MORPHOLOGYTheglandisfirm,withanintactcapsule,andmaybeunilaterallyorbilaterallyenlarged.Histologicexaminationrevealsdisruptionofthyroidfollicles,extravasationofcolloid,andinfiltratingneutrophils,whicharereplacedovertimebylymphocytes,plasmacells,andmacrophages.Theextravasatedcolloidprovokesanexuberantgranulomatousreactionwithgiantcells,somecontainingfragmentsofcolloid.Healingoccursbyresolutionofinflammationandfibrosis.
The onset of this form of thyroiditis often is acute. It is characterized by neck pain (particularly with swallowing), fever, malaise, and variable enlargement of the thyroid. Transient hyperthyroidism may occur, as in other cases of thyroiditis, as a result of disruption of thyroid follicles and release of excessive thyroid hormone. The leukocyte count and erythrocyte sedimentation rates are increased. With progression of the gland destruction, a transient hypothyroid phase may ensue. The condition typically is self-limited, with most patients returning to a euthyroid state within 6 to 8 weeks.
Subacute lymphocytic thyroiditis also is known as silent or painless thyroiditis; in a subset of patients, the onset follows pregnancy (postpartum thyroiditis). This disease is most likely autoimmune in etiology, as circulating antithyroid antibodies are found in a majority of patients. It mostly affects middle-aged women, who present with a painless neck mass or features of thyroid hormone excess. The initial phase of thyrotoxicosis (which is likely to be secondary to thyroid tissue damage) is followed by return to a euthyroid state within a few months. In a minority of affected individuals, the condition eventually progresses to hypothyroidism. Except for possible mild symmetric enlargement, the thyroid appears normal on gross inspection. The histologic features consist of lymphocytic infiltration and hyperplastic germinal centers within the thyroid parenchyma.
Riedel thyroiditis, a rare disorder that is a manifestation of IgG4-related disease (Chapter 5), is characterized by extensive fibrosis involving the thyroid and contiguous neck structures. Clinical evaluation demonstrates a hard and fixed thyroid mass, simulating a thyroid neoplasm. It may be associated with idiopathic fibrosis in other sites in the body, such as the retroperitoneum.
•Chroniclymphocytic(Hashimoto)thyroiditisisthemostcommoncauseofhypothyroidisminregionswheredietaryiodinelevelsaresufficient.
Hashimotothyroiditisisanautoimmunediseasecharacterizedbyprogressivedestructionofthyroidparenchyma,Hürthlecellchange,andmononuclear(lymphoplasmacytic)infiltrates,withorwithoutextensivefibrosis.
MultipleautoimmunemechanismsaccountforthyroidinjuryinHashimotodisease,includingcytotoxicitymediatedbyCD8+ Tcells,cytokines(IFN-γ),andanti-thyroidantibodies.
Subacutegranulomatous(deQuervain)thyroiditisisaself-limiteddisease,probablysecondarytoaviralinfection,andischaracterizedbypainandthepresenceofagranulomatousinflammationinthethyroid.
Subacutelymphocyticthyroiditisisaself-limiteddiseasethatoftenoccursafterapregnancy(postpartumthyroiditis),typicallyispainless,andischaracterizedbylymphocyticinflammationinthethyroid.
In 1835, Robert Graves reported on his observations of a disease characterized by “violent and long continued palpitations in females” associated with enlargement of the thyroid gland. Graves disease is the most common cause of endogenous hyperthyroidism. It is characterized by a triad of manifestations:
Thyrotoxicosis, caused by a diffusely enlarged, hyper-functional thyroid