The usual classification of thyroiditis includes acute thyroiditis, subacute thyroiditis, chronic thyroiditis, and Riedel’s struma.

Acute thyroiditis is generally defined as acute bacterial infection of the thyroid. Signs, symptoms, and laboratory data are those of acute localized infection.

Riedel’s struma consists of thyroid parenchymal replacement by dense connective tissue. In some cases at least this presumably represents scar tissue from previous thyroiditis. Thyroid function tests are either normal (if sufficient normal thyroid remains) or indicate primary hypothyroidism.

Subacute thyroiditis (granulomatous thyroiditis or de Quervain’s disease) features destruction of thyroid acini with a granulomatous reaction consisting of multinucleated giant cells of the foreign body reaction type and large histiocytes. The etiology is unknown but possibly is viral or autoimmune. The classic syndrome of subacute thyroiditis includes thyroid enlargement (usually less than twice normal size) with pain and tenderness, symptoms of thyrotoxicosis, substantially increased ESR, increased T4, T3-RIA, and THBR (T3U) values, and decreased RAIU values. Thyroid scans demonstrate patchy isotope concentration throughout the thyroid gland (occasionally, only in focal areas) or else very little uptake. Classic cases have been reported to progress through four sequential stages: hyperthyroidism, followed by transient euthyroidism, then hypothyroidism, and then full recovery. Recovery in most cases takes place in 3-5 months. The classic syndrome is estimated to occur in approximately 50%-60% of patients with subacute thyroiditis. Milder or nonclassic cases lack the symptoms and laboratory findings of thyrotoxicosis. However, the ESR is usually elevated, and the RAIU value is usually decreased.

Painless thyroiditis (also called “silent thyroiditis”) describes a group of patients with a syndrome combining some elements of subacute thyroiditis with some aspects of chronic thyroiditis (Hashimoto’s disease). These patients have nonpainful thyroid swelling with or without clinical symptoms of thyrotoxicosis. Laboratory data include increased T4, T3-RIA, and THBR values, decreased RAIU value, patchy thyroid scan, and normal or minimally elevated ESR. Painless thyroiditis thus differs from subacute thyroiditis by lack of pain in the thyroid area and by normal ESR. Although some consider this syndrome to be a painless variant of subacute thyroiditis, biopsies of most cases have disclosed histologic findings of chronic lymphocytic thyroiditis rather than subacute thyroiditis. The reported incidence of this condition has varied from 5%-30% of all cases of hyperthyroidism. However, one report suggests that the incidence varies with geographic location, with the highest rates being in the Great Lakes region of the United States and in Japan.

Postpartum transient toxicosis is a syndrome that is said to occur in as many as 5%-6% (literature range, 5%-11%) of previously euthyroid postpartum women. There is transient symptomatic or asymptomatic thyrotoxicosis with elevated T4 and low RAIU values, similar to the findings in thyrotoxic silent thyroiditis. This episode in some cases is followed by transient hypothyroidism. Thyroid autoantibody titers are elevated, suggesting lymphocytic thyroiditis.

Chronic thyroiditis is characterized histologically by dense lymphocytic infiltration of the thyroid with destruction of varying amounts of thyroid parenchyma. Chronic thyroiditis is frequently divided into two subdivisions: lymphocytic thyroiditis, most frequent in children and young adults, and Hashimoto’s disease, found most often in adults aged 30-50 years. In both cases females are affected much more often than males. In approximately one half of chronic thyroiditis patients, serum T4 levels are normal and the patients are clinically euthyroid. In 20%-40% the T4level is decreased, and there may be variable degrees of hypothyroidism. In some patients with decreased T4 levels the T3-RIA may be normal and presumably is responsible for maintaining clinical euthyroidism. The RAIU value is normal in 30%-50% of cases. In 10%-30% the RAIU value is increased, especially in the early stages of the disease. In fact, an elevated RAIU value with a normal T4 value definitely raises the possibility of active (early) chronic thyroiditis. The ESR is usually normal. Thyroid scan discloses generalized patchy isotope distribution in approximately 50% of cases and focal patchy or reduced uptake in 5%-10% more. In approximately one third of cases various precursors of T4 or abnormal thyroglobulin derivatives are released from damaged thyroid acini. In about 5% of patients with chronic thyroiditis, release of thyroid hormone derivatives produces hyperthyroidism with increased serum T4 levels. The RAIU value may be elevated or decreased. If the RAIU value is decreased, these patients might be considered part of the “thyrotoxic silent thyroiditis” group. On the other hand, some patients with chronic thyroiditis eventually develop sufficient damage to the thyroid to produce permanent hypothyroidism.

Lymphocytic thyroiditis and Hashimoto’s disease are very similar, and some do not differentiate between them. However, in lymphocytic thyroiditis the goiter tends to enlarge more slowly, abnormal iodoproteins tend to appear more often, and the RAIU value tends to be elevated more frequently. Hashimoto’s disease tends to have more histologic evidence of a peculiar eosinophilic change of thyroid acinar epithelial cells called “Askenazi cell transformation.” Exact diagnosis of chronic thyroiditis is important for several reasons: to differentiate the condition from thyroid carcinoma, because a diffusely enlarged thyroid raises the question of possible thyrotoxicosis, and because treatment with thyroid hormone gives excellent results, especially in childhood lymphocytic thyroiditis.

Thyroid autoantibodies. Both subgroups of chronic thyroiditis are now considered to be either due to or associated with an autoimmune disorder directed against thyroid tissue. Autoantibodies against one or another element of thyroid tissue have been detected in most cases. In addition, there is an increased incidence of serologically detectable thyroid autoantibodies in rheumatoid-collagen disease patients, conditions themselves associated with disturbances in the body autoimmune mechanisms. There are two major subgroups of thyroid autoantibodies, those active against thyroglobulin and those directed against the microsome component of thyroid cells. There are several different techniques available to detect these antibodies, including, in order of increasing sensitivity: latex agglutination (antithyroglobulin antibodies only), immunofluorescence, hemagglutination (also known as the tanned [tannic acid-treated] red blood cell [or TRC] test), and radioassay. At present radioimmunoassay and immunofluorescence are not widely available, and most reference laboratories use some modification of the hemagglutination test.

In general, antimicrosomal antibodies are found more often in chronic thyroiditis than antithyroglobulin antibodies. Antithyroglobulin antibodies are found less often in diseases other than chronic thyroiditis, but this increase in specificity is only moderate, and neither test has adequate selectivity for chronic thyroiditis (Table 29-1). High titers are much more likely to be associated with chronic thyroiditis than with nontoxic nodular goiter or thyroid carcinoma. High titers of antimicrosomal antibodies (or both antimicrosomal and antithyroglobulin antibodies) are not specific for chronic thyroiditis, because patients with Graves’ disease or primary hypothyroidism may have either high or low titers. Normal or only slightly elevated titers, however, constitute some evidence against the diagnosis of chronic thyroiditis.


Table 29-1 Thyroid autoantibody test results in thyroid diseases (hemagglutination method)*