Low T3 syndrome upon admission and response to nutritional support in malnourished medical inpatients


 
 
 During illness, deiodination of thyroxine (T4) to triiodothyronine (T3) is down regulated. This is called “low T3 syndrome”, an adaptive metabolic mechanism to reduce energy expenditure and prevent catabolism. We investigated the prognostic role of low T3 syndrome in patients at nutritional risk regarding mortality, clinical outcomes and response to nutritional support.
 
 
 
 This is a secondary analysis of the Effect of Early Nutritional Support on Frailty, Functional Outcomes, and Recovery of Malnourished Medical Inpatients Trial (EFFORT), a randomized-controlled Swiss multicenter trial comparing effects of individualized nutritional support with usual care in adult medical inpatients at nutritional risk. The primary endpoint was all-cause mortality over 30-,180-days and 5-years.
 
 
 
 We had complete data including fT3 concentration of 801/2028 (39.5%) patients from the initial trial. Of these 492 (61.4%) had low T3 syndrome (fT3 < 3.2 pmol/l). Low T3 syndrome was associated with higher mortality over 30 days (adjusted hazard ratio 1.97 [95%CI 1.17 to 3.31], p 0.011) and other adverse clinical outcomes. Nutritional support only lowered mortality in the group of patients with but not in those without low T3 syndrome (adjusted odds ratio of nutritional support of 0.82 [95%CI 0.47 to 1.41] vs. 1.47 [95%CI 0.55 to 3.94]). This finding, however, was not significant in interaction analysis (p for interaction = 0.401).
 
 
 
 Our secondary analysis of a randomized trial suggests that medical inpatients at nutritional risk with low T3 syndrome have a substantial increase in mortality and may show a more pronounced beneficial response to nutritional support interventions.
