TSH receptor antibodies

Cho, B. 2002. Clinical applications of TSH receptor antibodies in thyroid diseases. Journal of Korean Medical Science 17(3), 293-301. 

While this pattern of biochemistry does not exclude transient relapse of Graves hyperthyroidism (despite the finding of negative TSH receptor antibodies), or a transient thyroiditis, the authors speculated that indinavir (prescribed in this patient together with stavudine and lamivudine) had inhibited the glucuronidation of thyroxine and hence caused a rise in serum thyroid hormone concentrations. 

In five patients who presented in Tasmania during 1 year, all of whom were taking amiodarone 200 mg/day, serum TSH was undetectable and the free thyroxine and triiodothyronine concentrations were raised (46). In one case there was a low titer of TSH receptor antibodies and in another a high titer of antithyroid peroxidase antibodies. In all cases the hyperthyroidism was severe and occurred after at least 2 years of treatment with amiodarone. In one of two patients in whom it was measured the serum concentration of interleukin-6 was raised, as has been previously shown (SEDA-19, 193). In two cases the hyperthyroidism was refractory to treatment with propylthiouracil, lithium, and dexamethasone in these cases thyroidectomy was required. Two patients responded to propylthiouracil, lithium, and dexamethasone, and one responded to carbimazole. 

Antimicrosomal antibodies Antithyroid peroxidase antibodies TSH receptor antibodies... 

Shewring G, Rees-Smith B. An improved radioreceptor assay for TSH receptor antibodies. CHn Endocrinol 1982 17 409-17. 

Glinoer D. de Nayer P. Bex M Effects of 1-thyroxine administration, TSH-receptor antibodies and smok-... 

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). 

After parturition the mother s thyroid function tests were normal, as were thyroglobulin and thyroperoxidase TSH receptor antibodies were undetectable. Her thyroid was not palpable, but a scan showed diffuse enlargement and uptake was increased. She developed a multinodular goiter 4 years later, but free thyroxine and TSH concentrations remained normal. Three more children born to mothers using penicillamine all had subclinical hypothyroidism. The authors hypothesized that penicillamine inhibits thyroid hormone iodination and coupling reactions catalysed by thyroid peroxidase, and concluded that in utero exposure to penicillamine may cause congenital goitrous hypothyroidism and persistent subclinical hypothyroidism in older children. 

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. 

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

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

Congenital (cretinism) Athyreosis or ectopic thyroid, iodine deficiency TSH receptor-blocking antibodies Absent or present Severe... 

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. 

Hypothyroidism, known as myxedema in adults, when severe, is the most common disorder of the thyroid gland. Worldwide, hypothyroidism is most often the result of endemic iodine deficiency. In nonendemic areas, where iodine is sufficient in the diet, chronic autoimmune thyroiditis (Hashimoto s thyroiditis) accounts for the majority of cases. This disorder is primarily characterized by high levels of circulating antibodies against a key enzyme (thyroid peroxidase) in the processing of iodine in the thyroid gland. Blocking antibodies directed at the TSH receptor may also be present. Thyroid destruction may also occur via apoptotic cell death. 

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... 

Mariotti S (2002) Normal Physiology of the Hypothalmic-Pituitary-Thyroidal System and Relation to the Neural System and Other Endocrine Glands. [Internet resource] http //www.thyroidmanager.org/Chapter4/4-frame.htm Meinhold H, Altmann R, Bogner U, Finke R, Schleusener H (1994) Evaluation of various immunometric TSH assays. Exp Clin Endocrinol 102 23-26 Oda Y, Sanders J, Roberts S, Maruyama M, Kato R, Perez M, Petersen VB, Wedlock N, Furmaniak 1, Smith RB (1998) Binding characteristics of antibodies to the TSH receptor. J Mol Endocrinol 20 233-244... 

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. 

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