- Kenneth D Burman, MD
Kenneth D Burman, MD
- Chief, Endocrine Section
- Medstar Washington Hospital Center, Washington, DC
- Professor, Department of Medicine
- Georgetown University Medical Center
Most thyroidologists use the term subacute thyroiditis to apply specifically to subacute granulomatous thyroiditis. Other names for this disorder are subacute nonsuppurative thyroiditis, giant cell thyroiditis, painful thyroiditis, and de Quervain's thyroiditis. It is a relatively uncommon cause of hyperthyroidism and affects women more often than men (3 to 5:1) .
Subacute thyroiditis (subacute granulomatous thyroiditis) is characterized by neck pain or discomfort, a tender diffuse goiter, and a predictable course of thyroid function evolution. Hyperthyroidism is typically the presentation followed by euthyroidism, hypothyroidism, and ultimately restoration of normal thyroid function (figure 1).
The diagnosis and management of subacute thyroiditis will be provided here. Other types of thyroiditis are discussed separately. (See "Overview of thyroiditis".)
The best available incidence data for subacute thyroiditis comes from the Rochester Epidemiology Project in Olmsted county, Minnesota [2,3]. Between 1970 and 1997, 94 patients with subacute thyroiditis were identified. They report an incidence of 12.1 cases per 100,000/year with a higher incidence in females than in males (19.1 and 4.1 per 100,000/year, respectively). It is most common in young adulthood (24 per 100,000/year) and middle age (35 per 100,000/year), and decreases with increasing age.
Subacute thyroiditis is presumed to be caused by a viral infection or a postviral inflammatory process. Many patients have a history of an upper respiratory infection prior to the onset of thyroiditis (typically two to eight weeks beforehand). The disease was thought to have a seasonal incidence (higher in summer) , and clusters of cases have been reported in association with Coxsackievirus, mumps, measles, adenovirus, and other viral infections [1,5]. However, in other series, there was a relatively comparable distribution of presentation throughout the year [2,6]. Serial studies of viral antibody titers have implicated many of the same viruses, but the changes could equally be attributed to nonspecific anamnestic responses . Viral inclusion bodies are not seen in thyroid tissue.To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:
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- CLINICAL FEATURES
- Clinical manifestations
- Laboratory findings
- Imaging studies
- DIFFERENTIAL DIAGNOSIS
- Pain management
- Management of symptomatic hyperthyroidism
- Management of hypothyroidism
- INFORMATION FOR PATIENTS
- SUMMARY AND RECOMMENDATIONS