Abstract
T2′ plasma levels are measured under different conditions and correlated to the respective rT3 concentrations. Specific RIAs for T2′ and rT3 are used. Pharmacological doses of T3 cause an increase of plasma T2′; if T3 or T4 doses are administered to an athyroid patient which cause a similar level of plasma T3 the increase of T2′ is much larger during T4 treatment. Cord blood levels of T2′ are 2–3-fold higher than in normal adults whereas rT3 concentrations are about 10 times higher than normal. After birth rT3 and T2′ levels decrease in about a parallel manner. After a bolus iv injection of 500 μg rT3, T2′ starts to increase as early as 2 min after injection. PTU in therapeutic doses causes a rapid increase of plasma rT3 with a maximum 4 h after ingestion. A dose of 150 mg PTU causes a maximum of about 100% above baseline. T2′ also increases but to a lesser degree (about 50 % above baseline). We conclude that rT3 is the most important precursor of T2′ whereas T3 contributes only to a minor degree to the total T2′ production under physiological conditions.

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