Toxic multinodular goiter A toxic multinodular goiter (MNG; also known as Plummer disease) contains multiple autonomously functioning nodules, resulting in hyperthyroidism. These nodules function independently of thyroid-stimulating hormone (TSH) and are almost always benign. However, nonfunctioning thyroid nodules in the same goiter may be malignant.
It 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).
Toxic multinodular goiter is the second most common cause of hyperthyroidism (after Graves’ disease) in the developed world, whereas iodine deficiency is the most common cause of hypothyroidism in developing-world countries where the population is iodine-deficient. (Decreased iodine leads to decreased thyroid hormone.) However, iodine deficiency can cause goiter (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:
- heat intolerance
- muscle weakness/wasting
- weight loss
- increased appetite
- non-painful goitre (swelling of the thyroid gland)
- tachycardia (high heart rate – above 100 beats per minute at rest in adults)
- Tracheal compression
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 hyperthyroidism.
Toxic multinodular goiter can be treated with antithyroid medications such as propylthiouracil or methimazole, radioactive iodine, or with surgery. Another treatment option is injection of ethanol into the nodules.