This phenomenon is thus iodine-induced
hyperthyroidism, typically presenting in a patient with
endemic goiter (due to
iodine deficiency), who relocates to an iodine-abundant geographical area. People who have
Graves disease,
toxic multinodular goiter, or various types of
thyroid adenoma are also at risk of the Jod-Basedow effect when receiving iodine, because the thyroid will then not respond to the negative feedback from increased
thyroid hormones. The source of iodine may be from the diet, administration of
iodinated contrast for medical imaging, or
amiodarone (an
antiarrhythmic drug). The hyperthyroidism usually develops over 2 to 12 weeks following iodine administration. In some ways the Jod-Basedow phenomenon is the opposite of two physiological compensation mechanisms, the
Plummer effect and the
Wolff–Chaikoff effect, which in normal persons and in persons with thyroid disease, suppress the thyroid hormone after ingestion of large quantities of iodine or iodide. However, unlike the Plummer and Wolff-Chaikoff effects, the Jod-Basedow effect does not occur in persons with normal thyroid glands, as thyroid hormone synthesis and release in normal persons is controlled by pituitary TSH secretion, which does not allow hyperthyroidism when extra iodine is ingested. ==Precautions in medical imaging==