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Toxic multinodular goiter natural history, complications and prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Akshun Kalia M.B.B.S.[2]

Overview

If left untreated, toxic multinodular goiter may progress to develop hyperthyroidism. However, the progression of toxic multinodular goiter is quite slow. Untreated patients initially have a history of thyroid enlargement followed by a long period of subclinical hyperthyroidism. Overt hyperthyroidism occurs late in the course of toxic multinodular goiter. Common complications of toxic multinodular goiter include tachycardia, arrhythmia, atrial fibrillation, heart failure (dilated cardiomyopathy), pulmonary hypertension, facial plethora, inspiratory stridor, hoarseness, dysphagia, bone mineral loss and thyroid storm. Prognosis of toxic multinodular goiter is generally good with treatment. Both surgery and radioactive iodine therapy can confer a moderate long-term risk of hypothyroidism and such patients require lifelong hormone replacement therapy. Toxic multinodular goiter is commonly seen in elderly. Therefore, in elderly, presence of other conditions may influence the outcome of toxic multinodular goiter.

Natural History, Complications, and Prognosis

Natural History

Complications

Common complications of toxic multinodular goiter include:[5][6]

Prognosis

  • Prognosis of toxic multinodular goiter is generally good with treatment.
  • About 45% to 75% of patients stay euthyroid following I-131 therapy.
  • Both surgery and radioactive iodine therapy can confer a moderate long-term risk of hypothyroidism.
  • Patients with I-131 therapy who develop hypothyroidism require lifelong thyroid hormone replacement therapy
  • Toxic multinodular goiter is commonly seen in elderly. Therefore, in elderly, presence of other conditions may influence the outcome of toxic multinodular goiter.

References

  1. Wiener JD, de Vries AA (1979). “On the natural history of Plummer’s disease”. Clin Nucl Med. 4 (5): 181–90. PMID 582300.
  2. Elte JW, Bussemaker JK, Haak A (1990). “The natural history of euthyroid multinodular goitre”. Postgrad Med J. 66 (773): 186–90. PMC 2429462. PMID 2114018.
  3. Parle JV, Maisonneuve P, Sheppard MC, Boyle P, Franklyn JA (2001). “Prediction of all-cause and cardiovascular mortality in elderly people from one low serum thyrotropin result: a 10-year cohort study”. Lancet. 358 (9285): 861–5. doi:10.1016/S0140-6736(01)06067-6. PMID 11567699.
  4. Pearce EN, Braverman LE (2004). “Hyperthyroidism: advantages and disadvantages of medical therapy”. Surg. Clin. North Am. 84 (3): 833–47. doi:10.1016/j.suc.2004.01.007. PMID 15145238.
  5. Dahl P, Danzi S, Klein I (2008). “Thyrotoxic cardiac disease”. Curr Heart Fail Rep. 5 (3): 170–6. PMID 18752767.
  6. Ertek S, Cicero AF (2013). “Hyperthyroidism and cardiovascular complications: a narrative review on the basis of pathophysiology”. Arch Med Sci. 9 (5): 944–52. doi:10.5114/aoms.2013.38685. PMC 3832836. PMID 24273583.

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