A B S T R A C T The absorption of L-thyroxine (T4) and L-triiodothyronine (Ts) and the fractional rate of conversion of T4 to T3 were determined from the turnover rates of T4 and Ta in seven patients without endogenous thyroid function during separate treatment periods with these iodothyronines. Serum T3 concentration was measured by a radi-oimmunoassay procedure in which the iodothyronines are separated from the plasma proteins before incubation with anti-Ts antibody. Metabolic clearance rates were calculated by an integral (noncompartmental) approach since the use of single compartment kinetics led to a 40% overestimation of the metabolic clearance rate of T3. Based on the amount of hormone ingested and the observed hormonal turnover rates, the absorption of T4 and Ta (iodothyronine turnover/iodothyronine ingested) in man could be estimated. Absorption of T3 was complete in three subjects but decreased to 43% in a fourth who was suffering from mild congestive heart failure.Mean T4 absorption was 48.0±2.6% (SEM) for seven subjects. The mean fractional rate of T4 to Ta conversion determined during T4 replacement therapy (Ta turnover/ T4 turnover) was 42.6% (range 30.7-50.8%). Thus, approximately one-half of the T4 which was deiodinated was converted to T3 suggesting that monodeiodination is an obligatory step in the peripheral metabolism of T4. Calculations based on these results together with other available data suggest that under normal physiologic circumstances the major portion of the Ta pool is derived from monodeiodination of T4.

A B s T R A C T A niewN, proce(dure for the radlioitimutinoassay of i-triiodothyronine ( T:) inl h1uIm1ain plasima is (lescribed in whiclh the iodothivronine.s are separatedl frollm the pl)asma proteins before incubation with a specific anitiserumii to Ta. The antibody bound and free T. are separated with dextran-coated charcoal. In this system, the mean recovery of T added to l)lasma was 97.9% aand botlh in vitro conversion of L-thyroxine (T4) to T:. and crossreaction between T. and the anti-T3 antibody were undetectable (less thani 0.1% ). The assay procedure allowed the measuremiienit of T:, in up to 0.5 ml of plasma resulting in iml)roved assay sensitivity (6 ng/100 ml).The mean plasma T3 in normal subjects was 146±24 ng/100,ml (SD). Mean Ti concentration was increased in hyperthyroidism (665±289 ngj/100 ml') and decreased in hypothyroidism (44±26 ng/100 nml). In patients witlh severe hypothyroidism, pllasma T3 was betweeni 7 and 30 ng/100 nml. Plasnma T: concenitrationi was relatively constant throughout the day in three euthyroid subjects.In contrast, in hypothyroid subjects onI replacement therapy with T3, a T4: T3 comiibiniation or desiccated thyroid plasma T:, was markedly elevated for several hours after ingestion of the mledication. Plasma T. was unchanged throughout the day in patients treated with T.

Studies with L-[(125)l] triiodothyronine and L-[(125)l] thyroxine, and with equilibrium dialysis of plasma proteins indicate that rat pituitary binds L-triiodothyronine 9.8 times as strongly as it does L-thyroxine. Injection of even small doses of nonradioactive L-triiodothyronine reduces the pituitary/ plasma ratio of radioactive L-triiodothyronine, an indication of the existence of pituitary binding sites with a limited capacity for L-triiodothyronine. Limited capacity binding sites for L-thyroxine could not be demonstrated.

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