Enhanced proatherogenic inflammation after recombinant human TSH administration in patients monitored for thyroid cancer remnant

Objective To evaluate the effect of recombinant human TSH (rhTSH) on biomarkers of vascular endothelial cell and platelet activation in patients monitored for thyroid carcinoma remnant. Methods Circulating levels of soluble(s) intercellular adhesion molecule (sICAM)-1 and sE-selectin, as indices of vascular endothelial cell activation, of sP-selectin and sCD40 ligand (sCD40L), as indices of platelet activation, and of 8-iso-prostaglandin F(2 alpha) (8-iso-PGF(2 alpha)), as an index of lipid peroxidation, were evaluated in 20 patients (16 females, 48 center dot 0 +/- 13 center dot 6 years) at baseline and after intramuscular rhTSH injection (0 center dot 9 mg/day on two consecutive days). Results At baseline, serum TSH values were below normal whereas free T3 and free T4 were within the normal range. After rhTSH injection, serum TSH increased significantly but free T3 and free T4 remained unchanged. Concomitantly, plasma sICAM-1 concentrations increased significantly (from 155 center dot 9 +/- 39 center dot 1 to 183 center dot 6 +/- 38 center dot 1 ng/ml, P < 0 center dot 03), as did those of sE-selectin (from 74 center dot 8 +/- 15 center dot 4 to 91 center dot 4 +/- 12 center dot 2 ng/ml, P < 0 center dot 0006), sP-selectin (from 56 center dot 4 +/- 13 center dot 7 to 72 center dot 2 +/- 14 center dot 9 ng/ml, P < 0 center dot 002), sCD40L (from 2 center dot 1 +/- 0 center dot 9 to 2 center dot 8 +/- 1 center dot 1 ng/ml, P < 0 center dot 03) and total 8-iso-PGF(2 alpha)(from 238 center dot 5 +/- 47 center dot 0 to 307 center dot 8 +/- 41 center dot 2 pg/l, P < 0 center dot 0001). Changes in circulating levels of sCD40L were directly correlated with changes in levels of plasma total 8-iso-PGF(2 alpha) (r = 0 center dot 523, P < 0 center dot 02) and sP-selectin (r = 0 center dot 480, P < 0 center dot 03). Conclusions Supraphysiological concentrations of rhTSH might exert proatherogenic effects by promoting activation of vascular endothelial cells and platelets probably through enhanced oxidative stress.