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Clinical Chemistry, Vol 29, 1408-1410, Copyright © 1983 by American Association for Clinical Chemistry
JR Stockigt, V Stevens, EL White and JW Barlow
We have assessed the influence of albumin-bound thyroxin (T4) on apparent free T4 values obtained by two "unbound analog" free T4 methods (AmerlexR Free T4 and Clinical Assays one-step Free T4). We evaluated sera showing three different albumin anomalies: total hereditary analbuminemia, partially corrected analbuminemia, and familial dysalbuminemic hyperthyroxinemia, where abnormal albumin- binding of analog tracer is associated with high apparent free T4 values by these methods. In hereditary analbuminemia, free T4 was almost undetectable by both assays; in contrast, free T4 by equilibrium dialysis was normal. After addition of T4-free human serum albumin, the apparent free T4 concentration in total hereditary analbuminemia became normal by the analog methods. Immunoprecipitation of [125I]T4 and the unidentified labeled kit analogs by antiserum to human albumin was negligible in untreated total hereditary analbuminemia and approximately twice normal in familial dysalbuminemic hyperthyroxinemia. Therefore, alterations in tracer binding to albumin correlate with the apparent free T4 concentrations obtained by the analog methods. The interactions of the unidentified analog tracers and T4 with albumin are such that these techniques principally reflect the albumin-bound T4 moiety.
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