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Subacute thyroiditis

INTRODUCTION

There is some controversy concerning the nomenclature used to categorize the different forms of subacute thyroiditis. However, 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 an uncommon cause of hyperthyroidism and affects women more often than men (3 to 5:1) [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".)

EPIDEMIOLOGY

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.

PATHOGENESIS

Subacute thyroiditis is presumed to be caused by a viral infection or a postviral inflammatory process. The majority of 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) [4], and clusters of cases have been reported in association with Coxsackievirus, mumps, measles, adenovirus, and other viral infections [1]. However, in other series, there was a relatively comparable distribution of presentation throughout the year [2,5]. Serial studies of viral antibody titers have implicated many of the same viruses, but the changes could equally be attributed to nonspecific anamnestic responses [6]. Viral inclusion bodies are not seen in thyroid tissue.

Thyroid autoimmunity does not appear to play a primary role in the disorder, but it is strongly associated with HLA-B35 in many ethnic groups [7]. A unifying hypothesis might be that the disorder results from a common subclinical viral infection that provides an antigen, either of viral origin or resulting from virus-induced host tissue damage, that uniquely binds to HLA-B35 molecules on macrophages. The resulting antigen-HLA-B35 complex activates cytotoxic T lymphocytes that then damage thyroid follicular cells, because the cells have partial structural similarity with the infection-related antigen. Unlike autoimmune thyroid disease, however, the immune reaction is not self-perpetuating, so the process is limited.

          

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Literature review current through: Nov 2014. | This topic last updated: Aug 27, 2014.
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