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Orbital Autoimmunity in Graves’ Disease

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Part of the book series: Endocrine Updates ((ENDO,volume 14))

Abstract

Graves’ disease (GD) is an autoimmune syndrome characterized by hyperthyroidism and a diffusely enlarged thyroid gland. The most prominent extrathyroidal manifestation of this thyroid disease is thyroid-associated or Graves’ ophthalmopathy (GO), a medically incurable and chronic autoimmune process that affects all orbital tissue compartments and leads to various eye complications such as discomfort, lid retraction, proptosis, periorbital swelling, extraocular muscle dysfunction, diplopia, and sight loss. When assessed carefully, GO occurs in about 80–90% of patients with GD. In most instances, the orbital problems appear within 18 months after diagnosis of thyroid disease. The close clinical association of GD with GO and pretibial dermopathy (PTD), a less frequent extrathyroidal manifestation, suggests a common antigen or similar sequence of pathogenic events in these affected tissues (1,2). Enlargement of extraocular muscle bodies together with an increase of orbital connective/fatty tissue within the bony orbits is responsible for most of the orbital complications in patients with severe active GO. Tissue enlargement is effected by marked infiltration of immunocompetent cells, mainly macrophages and T lymphocytes, and some B cells and mast cells, as well as by abundant quantities of collagen and hydrophilic glycosaminoglycans (GAGs). It is entirely possible that the orbital immune process is triggered in a non-specific manner, and that antigen encounter by macrophages and dendritic cells facilitates T cell-dependent propagation and perpetuation of the disease.

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Heufelder, A.E., Joba, W. (2001). Orbital Autoimmunity in Graves’ Disease. In: Bahn, R.S. (eds) Thyroid Eye Disease. Endocrine Updates, vol 14. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1447-3_2

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