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Nutrition Support and Hyperglycemia
Published in Jeffrey I. Mechanick, Elise M. Brett, Nutritional Strategies for the Diabetic & Prediabetic Patient, 2006
Hyperglycemia in patients receiving nutrition support may be due to type-1 diabetes (T1DM), type-2 diabetes (T2DM), or stress hyperglycemia (SH). Stress hyperglycemia is defined as the presence of elevated glucose during an acute illness, in a patient without a prior diagnosis of diabetes, which normalizes after the illness. The majority of patients who receive nutrition support are hospitalized patients with acute illnesses in whom the need for nutrition support is temporary. A retrospective chart review of 1886 consecutive hospital admissions demonstrated hyperglycemia, defined as a fasting plasma glucose of > 126 mg/dL or random plasma glucose of > 200 mg/dL, in 38% of patients [1]. Of the patients that were hyperglycemic, 68% were known to have diabetes and 32% were hyperglycemic without a prior history of diabetes. In a study by Levetan et al. [2], 37.5% of medical and 33% of surgical admissions with hyperglycemia, defined as a glucose level > 200 mg/dL, did not have a prior diagnosis of diabetes. This latter group consists of patients with undiagnosed T2DM and SH. Compared with patients previously diagnosed with diabetes, patients with SH have a higher in-hospital mortality rate despite a lower average blood glucose level [1]. This suggests that new hyperglycemia in hospitalized patients may be an indicator of more severe stress.
Prognostic implications of stress hyperglycemia ratio in patients with myocardial infarction with nonobstructive coronary arteries
Published in Annals of Medicine, 2023
Side Gao, Sizhuang Huang, Xuze Lin, Li Xu, Mengyue Yu
Stress hyperglycemia emphasizes a relative acute increase of glycemia in response to stress reaction or critical illness [12]. It is commonly seen in AMI and has been reported as a powerful predictor of worse outcomes both in diabetic and nondiabetic patients with AMI [13–17]. Previous studies have revealed that stress hyperglycemia can activate the neuroendocrine system, release excessive catecholamine and cytokines, aggravate inflammatory response and oxidative stress, promote a prothrombotic state, induce endothelial dysfunction, and impair microcirculatory function [33–37]. In line with these pathophysiologic changes, patients with stress hyperglycemia tend to have larger infarct size, worse cardiac function, and a higher risk of plaque progression, heart failure, ventricular arrhythmia, and death after AMI [13–17]. Thus, it is critical to adequately evaluate stress hyperglycemia for early risk stratification and pre-emptive decision-making.
The effects of SIRT1/FoxO1 on LPS induced INS-1 cells dysfunction
Published in Stress, 2019
Xingxing Mo, Xiao Wang, Qinmin Ge, Fan Bian
Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection (Shankar-Hari et al., 2016). The key mechanism of sepsis is oxidative stress, which is characterized by redundant reactive oxygen species (ROS) without scavenging in time (Mantzarlis, Tsolaki, & Zakynthinos, 2017). Oxidative stress could result in hyperglycemia by stimulating a large number of inflammatory cytokines secretion from pancreatic β cells, which further aggravates islet dysfunction and insulin resistance (Tao et al., 2017). It was recently reported that stress hyperglycemia contributed to mortality increase in septic patients (Nugent, Edriss, & Selvan, 2016). However, the molecular mechanisms between sepsis and stress hyperglycemia have not been fully understood.
Glucose intolerance in intensive care patients: Incidence and outcome
Published in Egyptian Journal of Anaesthesia, 2021
Ahmed A. El Shebiny, Gamal M. Elewa, Ez Alregal G. Gouda, Reham Mustafa Hashim
Glucose intolerance frequently occurs in the critically ill, in both diabetics, and those who were previously glucose-tolerant. The term “stress hyperglycemia” reflects the pathogenesis of the latter group [4]. Stress hyperglycemia is defined as an increase in blood glucose above 200 mg/dl in presence of acute illness, without previously diagnosed diabetes [3].