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TSH receptor-stimulating antibody

Patients receiving amiodarone must receive monitoring for thyroid abnormalities. Baseline measurements of serum TSH, FT4, FT3, antithyroid peroxidase antibody (anti-TPOAb) and TSH receptor-stimulating antibodies (TSHR-SAb) should be performed. TSH, FT4, and FT3 should be checked 3 months after initiation of amiodarone and then every 3 to 6 months. [Pg.668]

TSH receptor-stimulating antibody or thyroid-stimulating immunoglobulin (TSI) < 125% Test not indicated Elevated in Graves disease... [Pg.856]

In Graves disease (see below), lymphocytes secrete a TSH receptor-stimulating antibody (TSH-R Ab [stim]), also known as... [Pg.857]

In Graves disease, hyperthyroidism results from the action of thyroid-stimulating antibodies (TSAb) directed against the thyrotropin receptor on the surface of the thyroid cell. These immunoglobulin G antibodies bind to the receptor and activate the enzyme adenylate cyclase in the same manner as TSH. [Pg.241]

Graves disease is considered to be an autoimmune disorder in which helper T lymphocytes stimulate lymphocytes to synthesize antibodies to thyroidal antigens. The antibody described previously (TSH-R Ab [stim]) is directed against the TSH receptor site in the thyroid cell membrane and has the capacity to stimulate growth and biosynthetic activity of the thyroid cell. Spontaneous remission occurs but some patients require years of antithyroid therapy. [Pg.867]

The leading cause of Graves disease occurs when there is a defect in the immune system that causes the production of autoantibodies to TSH receptors located on the surface of thyroid cells. These antibodies act as agonists to stimulate the thyroid, causing it to enlarge (goiter formation), with the overproduction of thyroid hormones... [Pg.155]

Q6 Graves disease is an autoimmune disease caused by the presence of thyroid stimulating antibodies which attack the TSH receptors in the thyroid gland, preventing the TSH from binding to its receptors. [Pg.144]

Thyrotoxicosis is most commonly caused by Graves disease, which is an autoimmune disorder in which thyroid-stimulating antibody (TSAb) directed against the thyrotropin receptor elicits the same biologic response as thyroid-stimulating hormone (TSH). [Pg.1369]

TR 82, TR/31, TRal thyroid hormone receptors TRH thyrotropin-releasing hormone TSAb thyroid-stimulating antibody TSH thyroid-stimulating hormone... [Pg.1387]

Biochemical mechanism The most frequent cause of hyperthyroidism, Graves disease, is an autoimmune process in which thyroid hypersecretion is caused by circulating immunoglobulins that bind to the TSH receptor on the thyroid follicular cells and stimulate thyroid hormone production. The diagnosis is confirmed by increased thyroid stimulating IgG antibodies and is frequently seen in other family members. [Pg.66]

Etiology Thyroid-stimulating antibodies bind to TSH receptors, causing release of thyroxin (current theory). [Pg.153]

In Chinese hamster ovary cells transfected with the recombinant human TSH receptor, lemon balm produced a dose-dependent inhibition of TSH-stimulated adenylate cyclase activity, inhibited the cAMP production stimulated by TSH receptor antibody, and produced a significant inhibition of TSH binding to its receptor and of antibody binding to TSH (Santini et al. 2003). [Pg.559]

Types of autoimmune diseases vary widely, from organ-specific diseases such as thyroiditis where there may be stimulation (thyrotoxicosis) by antibody against the receptor for pituitary thyroid-stimulating hormone (TSH) or inhibition (myxoedema) by cell destruction probably mediated by NK cells and autoantibody, through to non-... [Pg.298]


See other pages where TSH receptor-stimulating antibody is mentioned: [Pg.669]    [Pg.683]    [Pg.749]    [Pg.886]    [Pg.337]    [Pg.669]    [Pg.683]    [Pg.749]    [Pg.886]    [Pg.337]    [Pg.221]    [Pg.1189]    [Pg.563]    [Pg.564]    [Pg.499]    [Pg.564]    [Pg.2086]    [Pg.2086]    [Pg.2086]    [Pg.306]    [Pg.772]    [Pg.1380]    [Pg.551]    [Pg.254]    [Pg.969]    [Pg.892]    [Pg.193]    [Pg.499]    [Pg.382]    [Pg.36]    [Pg.37]    [Pg.670]    [Pg.24]    [Pg.1977]    [Pg.83]   


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