Clinical Chemistry
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Clinical Chemistry 51: 1065-1069, 2005. First published April 15, 2005; 10.1373/clinchem.2005.050518
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(Clinical Chemistry. 2005;51:1065-1069.)
© 2005 American Association for Clinical Chemistry, Inc.

Case Report

Dysprealbuminemic Hyperthyroxinemia in a Patient with Hyperthyroid Graves Disease

Scott J. Cameron1, Judith C. Hagedorn2, Lori J. Sokoll1, Patrizio Caturegli2 and Paul W. Ladenson1,2,a

1 Clinical Chemistry Division, Department of Pathology, and 2 Division of Endocrinology and Metabolism, Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, MD.

aAddress correspondence to this author at: Johns Hopkins Medical Institutions, 1830 E. Monument St., Suite 333, Baltimore, MD 21287-0003. Fax 410-955-3916; e-mail ladenson{at}jhmi.edu.

Rare mutant forms of circulating albumin and prealbumin [transthyretin (TTR)] have increased binding affinity for thyroxine (T4). Patients with these variant plasma proteins, as a result of inherited mutations or as a paraneoplastic phenomenon, typically present with increased serum total T4 and, by some assay methodologies, an increased free T4 as well. Although these individuals are, in fact, euthyroid, nonspecific symptoms may lead to inappropriate treatment for hyperthyroidism. We present a 34-year-old woman in whom a mutant form of TTR with increased T4 binding affinity and coexisting Graves disease was present. Subsequent 131I therapy led to development of postablative hypothyroidism, which was obscured by her higher serum free T4 concentration. Circulating thyroid-binding globulin (TBG), albumin, and TTR concentrations were all within their respective reference limits. A T4-binding protein panel confirmed that TTR-bound T4 was significantly increased, whereas TBG- and albumin-bound T4 was normal, indicating that this patient had euthyroid dysprealbuminemic hyperthyroxinemia, which had been masked by the initial presentation of hyperthyroidism. These findings indicate that hypothyroidism can be masked by coexisting euthyroid dysprealbuminemic hyperthyroxinemia.






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