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. Author manuscript; available in PMC: 2016 Sep 27.
Published in final edited form as: Lancet. 2016 Mar 30;388(10047):906–918. doi: 10.1016/S0140-6736(16)00278-6

Table 1.

Pathogenic mechanisms and causes of thyrotoxicosis

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.