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outstanding papers ( 5 , 6 , 7 , 8 ). Thyroid antigens in AITD The autoantigens targeted during autoimmune attack in AITD are proteins expressed by the thyroid tissue, indispensable for its physiological function. The key features of thyroid
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What Is Known about This Topic? Graves’ orbitopathy is believed to be the consequence of autoimmunity against antigens present both in the thyroid and in orbital tissues. Massive release of thyroid antigens causes the appearance or
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Graves’ disease (GD) is a systemic autoimmune disorder characterized by the infiltration of thyroid antigen-specific T cells into thyroid-stimulating hormone receptor (TSH-R)-expressing tissues. Stimulatory autoantibodies (Ab) in GD activate the TSH-R leading to thyroid hyperplasia and unregulated thyroid hormone production and secretion. Diagnosis of GD is straightforward in a patient with biochemically confirmed thyrotoxicosis, positive TSH-R-Ab, a hypervascular and hypoechoic thyroid gland (ultrasound), and associated orbitopathy. In GD, measurement of TSH-R-Ab is recommended for an accurate diagnosis/differential diagnosis, prior to stopping antithyroid drug (ATD) treatment and during pregnancy. Graves’ hyperthyroidism is treated by decreasing thyroid hormone synthesis with the use of ATD, or by reducing the amount of thyroid tissue with radioactive iodine (RAI) treatment or total thyroidectomy. Patients with newly diagnosed Graves’ hyperthyroidism are usually medically treated for 12–18 months with methimazole (MMI) as the preferred drug. In children with GD, a 24- to 36-month course of MMI is recommended. Patients with persistently high TSH-R-Ab at 12–18 months can continue MMI treatment, repeating the TSH-R-Ab measurement after an additional 12 months, or opt for therapy with RAI or thyroidectomy. Women treated with MMI should be switched to propylthiouracil when planning pregnancy and during the first trimester of pregnancy. If a patient relapses after completing a course of ATD, definitive treatment is recommended; however, continued long-term low-dose MMI can be considered. Thyroidectomy should be performed by an experienced high-volume thyroid surgeon. RAI is contraindicated in Graves’ patients with active/severe orbitopathy, and steroid prophylaxis is warranted in Graves’ patients with mild/active orbitopathy receiving RAI.
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reactivation of GO following total thyroidectomy for GD, and radioiodine treatment after rhTSH for thyroid cancer. Radioiodine treatment may cause worsening of GO by the release of thyroid antigen resulting from radiation injury, inducing a long
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]. Interestingly, Kriss was convinced that the shift in gravity between the thyroid and the orbit during sleep might have favoured a retrograde flow of lymph and, therefore, of thyroid antigens [ 10 ]. On the other hand, Wiersinga et al. [ 11 ] failed to
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1 year, including TPO Ab, considered an immune response secondary to the release of thyroid antigens ( 12 , 13 , 14 ). To date, the role of the TPO Ab status in patients with hyperthyroidism due to Graves’ disease prior to RAI administration has
Department of Clinical Sciences, Skåne University Hospital, Malmö, Sweden
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Department of Clinical Sciences, Skåne University Hospital, Malmö, Sweden
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Department of Clinical Sciences, Skåne University Hospital, Malmö, Sweden
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thyroid antigens [ 11 , 12 ]. However, in some patients, the increase in TRAb persists for several years, indicating the existence of other mechanisms involving the activation of specific immunocompetent cells. Indeed, irradiated Hashimoto lymphocytes
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’s thyroiditis [ 25 ], suggesting that TgAb produced in acute thyroid destruction is not similar to that produced in a chronic autoimmune reaction, but represents a nonspecific response to the release of thyroid antigens. Table 3. Reported frequency of
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Discussion In this study, the genetic factors we chose to analyze were the costimulatory genes, which are not involved in the initiating of autoimmune response to thyroid antigens, but required to generate subsequent cytokines and cell surface molecules
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autoantibodies, probably due to a release of thyroid antigens following irradiation-induced follicular damage [ 5 , 20 , 21 ]. To the best of our knowledge, no study has yet looked at a possible influence of the RAI dose on the subsequent course of TSI
