Tissue Distribution and Quantitation of a Gene Expressing a 64-kDa Antigen Associated with Thyroid-Associated Ophthalmopathy

Zhang, Z.-G.; Wall, Jack R.; Bernard, Nicole F.

doi:10.1006/clin.1996.0119

“…Other eye muscle autoantigens possibly involved in GO include 1) a 63-kDa calcium-binding protein, called calsequestrin, expressed in extraocular muscle and skeletal muscle, but not in the thyroid (67); 2) a 53-kDa protein, identified as another calcium-binding glycoprotein, sarcalumenin, expressed in extraocular muscle and skeletal muscle, but not in the thyroid (68); 3) a different 63-to 64-kDa protein, called 1D protein, cloned from a thyroid cDNA expression library (62), which is expressed in extraocular muscles, skeletal muscles, thyroid, testis, and other tissues (69,70); and 4) a novel eye muscle protein, called G2s, with an estimated molecular mass of about 220 kDa, expressed in extraocular muscles, skeletal muscles, and thyroid (68). A higher prevalence of circulating antibodies directed against two porcine eye muscle antigens (64-kDa and 95-kDa) has been found by immunoblotting in GO patients compared with those without eye involvement or to normal controls (71).…”

Section: Pathogenesismentioning

confidence: 99%

Management of Graves' Ophthalmopathy: Reality and Perspectives

Bartalena¹

2000

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Graves' ophthalmopathy is an debilitating disease impairing the quality of life of affected individuals. Despite recent progress in the understanding of its pathogenesis, treatment is often not satisfactory. In mild cases, local therapeutic measures (artificial tears and ointments, sunglasses, nocturnal taping of the eyes, prisms) can control symptoms and signs. In severe forms of the disease (3-5%), aggressive measures are required. If the disease is active, high-dose glucocorticoids and/or orbital radiotherapy, or orbital decompression represent the mainstay of treatment. If the disease is severe but inactive, orbital decompression is preferred. Novel treatments such as somatostatin analogs or intravenous immunoglobulins are under evaluation. Rehabilitative (extraocular muscle or eyelid) surgery is often needed after treatment and inactivation of eye disease. Correction of both hyper-and hypothyroidism is crucial for the ophthalmopathy. Antithyroid drugs and thyroidectomy do not influence the course of the ophthalmopathy, whereas radioiodine treatment may cause the progression of preexisting ophthalmopathy, especially in smokers. The exacerbation, however, is prevented by glucocorticoids. In addition, thyroid ablation may prove beneficial for the ophthalmopathy in view of the pathogenetic model relating eye disease to autoimmune reactions directed against antigens shared by the thyroid and the orbit.

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“…Other eye muscle autoantigens possibly involved in GO include 1) a 63-kDa calcium-binding protein, called calsequestrin, expressed in extraocular muscle and skeletal muscle, but not in the thyroid (67); 2) a 53-kDa protein, identified as another calcium-binding glycoprotein, sarcalumenin, expressed in extraocular muscle and skeletal muscle, but not in the thyroid (68); 3) a different 63-to 64-kDa protein, called 1D protein, cloned from a thyroid cDNA expression library (62), which is expressed in extraocular muscles, skeletal muscles, thyroid, testis, and other tissues (69,70); and 4) a novel eye muscle protein, called G2s, with an estimated molecular mass of about 220 kDa, expressed in extraocular muscles, skeletal muscles, and thyroid (68). A higher prevalence of circulating antibodies directed against two porcine eye muscle antigens (64-kDa and 95-kDa) has been found by immunoblotting in GO patients compared with those without eye involvement or to normal controls (71).…”

Section: Pathogenesismentioning

confidence: 99%

Management of Graves’ Ophthalmopathy: Reality and Perspectives*

Bartalena

¹

,

Pinchera

²

,

Marcocci

³

2000

View full text Add to dashboard Cite

Graves' ophthalmopathy is an debilitating disease impairing the quality of life of affected individuals. Despite recent progress in the understanding of its pathogenesis, treatment is often not satisfactory. In mild cases, local therapeutic measures (artificial tears and ointments, sunglasses, nocturnal taping of the eyes, prisms) can control symptoms and signs. In severe forms of the disease (3-5%), aggressive measures are required. If the disease is active, high-dose glucocorticoids and/or orbital radiotherapy, or orbital decompression represent the mainstay of treatment. If the disease is severe but inactive, orbital decompression is preferred. Novel treatments such as somatostatin analogs or intravenous immunoglobulins are under evaluation. Rehabilitative (extraocular muscle or eyelid) surgery is often needed after treatment and inactivation of eye disease. Correction of both hyper- and hypothyroidism is crucial for the ophthalmopathy. Antithyroid drugs and thyroidectomy do not influence the course of the ophthalmopathy, whereas radioiodine treatment may cause the progression of preexisting ophthalmopathy, especially in smokers. The exacerbation, however, is prevented by glucocorticoids. In addition, thyroid ablation may prove beneficial for the ophthalmopathy in view of the pathogenetic model relating eye disease to autoimmune reactions directed against antigens shared by the thyroid and the orbit.

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“…Based on serological methods, putative muscle antigens have been identified in EOM as well as in peripheral muscle tissue [29,30]. On clinical grounds, Graves' disease can present features such as myalgia, swelling of the calves and fasciitis [31].…”

Section: Introductionmentioning

confidence: 99%