83 - Nonthyroidal Illness Syndrome

Abstract

The nonthyroidal illness syndrome (NTIS) was first reported in the 1970s as a remarkable ensemble of changes in serum thyroid hormone (TH) concentrations occurring during severe illness. Ever since, NTIS has remained an intriguing phenomenon not only because of the robustness of the decrease in serum T3, but also by its clear correlation with morbidity and mortality. Both experimental and clinical studies have shown that tissue TH concentrations during NTIS do not necessarily reflect serum concentrations and may decrease, remain unaltered, or even increase according to the organ and type of illness studied. In recent years, it has become clear that parenteral feeding in patients with critical illness is a major determinant not only of NTIS but also of clinical outcome. The altered serum and tissue TH concentrations have a solid basis in organ-specific molecular changes in TH transporters, receptors and deiodinases. The role of inflammatory pathways in these non-systemic changes has begun to be clarified. A novel role for TH metabolism in innate immune cells, including neutrophils and monocytes/macrophages, was shown in recent years, but there is no evidence at this stage that this is a determinant of susceptibility to infections. Although it may be tempting to correct NTIS by TH supplementation, there is at present insufficient evidence that this is beneficial. Thus, there is a clear need for adequately powered randomized controlled trials (RCTs) with clinically relevant endpoints to fill this knowledge gap.