Clinical Chemistry
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Clinical Chemistry 30: 1179-1181, 1984;
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Clinical Chemistry, Vol 30, 1179-1181, Copyright © 1984 by American Association for Clinical Chemistry

Familial dysalbuminemic hyperthyroxinemia: a study of four probands and the kindred of three

AG Scottolini, NV Bhagavan, T Oshiro and L Powers

We investigated four probands, and the kindred of three, with familial dysalbuminemic hyperthyroxinemia, using the one- and two-step tests for free thyroxin and other thyroid-function tests. The results indicate that this is an autosomal dominant trait. The discovery of eight cases in our patient population, which represents about 4% of our hyperthyroxinemic patients (8/320), during eight months indicates that this aberration is more common than suspected. Its importance lies in the misinterpretation of test results and the consequent inappropriate treatment for thyrotoxicosis.


The following articles in journals at HighWire Press have cited this article:


Home page
 Clin. Chem.Home page
C. E. Petersen, C.-E. Ha, K. Harohalli, D. S. Park, J. B. Feix, O. Isozaki, and N. V. Bhagavan
Structural Investigations of a New Familial Dysalbuminemic Hyperthyroxinemia Genotype
Clin. Chem., August 1, 1999; 45(8): 1248 - 1254.
[Abstract] [Full Text] [PDF]

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 J. Biol. Chem.Home page
C. E. Petersen, C.-E. Ha, D. M. Jameson, and N. V. Bhagavan
Mutations in a Specific Human Serum Albumin Thyroxine Binding Site Define the Structural Basis of Familial Dysalbuminemic Hyperthyroxinemia
J. Biol. Chem., August 9, 1996; 271(32): 19110 - 19117.
[Abstract] [Full Text] [PDF]


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