1.
Hospital related hyperglycemia as a predictor of mortality in non-diabetes patients: A systematic review.
Pratiwi, C, Zulkifly, S, Dahlan, TF, Hafidzati, A, Oktavia, N, Mokoagow, MI, Epriliawati, M, Nasarudin, J, Made Kshanti, IA
Diabetes & metabolic syndrome. 2021;(6):102309
Abstract
BACKGROUND AND AIMS Hyperglycemia is a condition often found in hospitalized patients due to stress injury, parenteral nutrition or medications administered during hospitalization. According to previous studies, hyperglycemia could be an independent predictor of mortality. The objective of the study is to assess the risk of mortality in non-diabetic patients with hyperglycemia during hospitalization. METHODS In this systematic review, we conducted literature reviews on several databases. Twelve studies were retrieved and critically reviewed using NOS. RESULTS A majority of the studies reported that hospital related hyperglycemia increased the mortality rate. CONCLUSIONS Hospital related hyperglycemia is an independent predictor factor for both in-hospital and long-term mortality.
2.
Signaling mechanisms of altered cellular responses in trauma, burn, and sepsis: role of Ca2+.
Sayeed, MM
Archives of surgery (Chicago, Ill. : 1960). 2000;(12):1432-42
Abstract
Alterations in cellular responses in various organ systems contribute to trauma-, burn-, and sepsis-related multiple organ dysfunction syndrome. Such alterations in muscle contractile, hepatic metabolic, and neutrophil and T-cell inflammatory-immune responses have been shown to result from cell-signaling modulations and/or impairments in the respective cell types. Altered Ca(2+) signaling would seem to play an important role in the myocardial and vascular smooth muscle contractile dysfunction in the injury conditions; Ca(2+)-linked signaling derangement also plays a crucial role in sepsis-induced altered skeletal muscle protein catabolism and resistance to insulin-mediated glucose use. The injury-related increased hepatic gluconeogenesis and acute-phase protein response could also be caused by a pathophysiologic up-regulation of hepatocyte Ca(2+)-signal generation. The increased oxidant production by neutrophil, a potentially detrimental inflammatory response in early stages after burn or septic injuries, seems to result from an up-regulation of both the Ca(2+)-dependent as well as Ca(2+)-independent signaling pathways. The injury conditions would seem to cause an inappropriate up-regulation of Ca(2+)-signal generation in the skeletal myocyte, hepatocyte, and neutrophil, while they lead to a down-regulation of Ca(2+) signaling in T cells. The crucial signaling derangement that causes T-cell proliferation suppression seems to be a decrease in the activation of protein tyrosine kinases, which subsequently down-regulates Ca(2+) signaling. The delineation of cell-signaling derangements in trauma, burn, or sepsis conditions can lead to development of therapeutic interventions against the disturbed cellular responses in the vital organ systems.