Aetiology
The aetiology is presumed to be viral or autoimmune.[7] A seasonal variation has been noted in several studies in many countries, with the highest incidence in the summer and autumn (July to December), which is typical for viral infections.[8] The disease tends to occur after an upper respiratory infection. Post-convalescent viral titres of many common viruses (influenza, adenovirus, mumps, coxsackie, echo, H1N1) are elevated and then decrease in patients after the diagnosis of subacute thyroiditis.[9][10] Often, a patient may have multiple viral antibody levels that fall quickly after diagnosis, suggesting that this is an anamnestic response to the inflammatory condition rather than the cause.
Histocompatibility studies show a predominance of certain HLA genotypes in patients with subacute thyroiditis.[7][11][12] Familial cases of this thyroiditis occur and are associated with HDL-B35.[13]
One hypothesis is that the condition is a result of a viral infection in a genetically predisposed person, but it is not clear whether this is a host response to the viral infection or a viral infection of the thyroid. Virus-like particles have been identified in some patients.[14]
Pathophysiology
Subacute thyroiditis is a destructive thyroiditis that results in the release of preformed thyroid hormones, in the form of thyroglobulin, into the circulation. Thyroglobulin is degraded by serum proteases into the thyroid hormones, thyroxine (T4) and triiothyronine (T3). The thyroid is often enlarged and firm to palpation.[15] The elevated thyroid hormone levels in the blood can result in the symptoms of thyrotoxicosis (e.g., palpitations, tremor, heat intolerance) and suppress the pituitary secretion of thyroid-stimulating hormone (TSH). The thyroid destruction plus the TSH suppression results in low iodine uptake by the entire thyroid gland, even if the inflammation is focal within one part of the thyroid. Of note, because the thyrotoxicosis is caused by release of preformed hormone, antithyroid medications such as thiamazole, propylthiouracil, and carbimazole are ineffective in reducing thyroid hormone levels and are not indicated in subacute thyroiditis. Thyroid histology shows thyroid follicle destruction, infiltrates of mononuclear cells, and characteristic multinucleated giant cell granulomas.[16]
Classification
Phases of subacute thyroiditis[5]
Thyrotoxic phase (up to 6 weeks in length)
Acute viral-like illness with thyroid (neck) pain, fever, myalgias, malaise, and pharyngitis, which precedes severe neck pain; the neck pain may start on one side and migrate to the contralateral side.
Thyroid destructive phase with elevated serum T4 and T3 levels.
Radioiodine thyroidal uptake with I-123 or Tc-99m is very low (<1% at 24 hours).
Serum ESR and CRP levels are usually elevated.
Hypothyroid phase (up to 6 months in length)
Serum thyroid hormone levels are usually mildly or moderately low. Low levels may sometimes benefit from thyroid hormone replacement.
Radioiodine thyroidal uptake is variable.
Serum thyroid autoantibody levels are variably positive.
Euthyroid phase
Serum thyroid function returns to normal in ≥90% of patients; the remainder remain permanently hypothyroid and will require indefinite thyroid hormone replacement therapy.
Thyroid histology returns to normal.
Use of this content is subject to our disclaimer