Literature
Clinical Pearls & Morning Reports
Published February 14, 2024
What is the typical course of disease in cases of subacute thyroiditis?
Before the coronavirus disease 2019 pandemic, coxsackievirus and mumps virus were the viruses that were most often associated with subacute thyroiditis. Read the NEJM Case Records of the Massachusetts General Hospital here.
Clinical Pearls
Q: What causes subacute thyroiditis?
A: Subacute granulomatous thyroiditis, commonly called subacute thyroiditis, is the prototype for several causes of destructive thyroiditis. The precise pathophysiological mechanism of subacute thyroiditis is poorly understood; it is thought to be a postviral inflammatory process caused by common antigens in viruses and thyroid follicular cells.
Q: Which viruses have been associated with subacute thyroiditis?
A: Several vaccine-preventable viral infections are associated with subacute thyroiditis, including measles, mumps, and rubella. Exposure to children in congregate settings, such as day care centers or schools, is a risk factor for exposure to viruses associated with subacute thyroiditis, including echovirus, parvovirus B19, coxsackievirus, and varicella–zoster virus. A third group of viruses that are associated with the development of subacute thyroiditis are acquired through sexual and other close intimate contact. These include cytomegalovirus, herpes simplex virus types 1 and 2, Epstein–Barr virus, and human immunodeficiency virus. Typically, only recently acquired infections trigger subacute thyroiditis.
Morning Report Questions
Q: What are some of the clinical and imaging features of subacute thyroiditis?
A: Patients with subacute thyroiditis classically present with a preceding upper respiratory illness, thyrotoxicosis, and thyroid pain that may start in one lobe and migrate to the other lobe, with radiation to the jaw or ear. Fever is present in 28% of patients. On examination, the thyroid is characteristically firm or hard, and it is tender or quite painful. Rarely, a patient with subacute thyroiditis will present without pain. The cause of thyrotoxicosis is traditionally determined by thyroid scintigraphy with measurement of radioactive iodine uptake over a 24-hour period. Patients with Graves’ disease and those with a toxic adenoma or toxic nodular goiter all present with a high or normal level of radioactive iodine uptake; scintigraphy shows diffuse uptake in patients with Graves’ disease and focal uptake in those with toxic nodular goiter with one or more toxic adenomas. By contrast, destructive subacute thyroiditis results in thyrotoxicosis with near-absent radioactive iodine uptake.
Q: What is the typical course of disease in cases of subacute thyroiditis?
A: Thyrotoxicosis that develops in patients with subacute thyroiditis is caused by leakage of preformed hormone from thyroid follicles which results in a transient hyperthyroid phase that lasts an average of 2 to 8 weeks. During the thyrotoxic phase, beta-adrenergic blockers may be used to ameliorate symptoms of hyperthyroidism, and in older patients or patients with cardiovascular disease, beta-adrenergic blockers may reduce the risk of atrial arrhythmia. When thyroid stores become exhausted and the inflammation subsides, blood levels of thyroid hormone decrease through the normal range and usually become transiently subnormal, resulting in a brief euthyroid phase followed by a variable period of hypothroidism. After the thyrotoxicosis resolves, resumption of thyrotropin production may take a month or longer. Thus, the hypothyroid phase lasts until damaged thyroid follicular cells and the pituitary–thyroid axis recover. Full recovery occurs in more than 85% of patients.