Prophylactic application of thyrostatic drugs during excessive iodine exposure in euthyroid patients with thyroid autonomy: a randomized study

Nolte, W.; Müller, Ralf; Siggelkow, Heide; Emrich, D.; Hüfner, M.

doi:10.1530/eje.0.1340337

Cited by 78 publications

(33 citation statements)

References 11 publications

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Section: Discussioncontrasting

confidence: 84%

“…Based on our observations, we do not support preventive measures as recommended by others (18). The study of Nolte et al (18) even shows that iodine-induced hyperthyroidism cannot be prevented by prophylactic therapy in every case. At this point it should be mentioned that the risk for side-effects of carbimazole (leukopenia 0.4%, thrombocytopenia 0.2%, agranulocytosis 0.2%) (19) is even higher than the risk of iodine-induced hyperthyroidism.…”

Section: Discussioncontrasting

confidence: 84%

“…According to these facts it cannot be established which patients should be selected to receive a prophylactic therapy. In one study the effect of prophylactic therapy on the development of iodine-induced hyperthyroidism has been examined; Nolte et al (18) investigated 51 patients undergoing coronary angiography. They received 20 mg thiamazole or 900 mg sodium perchlorate before and after coronary angiography or received no therapy.…”

Section: Discussionmentioning

confidence: 99%

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Risk of iodine-induced thyrotoxicosis after coronary angiography: an investigation in 788 unselected subjects

Hintze¹,

Blombach²,

Fink³

et al. 1999

European Journal of Endocrinology

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In this study, the risk of iodine-induced thyrotoxicosis in unselected patients from an iodine-deficient area was investigated. The patients were consecutively enrolled. Thyroid hormone values and urinary iodine excretion were determined before, as well as 1, 4 and 12 weeks after iodine contamination by coronary angiography. Two of 788 unselected patients developed hyperthyroidism within 12 weeks. The two patients did not belong to a risk group for iodine-induced thyrotoxicosis (i.e. old people, patients with goiter or possible thyroid autonomy, low TSH). Both patients had normal TSH levels at baseline and ultrasound of the thyroid was without evidence of nodules. The study shows that in euthyroid unselected patients from an iodine-deficient area short-term iodine contamination by contrast media rarely leads to hyperthyroidism. On account of these facts, prophylactic therapy, e.g. by perchlorate or thiamazole, is not generally recommended, because the risk of side-effects is perhaps even greater than the risk of iodine-induced thyrotoxicosis.

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Section: Discussioncontrasting

confidence: 84%

Section: Discussioncontrasting

confidence: 84%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Risk of iodine-induced thyrotoxicosis after coronary angiography: an investigation in 788 unselected subjects

Hintze¹,

Blombach²,

Fink³

et al. 1999

European Journal of Endocrinology

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“…These collective data bear great clinical relevance given the known adverse effects of hyperthyroidism on multiple organ systems (i.e., bone, neuropsychiatric) 16 particularly the cardiovascular system (e.g., atrial fibrillation, high-output heart failure, angina, and possibly greater cardiovascular mortality). 17,18 Although untested, it has been suggested that prophylactic treatment with methimazole or perchlorate may be warranted in high-risk patients in advance of anticipated iodide exposure such as elective ICM-based procedures; 2,19,20 further studies are needed to evaluate the safety and effectiveness of this approach.…”

Section: Discussionmentioning

confidence: 99%

Iodinated contrast media exposure and incident hyperthyroidism and hypothyroidism in a community-based cohort

et al. 2013

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Recent data suggest iodinated contrast media (ICM) exposure is associated with increased risk of incident hyperthyroidism among patients receiving care from two tertiary care medical centers. We sought to confirm and generalize these findings by conducting a casecontrol study among a broadly-representative community-based cohort of patients receiving care within Harvard Vanguard Medical Associates from 1996 to 2012. Incident hyperthyroid and hypothyroid cases were defined by change in thyrotropin (TSH) from normal (at baseline), to low or high (at follow-up), respectively. In parallel analyses, hyper-and hypothyroid cases were matched to euthyroid controls using incidence density sampling, and ICM exposure was ascertained using claims data. Secondary analyses examined associations with incident overt hyperthyroidism and overt hypothyroidism (follow-up TSH≤0.1 mIU/L and TSH>10 mIU/L, respectively). We observed that ICM exposure was associated with increased risk of incident hyperthyroidism [odds ratio, 1.61 (95% CI) 1.27-2.04], incident overt hyperthyroidism [odds ratio, 1.62 (95% CI) 1.08-2.43], and incident overt hypothyroidism [odds ratio 2.01 (95% CI) 1. 25-3.23]. These data confirm that ICM exposure is associated with increased risk of incident thyroid functional disease in a community-based cohort of patients in an iodine-sufficient region.

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“…In one prospective, randomized study of 1177 patients undergoing elective coronary angiography, 51 patients with euthyroid autonomy (i.e., suppressed TSH but normal thyroid hormone levels, negative thyrotropin-releasing hormone test and normal thyroidal radioisotope uptake study) identified as at increased risk of iodine-induced hyperthyroidism were randomly assigned to prophylactic treatment with perchlorate or thiamazole, or no treatment. 7 Hyperthyroidism developed in 2 patients in the control group and 1 in each of the treatment groups. The authors concluded that short-term prophylactic thyrostatic therapy appeared to have a protective effect against iodine excess in patients with euthyroid autonomy.…”

Section: Preventionmentioning

confidence: 98%

Iodinated contrast–induced thyrotoxicosis

Dunne

Kaimal

MacDonald

et al. 2012

CMAJ

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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 ...

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Prophylactic application of thyrostatic drugs during excessive iodine exposure in euthyroid patients with thyroid autonomy: a randomized study

Cited by 78 publications

References 11 publications

Risk of iodine-induced thyrotoxicosis after coronary angiography: an investigation in 788 unselected subjects

Risk of iodine-induced thyrotoxicosis after coronary angiography: an investigation in 788 unselected subjects

Iodinated contrast media exposure and incident hyperthyroidism and hypothyroidism in a community-based cohort

Iodinated contrast–induced thyrotoxicosis

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