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• W2186868954 abstract "In fact, the finding of high levels of thyroid hormones in the presence of detectable serum TSH concentration may also depend from the presence of circulating factors interfering with the measurement of either thyroid hormones or TSH . The presence of circulating anti-iodothyronine autoantibodies (anti-T4 and/or anti-T3) or abnormal albumin/transthyretin forms may cause FT4 and/or FT3 to be overestimated, particularly when one-step analog methods are employed. The more common factors interfering in TSH measurement are the circulating heterophilic antibodies or anti-TSH antibodies. Anti-TSH antibodies, however, usually lead to an underestimation of the actual levels of TSH and very rarely to over-estimation, since they frequently prevent the formation of the sandwich between the two monoclonal anti-TSH antibodies used in the non-competitive immunometric assays, and the circulating TSH molecules. In patients with RTH never treated by thyroidectomy or radioiodine, serum TSH levels have been found within the normal range in about 85% of cases, in the presence of elevated levels of total and free thyroid hormone, thyroglobulin, and reverse T3. These findings prompted studies on the bioactivity of the secreted TSH molecules. Indeed, an enhanced biological activity was documented in all patients studied. Modifications in oligosaccharide structure of the circulating TSH molecules seem to account for the above findings. RTH presents with highly variable clinical features ranging from mental retardation and delayed bone maturation (generalized RTH: GRTH) to signs and symptoms of thyrotoxicosis (pituitary RTH : PRTH). The majority of RTH patients were described as euthyroid, the distinctive feature being the presence of goiter. The astounding achievement in molecular biologic studies of thyroid hormone receptors had immediate ramification for clinical research and opened a new era in the understanding of etiopathogenesis of RTH. Using DNA amplification and sequencing techniques, about 60 different mutations in TRb1 gene have now been identified in RTH patients belonging to 100 families, similar mutations occurring therefore in more than one family. No mutations have been so far detected in the TRa gene, suggesting that its products may play a minor role in the regulation of TSH secretion. Functional studies have definitively showed that the etiopathogenesis of the disease is due to TRb mutations and their identification is today mandatory in the diagnosis of RTH. However, in about one sixth of patients with clinical and biochemical phenotype of RTH no mutation could be found in either TRb or TRa genes. These data suggest that other still unknown isoforms of TRs (TRg?) may exist and may be mutated, or novel, nonreceptor mechanisms may be disrupted to produce RTH. Almost all patients with RTH" @default.
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• W2186868954 date "1999-01-01" @default.
• W2186868954 modified "2023-09-27" @default.
• W2186868954 title "SYNDROMES OF HORMONE RESISTANCE IN THYROID FIELD" @default.
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