The euthyroid
hyperthyroxinemia (EHT) is characterized on the one hand by a normal basal THS or TRH-TSH response but also by high plasma values of total
thyroxine (TT4) on the other. However if only TT4 is assessed, "
hyperthyroidism" may be diagnosed erroneously. EHT may be caused by an increase of specific
thyroxine binding proteins which may be hereditary (permanent) or acquired (transient). The most frequent disturbance is due to an
estrogen induced increase of
thyroxine binding globulin (TBG) in the course of pregnancy, anticonceptive drugs or
estrogen treatment. The
albumin associated HT (FDH syndrome), first reported in 1979, has autosomal dominant traits. 144 patients with FDH syndrome were observed during the period between 1984 and 1990, i.e. 7% (1986) of all
hyperthyroid patients explored. Family screening is required to prevent unjustified treatment. Additionally existing disturbances of thyroid function as well as other protein binding anomalies may both cause problems in differential diagnosis.
Prealbumin associated
hyperthyroxinemia (PAAH), first published in 1982, may be due to an inherited increase in affinity, but may also be the consequence of a true elevation of
prealbumin plasma concentration in the course of an islet cell
cancer; both conditions are extremely rare. Nearly as rare are patients with plasma
autoantibodies directed against T4 and/or T3 (5 cases); yet, a reverse T3
autoantibody could be observed in merely 1 case. By means of our modified radio-
thyroxine-agarosegel-iceelectrophoresis all such
protein anomalies may be diagnosed and differentiated in 1 procedure. Moreover, all other types of EHT must be taken into consideration by differential diagnosis.