Received on March 3, 2005
Accepted on March 25, 2005
Dysprealbuminemic Hyperthyroxinemia in a Patient with Hyperthyroid Graves Disease
Scott J. Cameron 1,
Judith C. Hagedorn 2,
Lori J. Sokoll 1,
Patrizio Caturegli 2,
Paul W. Ladenson 3*
1 Clinical Chemistry Division, Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD
2 Division of Endocrinology and Metabolism, Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, MD
3 Clinical Chemistry Division, Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD and Division of Endocrinology and Metabolism, Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, MD
* To whom correspondence should be addressed. 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 131-I 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 hyperthyroidism can mask coexisting euthyroid dysprealbuminemic hyperthyroxinemia.
