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In conclusion: the high incidence of TSH-receptor antibodies in Graves' disease confirms their pathogenetic role in the development of hyperthyroidism; TSH-receptor antibodies in Graves' disease are not significantly associated with the presence of ophthalmopathy or pretibial myxoedema; TSH-receptor antibody assays may be useful for the diagnosis of Graves' disease in the absence of other signs of autoimmunity.
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In a 1971 study of myxedematous patients in whom therapy with LT 4 was initiated, lowering of their elevated serum TSH values was shown to correlate with the dose of LT 4 given ().
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All patients tolerated the weekly regimen well and the tissue markers of thyroid hormone effect were not different between both groups, with no evidence of toxicity.
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Congenital TSH deficiency may rarely be an isolated problem (caused by mutations in the TSH β subunit gene), but most commonly it is associated with other pituitary hormone deficiencies, as part of congenital hypopituitarism.
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Because of its rapid and less predictable absorption from the intestinal tract, it is generally not used as the primary medication to treat hypothyroidism.
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The most common cause of hyperthyroidism is Graves' disease, an autoimmune condition in which the body produces an antibody that causes the thyroid gland to release too much hormone.
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Three factors were likely responsible for LT 4 becoming the predominant therapy in the latter half of the 20th century: first, the isolation of T 4 in 1927 by Kendall (); second, the synthesis of T 4 () and its better-absorbed sodium salt by Chalmers et al.
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Infants born with permanent congenital (inborn) hypothyroidism need to receive treatment as soon as possible after birth to prevent mental retardation, stunted growth, and other aspects of abnormal development (a syndrome referred to as cretinism).
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