Abstract

Serum triiodothyronine (T3) and thyroxine (T4) levels were measured in 103 adult patients receiving sodium L-thyroxine (Synthroid), 0.2 or 0.3 mg daily for at least 3 mo, as suppression or replacement therapy. All were judged to be clinically euthyroid at the time of the measurements. The mean +/-SD T3 level during treatment was 130.3 +/-47.5 ng% and the mean T4 level was 11.0 +/-2.0 mug%. In normal untreated euthyroid subjects, the mean T3 level was 115.4 +/-26.0 ng% and the mean T4 level was 8.0 +/-1.7mug%. When sodium L-thyroxine was added in vitro to the stored sera of 10 hypothyroid patients to produce serum T4 levels equivalent to those that the patients later showed in vivo while on therapy, the cross-reaction was 0.85%. Thus at a mean T4 level of 11.0 mug%, there was a mean T3 level of 93.5 ng% that could be attributed to the added thyroxine itself. This cross-reaction was found to be due to contamination of the added sodium L-thyroxine with T3 and not due to cross-reactivity of the T3 antibody in the immunoassay system with T4. For 3 other brands of sodium L-thyroxine, the T3 contamination of the added T4 was 0.75%, 0.55%, and 0.40%. When 6 hypothyroid patients were given 5 mug of L-triiodothyronine (Cytomel) daily for 4 wk, there was no rise in serum T3 levels. When the same patients were switched to sodium L-thyroxine, 0.2 mg daily, serum T3 levels rose from a mean +/-SD of 60.0 +/-16.3 ng% to a mean of 130.0 +/-38.0 ng%. It would thus appear that in patients receiving sodium L-throxine therapy, the resulting serum T3 levels are due to extrathyroidal conversion of the administered T4 to T3, and not to the T3 present in the L-thyroxine administered.

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