Hyperthyroxinemia

Displacement of T3 and T4 from TBG with transient hyperthyroxinemia Salicylates, fenclofenac, mefenamic acid, furosemide... 

The major adverse effect on the fetus is altered thyroid function (SEDA-13, 141 SEDA-14, 149 SEDA-19, 194 SEDA-20, 176). There have been individual reports of neonatal hyperthyroxinemia (79), goiter (80), and hypothyroidism (81). In the patient with goiter there was associated hypotonia, bradycardia, large fontanelles, and macroglossia (80). 

Propranolol inhibits the conversion of thyroxine (T4) to tri-iodothyronine (T3) by peripheral tissues (180), resulting in increased formation of inactive reverse T3. There have been several reports of hyperthyroxinemia in clinically euthyroid patients taking propranolol for non-thyroid reasons in high dosages (320-480 mg/day) (181,182). The incidence was considered to be higher than could be accounted for by the development of spontaneous hyperthyroidism, but the mechanism is unknown. 

Cooper DS, Daniels GH, Ladenson PW, Ridgway EC. Hyperthyroxinemia in patients treated with high-dose propranolol. Am J Med 1982 73(6) 867-71. 

Mooradian A, Morley JE, Simon G, Shafer RB. Propranolol-induced hyperthyroxinemia. Arch Intern Med 1983 143(11) 2193—5. 

The function of most albumin isoforms is normal, although some have abnormal binding affinities for thyroxine (T4). Binding may be increased, as in familial dysalbu-minemic hyperthyroxinemia, or decreased. Individuals with famihal dysalbuminemic hyperthyroxinemia are euthyroid but have elevated serum T4 and free T4 index the variant albumin comigrates with Alb A. Two glycosylated variants. Alb RedhiU and Alb Casebrook, have altered fatty acid binding properties. 

Many disorders are associated with thyroid hormone excess or deficiency in the absence of definable thyroid disease. These states of euthyroid hyperthyroxinemia or euthyroid hypothyroxinemia often result from alterations in the concentration of thyroid hormone—binding proteins, the actions... 

Mutations in a human serum albumin gene that substitute either histidine or proline for arginine at position 218 increase binding affinity for T4. These mutations are autosomal dominant and occur with relatively high frequency. Carriers of these mutations have high levels of total serum T4 but their free-T4 and TSH concentrations are within the normal range. Individuals are euthyroid (normal thyroid) and their conditions are known as familial dysalbumine-mic hyperthyroxinemia (FDH). 

Steinrauf, L.K. Hamilton, J.A. Braden, B.C. Murrel, J.R. Benson. M.D. X-ray crystal structure of the ala-109 thr variant of human transthyretin which produces euthyroid hyperthyroxinemia. J. Biol. Chem. 1993, 268. 2425-2430. 

A patient taking amiodarone for atrial fibrillation developed hyperthyroxinemia, which led to a diagnosis of thyroid hormone resistance syndrome [3(r]. Although thyroid hormone resistance is not a complication of amiodarone treatment, hyperproduction of hormone, accompanied by high concentrations of thyroid hormone without TSH suppression, is a rare genetic disorder that is worth being aware of. 

Goichot B, Savagner F, Sapin R, Luca F, Schlienger J-L. Marked hyperthyroxinemia during amiodarone treatment revealing thyroid hormone resistance syndrome. Thyroid 2008 18(9) 1019-20. 

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