Table 1.
Cause | |
---|---|
Thyrotoxicosis with hyperthyroidism (normal or high radioactive iodine uptake) | |
| |
Effect of increased thyroid stimulators | |
TSH-receptor antibody | Graves’ disease |
Inappropriate TSH secretion | TSH-secreting pituitary adenoma; pituitary resistance to thyroid hormone |
Excess hCG secretion | Trophoblastic tumours (choriocarcinoma or hydatidiform mole); hyperemesis gravidarum |
Autonomous thyroid function | |
Activating mutations in TSH receptor or Gsα protein |
Solitary hyperfunctioning adenoma; multinodular goitre; familial non-autoimmune hyperthyroidism |
| |
Thyrotoxicosis without hyperthyroidism (low radioactive iodine uptake) | |
| |
Inflammation and release of stored hormone | |
Autoimmune destruction of thyroid gland | Silent (painless) thyroiditis; post-partum thyroiditis |
Viral infection* | Subacute (painful) thyroiditis (De Quervain thyroiditis) |
Toxic drug effects | Drug-induced thyroiditis (amiodarone, lithium, interferon α) |
Bacterial or fungal infection | Acute suppurative thyroiditis |
Radiation | Radiation thyroiditis |
Extrathyroidal source of hormone | |
Excess intake of thyroid hormone | Excess exogenous thyroid hormone (iatrogenic or factitious) |
Ectopic hyperthyroidism (thyroid hormone produced outside the thyroid gland) |
Struma ovarii; functional thyroid cancer metastases |
Ingestion of contaminated food | Hamburger thyrotoxicosis1 |
Exposure to excessive iodine | |
Jod-Basedow effect | Iodine-induced hyperthyroidism (iodine, iodine-containing drugs, radiographic contrast agents) |
TSH=thyroid-stimulating hormone. hCG=human chorionic gonadotropin. Gsα=G protein alpha subunit.
Aetiology is not definitive.