Involvement of circulating interleukin-6 and its receptor in the development of euthyroid sick syndrome in patients with acute myocardial infarction

Abstract

Objective: In patients with acute myocardial infarction (AMI), low triiodothyronine (T3) levels with normal or subnormal levels of thyrotropin (TSH), the euthyroid sick syndrome (ESS), have been reported, however, the mechanism of altered thyroid hormone metabolism is unknown. Recent reports have shown that interleukin-6 (IL-6) plays a key role in the pathogenesis of AMI and ESS. This preliminary study investigates the relationship between thyroid states and plasma levels of IL-6, the soluble IL-6 receptor (sIL-6R), and the soluble transducing 130 kDa glycoprotein (sgp130) in AMI. Design and methods: We measured the concentration of TSH, free T3 (FT3), free thyroxine (FT4), IL-6, sIL-6R and sgp130 in plasma from 24 patients with AMI and 20 normal controls. Results: All 24 AMI patients showed significantly lower concentrations of FT3 with normal or subnormal levels of TSH, and higher concentrations of IL-6 and sIL-6R than controls, IL-6 level was correlated with creatine phosphokinase (CPK) and FT3 levels but not with FT4 or TSH levels in patients with AMI. The time course of IL-6 and FT3 concentration seemed to be closely linked, sIL-6R level was correlated with CPK and sgp130 levels, but not with FT3, FT4 or TSH levels. FT4 level was correlated with sgp130 level. Conclusion: Patients with AMI develop ESS through activation of IL-6 and its receptor system.