Thyroid hormone levels after acute L-thyroxine loading in hypothyroidism.

While extrathyroidal conversion of T4 to T3 sustains circulating T3 blood levels in patients receiving maintenance doses of L-T4, the serum T3 rise after the acute administration of large doses of L-T4 may involve an additional mechanism, T3 contamination in L-T4 preparations. L-T4 (1000 micrograms; Synthroid) was given orally to four noncompliant hypothyroid individuals (mean T4, 1.0 micrograms/dl; mean T3, 28 ng/dl). Continuously withdrawn blood sampling revealed a mean rise in serum T4 to 7.7 micrograms/dl at 4 h and a parallel rapid mean rise in serum T3 to 66 ng/dl (136% over baseline) at 4 h. RIA analysis of the experimental batches of Synthroid revealed 0.7-0.9% T3 contamination. Oral administration of 5 or 10 micrograms Cytomel (T3; corresponding to 0.5% and 1% T3 contamination in 1000 micrograms Synthroid) to two of the hypothyroid subjects at a later date resulted in T3 serum elevations 12% and 68% as great as post 1000 micrograms L-T4. To eliminate basal hormone changes between these experiments, a third subject received 7.5 micrograms Cytomel on day 1 (corresponding to the measured T3 contamination in 1000 micrograms Synthroid), followed by 1000 micrograms Synthroid on day 2. Resulting peak T3 levels were identical. In summary, hypothyroid individuals rapidly absorb acute L-T4 loads, with parallel increases in T4 and T3 blood levels. The major source of this T3 elevation is the contaminant in L-T4 preparations. This degree of T3 contamination becomes clinically significant in acute large dose T4 regimens and results in euthyroid levels of T3.