Hashimoto Thyroiditis

Abstract

More than a century has passed since the first description of Hashimoto thyroiditis (HT) as a clinicopathologic entity. HT is an autoimmune disease in which a breakdown of immune tolerance is caused by interplay of a variety of immunologic, genetic, and environmental factors. Thyrocyte injury resulting from environmental factors results in expression of new or hidden epitopes that leads to proliferation of autoreactive T and B cells. Infiltration of thyroid by these cells results in HT. In addition to the usual type of HT, several variants such as the fibrous type and Riedal thyroiditis are also recognized. The most recently recognized variant is immunoglobulin G4(+) HT, which may occur as isolated thyroid limited disease or as part of a generalized Ig4-related sclerosing disease. The relationship between HT and Riedel thyroiditis remains unclear; however, recent evidence seems to suggest that it may also be part of the spectrum of Ig4-related sclerosing disease. HT is frequently associated with papillary thyroid carcinoma and may indeed be a risk factor for developing this type of cancer. The relationship between thyroid lymphoma and HT on the other hand appears well established.

Elevated blood Hsp60, its structural similarities and cross-reactivity with thyroid molecules, and its presence on the plasma membrane of oncocytes point to the chaperonin as an immunopathogenic factor in Hashimoto's thyroiditis

“…Clinical features include increased levels of antibodies to thyroglobulin (TG) and thyroid peroxidase (TPO), two proteins localized within the thyroid gland cells (Lorini et al 2003). It has been postulated that, as a result of interaction of the antibodies with TG and TPO, inflammation develops in the thyroid gland, the gland is destroyed, and the patient ultimately is rendered hypothyroid (Ahmed et al 2012). However, since TG and TPO are localized inside the cells, other mechanisms must also be implicated in cell lysis and gland destruction.…”

“…It is an autoimmune disease characterized by a prolonged autoimmune response against thyroid tissue that alters significantly the morphology of the gland (Ahmed et al 2012). Classic histological features of HT include small, degenerated follicles, oncocytic (Hurthle cell) metaplasia, and lymphoid infiltrates arranged in follicles (Lorini et al 2003;Ahmed et al 2012). Clinical features include increased levels of antibodies to thyroglobulin (TG) and thyroid peroxidase (TPO), two proteins localized within the thyroid gland cells (Lorini et al 2003).…”

The association between papillary thyroid carcinoma and histologically proven Hashimoto's thyroiditis: a meta-analysis

“…HT is characterized by hypothyroidism, the presence of serum antithyroglobulin and antiperoxidase antibodies, and widespread lymphocytic infiltration with depletion of follicular cells. In addition to the classical HT, recent studies have proposed that IgG4-related thyroiditis may be considered as a variant of HT (2). The association between HT and PTC has been a subject of long and ongoing debate (1,2).…”

“…In addition to the classical HT, recent studies have proposed that IgG4-related thyroiditis may be considered as a variant of HT (2). The association between HT and PTC has been a subject of long and ongoing debate (1,2).…”

Association of CTLA-4 gene polymorphisms −318C/T and +49A/G and Hashimoto's thyroidits in Zahedan, Iran

“…Primary HT is the most common form of thyroiditis; it has a wide pathologic variety and includes six forms: Classic (8), juvenile (9) and immunoglobulin G4-dependent HT (10), the fibrous variant, Hashitoxicosis and painless thyroiditis (10,11), and its etiology has remained elusive. The common feature in all types of HT is lymphocyte infiltration and fibrosis (12,13).…”