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J G Wiswell

Publications and source records attributed to J G Wiswell.

11 recordsLinked to original sources

Circulating thyroid hormone changes in acute trauma: prognostic implications for clinical outcome.

Alterations in circulating thyroid hormone concentrations occur in a variety of nonthyroidal disease states. In the present study, thyroid hormone levels were measured every 8 to 12 hours in 19 otherwise healthy individuals suffering acute severe trauma necessitating admission to the Maryland Institute for Emergency Medical Services Systems. Four fatalities occurred within 48 hours of admission. The mean total T3 level fell rapidly after the onset of trauma and remained low throughout the observation period. Reverse T3 rose concurrent with the fall in T3 but gradually returned to normal in the survivors. Total and free T4 levels remained normal in the survivors but fell below normal in the fatalities on the samples obtained preceding death. Changes in free T4 were consistent in three separate radioimmunoassay systems. Pharmacologic doses of glucocorticoids administered to seven of the 15 survivors and to the four fatalities did not result in an acute depression in total and free T4 levels in the survivors. Post-mortem examination of three fatalities did not reveal evidence of significant thyroid or pituitary disease. These results suggest that in acutely traumatized patients: 1) T3 declines rapidly and remains depressed throughout the illness; 2) continued fall of T4 to subnormal levels is associated with a poor prognosis; and 3) steroid therapy alone cannot explain the acute changes observed in hormone levels.

Acute Disease

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 Continuously withdrawn blood sampling revealed a mean rise in serum T4 to 7.7 micrograms/dl at 4 h and a parallel rapid mean rise in serum T3 to 66 ng/dl (136% over baseline) at 4 h.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.

Fasting