Both high and low plasma glutamine levels predict mortality in critically ill patients.

PURPOSE: Plasma amino acids are important indicators for understanding human kinetics and amino acid dynamics. We aimed to investigate the association between the plasma glutamine levels and the mortality rates and determine whether plasma glutamine can predict the prognosis of critically ill patients. METHODS: The clinical records of adult patients who were admitted to an ICU were retrospectively evaluated to investigate the plasma levels of amino acids, including glutamine. RESULTS: Two hundred fourteen patients were included in this study (male, 62%; median age, 64 years; range 20-97 years). The patients' diagnoses included sepsis (45%), trauma (14%), cardiovascular disease (9%), fulminant hepatitis (9%), burns (4%), and others (19%). The mortality rates in patients with plasma glutamine <400 nmol/mL (group L; 39%, 28/71) or ≥700 nmol/mL (group H; 50%, 15/30) were significantly higher (p < 0.05 and p < 0.01, respectively) than those in patients with plasma glutamine levels of 400-700 nmol/mL (group M; 21%, 24/113). Among patients with sepsis, the mortality rates of group L (46%) and group H (67%) were significantly higher (p < 0.05 or p < 0.01, respectively) in comparison with group M (26%). CONCLUSION: Both lower and higher plasma glutamine levels were risk factors for mortality in critically ill patients.

Evaluation of a model of latent pathologic factors in relation to serum ferritin elevation.

OBJECTIVES: Serum ferritin increases in various disorders and clinical conditions. However, causal associations between the serum ferritin level and clinical factors that influence serum ferritin level are not well characterized. We report a model that quantitatively analyzes the causal relations between the serum ferritin level and clinical factors. DESIGN AND METHODS: We analyzed the ferritin level and other laboratory data in the sera of 274 patients. Structural equation modeling was used to verify causal relations and the adequacy of latent factors. RESULTS: Three factors representing clinical status were identified: cell damage, hepatic function, and inflammation. Serum iron (SI) had the strongest effect on serum ferritin elevation. The effect of the cell damage factor on serum ferritin indicated cell destruction, and that of the hepatic function factor represented decreased serum ferritin clearance. The cell damage factor also indirectly increased the ferritin level via SI or the hepatic function factor. The total effect of the inflammatory status factor on ferritin level was very weak. CONCLUSIONS: These causal relations may explain the mechanism of serum ferritin level elevation in various clinical conditions.