Cardiovasc Diabetol. 2025 May 2;24(1):188. doi: 10.1186/s12933-025-02751-3.
ABSTRACT
Stress-induced hyperglycemia (SIH) is a physiological response to acute or chronic stress characterized by elevated blood glucose levels. It is prevalent in both patients with and without diabetes, particularly those with acute or critical illnesses. The development of SIH is characterized by complex interactions among catecholamines, cortisol, and inflammatory mediators such as cytokines, resulting in increased hepatic glucose production and insulin resistance. While mild to moderate SIH may provide a protective mechanism during stress, prolonged or excessive hyperglycemia can exacerbate inflammation and oxidative stress, contributing to adverse outcomes in conditions such as acute myocardial infarction, heart failure, and cerebrovascular diseases. The stress-hyperglycemia ratio (SHR), defined as the ratio of admission glucose to estimated mean glucose (derived from glycated hemoglobin [HbA1c]), has emerged as a valuable tool for quantifying stress hyperglycemia. Unlike absolute glucose levels, the SHR accounts for background hyperglycemia and provides a more accurate indicator of the relative glucose elevation associated with critical illness. Extensive research has demonstrated a U-shaped or J-shaped relationship of the SHR with disease outcomes, indicating that both low and high SHRs are associated with increased mortality and morbidity. The SHR has shown significant predictive value in cardiovascular diseases (e.g., acute coronary syndrome, heart failure), cerebrovascular diseases (e.g., acute ischemic stroke, intracerebral hemorrhage), and infectious diseases (e.g., sepsis, pneumonia). It also plays a role in other conditions, such as acute pancreatitis and certain cancers. The ease of calculating the SHR from widely available admission glucose and HbA1c tests makes it a practical and valuable prognostic marker in clinical settings. This review examines the relationship between the SHR and critical illnesses, highlighting its mechanisms and predictive value across various diseases.
PMID:40317019 | PMC:PMC12049067 | DOI:10.1186/s12933-025-02751-3