Abstract
Hyperglycemia is a common manifestation in the course of severe disease and is the result of acute metabolic and hormonal changes associated with various factors such as trauma, stress, surgery, or infection. Numerous studies demonstrate the association of adverse clinical events with stress hyperglycemia. This article briefly describes the pathophysiological mechanisms which lead to hyperglycemia under stressful circumstances particularly in the pediatric and adolescent population. The importance of prevention of hyperglycemia, especially for children, is emphasized and the existing models for the prediction of diabetes are presented. The available studies on the association between stress hyperglycemia and progress to type 1 diabetes mellitus are presented, implying a possible role for stress hyperglycemia as part of a broader prognostic model for the prediction and prevention of overt disease in susceptible patients.
Highlights
The term stress hyperglycemia (SH) refers to a transient increase in plasma glucose levels during acute illness or physical or psychological stress, which subsides when the stressful condition resolves [1]
Stress hormones decrease the translocation of glucose transporter protein 4 (GLUT-4) to the cell membrane, diminishing glucose cellular uptake, and a similar result is exerted by proinflammatory cytokines, mainly interleukin 1 (IL-1), interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α) [10, 11]
type 1 diabetes mellitus (T1DM) is a disease with a clear genetic origin, but genetic screening cannot be applied to the general population and, even more importantly, genetic susceptibility alone is not sufficient to predict whether a child will ever develop the overt disease
Summary
The term stress hyperglycemia (SH) refers to a transient increase in plasma glucose levels (usually above 150 mg/dl) during acute illness or physical or psychological stress, which subsides when the stressful condition resolves [1]. Stress hyperglycemia is considered a normal metabolic response to acute stress [4] It develops through complex pathophysiologic pathways, where counter-regulatory hormones such as cortisol, catecholamines, glucagon, and proinflammatory cytokines stimulate glycogenolysis and gluconeogenesis, leading to increased hepatic glucose output and peripheral insulin resistance. This condition was initially considered a protective homeostatic response, studies both in children and adults have associated stress hyperglycemia with adverse clinical outcomes and complications [1]. We discuss in brief the factors which are currently used for prediction of T1DM, and we present the main studies on the association of stress hyperglycemia with T1DM and its possible role as a predictive factor in children and adolescents
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