Abstract

We have demonstrated previously that heparin produces an increase in serum free thyroxine (FT4) measured by 2 step radio-immunoassay or equilibrium dialysis in some patients. The mechanism by which heparin administration acts to increase serum concentrations of FT4 was investigated in 12 patients. Blood was collected from each patient before and after an intravenous dose of heparin. Each sample was divided into 2 portions. Paraoxon, an inhibitor of lipase activity, was added to 1 portion. FT4 and non-esterified fatty acids were analyzed. FT4 was 1.4±0.2 (Mean±SD) and 1.4±0.3 ng/dl in the samples before heparin administration with and without paraoxon, respectively. After heparin administration, FT4 was 1.8±0.7 ng/dl in the samples not containing paraoxon (p < 0.01) and 1.5±0.2 ng/dl in the samples containing paraoxon (NS). Non-esterlfied fatty acid concentrations increased 10 fold on the average after heparin administration in the samples without paraoxon (p < 0.01). In the samples containing paraoxon, there was no Increase in non-esterified fatty acid concentrations after heparin administration. There was significant correlation between FT4 and non-esterified fatty acid concentrations (r = 0.93, p <0.01) In serum after heparin administration which did not contain paraoxon. There was a significant correlation between plasma triglyceride concentrations and non-esterified fatty acid concentrations after heparin administration in the samples not containing paraoxon. The effect of heparin administration on non-esterified fatty acids occurs primarily in vitro after blood withdrawal by continued hydrolysis of plasma triglycerides. The resultant elevated non-esterified fatty acids in turn appear to displace thyroxine from its binding sites on plasma proteins. Caution should be exercised in the interpretation of FT4 after administration of heparin.

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