JodBasedowPhänomen

Jod-Basedow phenomenon, also known as iodine-induced hyperthyroidism, is a form of thyrotoxicosis that occurs after exposure to a large iodine load in people who already have thyroid autonomy, such as multinodular goiter or latent autoimmune thyroid disease. The mechanism involves uptake of excess iodide by autonomous thyroid tissue, which can increase thyroid hormone synthesis and release despite the normal regulatory response, the Wolff-Chaikoff effect.

Risk factors include preexisting goiter with autonomous nodules, autoimmune thyroid disease, and regional iodine deficiency followed by abrupt iodine exposure. Iodinated contrast media used in imaging studies and certain iodine-containing medications are common sources of the trigger.

Clinically, onset is typically days to weeks after iodine exposure. Hyperthyroid symptoms such as weight loss, heat intolerance, palpitations, anxiety, tremor, and fatigue may be present, with older patients at higher risk for atrial fibrillation or heart failure. Laboratory testing shows suppressed TSH with elevated free T4 and/or T3. Radionuclide imaging often reveals high uptake in autonomous nodules, consistent with focal hyperfunctioning tissue.

Management centers on eliminating further iodine exposure and treating thyrotoxicosis. Antithyroid drugs (for example methimazole) reduce hormone synthesis, while beta-blockers alleviates adrenergic symptoms. In persistent or severe cases, radioactive iodine therapy or surgical resection of autonomous tissue may be required. The condition generally has a good prognosis with appropriate treatment, but prevention hinges on recognizing at-risk individuals prior to iodine administration.

In German-language literature, the term Jod-Basedow-Phänomen is used as well; the English terminology remains Jod-Basedow phenomenon.