Iodine-Induced Hyperthyroidism

Iodine induced hyperthyroidism (the Jod-Basedow phenomenon) is hyperthyroidism triggered by an excess of iodine in a thyroid that cannot switch off hormone synthesis. It occurs mainly in nodular goitre, latent Graves disease, and people with long standing iodine deficiency.

Sources are iodinated contrast, amiodarone, kelp and other iodine rich supplements, topical iodine antiseptics, and population iodine supplementation programmes.

Risk is greatest in older adults with multinodular goitre and in regions with iodine deficiency. Onset is within weeks to a few months of exposure and it may last months.

Pathophysiology.

In normal glands, a large iodine load briefly inhibits hormone synthesis (acute inhibition), and then the gland escapes from it. Autonomous nodules and Graves tissue do not respond to this inhibition, so the extra iodine becomes substrate for more hormone.

Uptake of radioiodine is low because the iodine pool is already large, so scanning is unreliable for months.

• Palpitations, atrial fibrillation, weight loss, tremor, heat intolerance and anxiety, often with heart failure in older adults.
• Goitre or palpable nodules. Onset is usually within 4 to 12 weeks after iodine exposure.

Red flags.

• Atrial fibrillation or heart failure.
• Fever, delirium or vomiting (thyroid storm).

• Suppressed thyroid stimulating hormone with raised free thyroxine or free triiodothyronine, after documented iodine exposure.
• Urinary iodine raised (single spot over 300 micrograms/L, higher after contrast).
• Thyrotropin receptor antibodies (to exclude Graves disease) and ultrasound of the thyroid for nodules.
• Radioiodine uptake is low for 2 to 3 months after a contrast load and cannot be used to distinguish causes in that period.

Differential diagnosis.

• Amiodarone induced thyrotoxicosis.
• Graves disease and destructive thyroiditis.
• Toxic nodular goitre unrelated to iodine, and exogenous thyroid hormone.

• Remove the iodine source where possible.
• Carbimazole 15 to 40 mg daily, reducing to the lowest effective dose once euthyroid. Response is slow because of the iodine load.
• Propranolol 10 to 40 mg three to four times daily for symptoms. Potassium perchlorate 200 mg four times daily for up to 4 weeks can speed recovery in severe disease (not over 1 g daily; check blood counts).
• When the iodine load has cleared, treat the underlying nodular disease definitively with radioiodine or surgery, because relapse is likely.
• Before iodinated contrast in a patient with nodular goitre or older age with heart disease, check thyroid stimulating hormone. Do not withhold contrast when it is clinically needed. Recheck thyroid function 3 to 4 weeks later.

Special groups. Pregnancy: avoid radioiodine; manage with the lowest effective antithyroid drug dose. Older adults: have a low threshold to treat early because of arrhythmia risk.

Monitoring. Thyroid function at 4 weeks after contrast in high risk patients, then every 4 to 6 weeks during treatment.

Referral and escalation. Endocrinology for all overt cases; urgent review for atrial fibrillation, heart failure or storm.