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dc.contributor.authorThongkum Sunthornthepvarakulen_US
dc.contributor.authorSupawadee Likitmaskulen_US
dc.contributor.authorSupunnee Ngowngarmratanaen_US
dc.contributor.authorKitti Angsusinghaen_US
dc.contributor.authorSureerat Kitvitayasaken_US
dc.contributor.authorNeal H. Scherbergen_US
dc.contributor.authorSamuel Refetoffen_US
dc.contributor.otherRajavithi Hospitalen_US
dc.contributor.otherMahidol Universityen_US
dc.contributor.otherUniversity of Chicagoen_US
dc.identifier.citationJournal of Clinical Endocrinology and Metabolism. Vol.83, No.5 (1998), 1448-1454en_US
dc.description.abstractWe report the abnormal albumin in members of a Thai family that presented with high serum total T3but not T4when measured by radioimmunoassay. In contrast, total T3values were very low when measured by ELISA and chemiluminescence. The subjects have no goiter, and clinically euthyroid. Their serum free T4, free T3, and TSH were normal. Spiking of T3to affected serum showed good recovery by radioimmunoassay but very poor recovery by ELISA and by chemiluminescence. The immunoprecipitation with labeled T3bound to albumin showed high percent precipitation in affected serum. T3- binding studies showed that the association constant of serum albumin in affected subjects was 1.5 x 106M-1or 40-fold that of unaffected relatives of 3.9 x 104M-1. In contrast, the K(a) of HSA for T4in an affected subject was only 1.5-fold that of a normal. Albumin complementary DNA from leukocytes of affected member was amplified and sequenced. We found the second nucleotide of normal codon 66 (CTT), a thymine, was substituted by a cytosine (CCT), resulting in the replacement of the normal leucine by proline. This is the first report of variant albumin causing familial dysalbuminemic hypertriiodothyroninemia.en_US
dc.rightsMahidol Universityen_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.titleFamilial dysalbuminemic hypertriiodothyroninemia: A new, dominantly inherited albumin defecten_US
Appears in Collections:Scopus 1991-2000

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