condition with multiple aetiologies ( 1 ). It is commonly caused by Graves’ disease (GD), toxic multinodular goitre (TMNG) or toxic adenoma and less commonly by thyroiditis, administration of iodinated contrast ( 2 ), immune checkpoint inhibitors ( 3 ), and extra-thyroidal causes such as struma ovarii, factitious thyrotoxicosis, trophoblastic tumours producing human chorionic gonadotrophin (hCG) ( 4 ), and TSH-producing pituitary adenomas.…”

Endovascular management of acute mesenteric ischemia in a young patient with thyrotoxicosis and atrial fibrillation: A case report and review of the literature

“…In addition, the patient’s condition was considered a high risk as he was thyrotoxic and have atrial fibrillation, so the least invasive procedure would be the most appropriate for him. These considerations of the condition of the patient led us to take the decision of endovascular management followed by observation, although endovascular procedure is still risky for him as a thyrotoxic patient with the need to take all perioperative preparations to prevent or manage a thyroid storm [ [12] , [13] , [14] ]. The open surgical management was spared due to the absence of peritoneal signs, and it would have been considered in case they developed on serial physical examination.…”

Thyrotoxicosis: an under-recognised aetiology

“…Jod-Basedow syndrome, or iodine-induced hyperthyroidism, is commonly unrecognised as a side effect of contrast medium, and acute thyrotoxicosis can be deadly. It typically presents in patients living in iodine deficient areas, the elderly and in those with a history of thyroid dysfunction (such as multinodular goitre) 2. This case report is important as it illustrates Jod-Basedow syndrome following iodinated contrast in a patient without any of the typical risk factors, who resides in an iodine-replete environment.…”