Toxic multinodular goiter (also known as toxic nodular goiter, toxic nodular struma) is a common cause of hyperthyroidism in which there is excess production of thyroid hormones from functionally autonomous thyroid nodules, which do not require stimulation from thyroid stimulating hormone (TSH).
It is the second most common cause of hyperthyroidism (after Graves’ disease) in the developed world. In countries where the population is iodine-deficient i.e. the developing world, iodine deficiency is the most common cause of hypothyroidism. (Decreased iodine leads to decreased thyroid hormone.) However, iodine deficiency can cause goitre (thyroid enlargement); within a goitre, nodules can develop. Risk factors for toxic multinodular goiter include individuals over 60 years of age and being female.
Symptoms of toxic multinodular goitre are similar to that of hyperthyroidism, including:
goitre (swelling of the thyroid gland)
tachycardia (high heart rate – above 100 beats per minute at rest in adults)
Sequence of events:
Iodine deficiency leading to decreased T4 production.
Induction of thyroid cell hyperplasia due to low levels of T4. This accounts for the multinodular goitre appearance.
Increased replication predisposes to a risk of mutation in the TSH receptor.
If the mutated TSH receptor is constitutively active, it would then become ‘toxic’ and produces excess T3/T4 leading to hyperthryoidism.
Toxic multinodular goiter can be treated with antithyroid medications such as propylthiouracil or methimazole, radioactive iodine, or with surgery. Another treatment option in recent years (2013) is ethanol ablation of the nodules.