Subacute granulomatous 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, subacute granulomatous thyroiditis, giant cell 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 granulomatous thyroiditis is characterized by neck pain, 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 (graph 1). An overview of subacute granulomatous thyroiditis will be provided here. Other types of thyroiditis are discussed separately. (See "Overview of thyroiditis".)

EPIDEMIOLOGY

The best available incidence data for subacute granulomatous thyroiditis comes from the Rochester Epidemiology Project in Olmsted county, Minnesota [2,3]. 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.

Between 1970 and 1997, 94 patients were identified, almost all of whom presented with pain, as described below [2]. (See 'Clinical manifestations' below.)

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 has been 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]. Serial studies of viral antibody titers have implicated many of the same viruses, but the changes could equally be attributed to nonspecific anamnestic responses [5]. Viral inclusion bodies are not seen in thyroid tissue. Furthermore, there appears to be a relatively comparable distribution of presentation throughout the year [2,6].