Stress hyperglycemia in acute pancreatitis: From mechanisms to prognostic implications

Abstract

Acute pancreatitis (AP) is an inflammatory reaction of the pancreas. When the disease is severe, it is often accompanied by destruction of the pancreatic islets, resulting in dysfunction of the endocrine system of the pancreas. Stress hyperglycemia is a transient increase in glucose during a critical illness, and its possible mechanism is related to abnormal glucose metabolism and insulin resistance due to the increased release of counterregulatory hormones and cytokines, such as glucagon, cortisol, and catecholamines. Numerous studies have shown that stress hyperglycemia is strongly associated with morbidity, mortality, and increased risk of post-acute pancreatitis diabetes in AP patients. Therefore, stress hyperglycemia may be a significant independent risk factor for poor clinical outcomes and prognosis in patients with AP. This article reviews the clinical features, risk factors, and mechanisms of action of stress hyperglycemia in AP and its influence on adverse clinical outcomes and the prognosis of inpatients with AP. For AP patients with stress hyperglycemia, it is necessary to comprehensively consider their blood glucose levels, daily habits, and complications to develop an appropriate treatment plan for hyperglycemia. Limited evidence indicates that in the case of acute hyperglycemia in critically ill patients, especially during the first 3 days of hospitalization, insulin therapy should not be undertaken if the blood glucose level does not exceed 10 mmol/L. However, some important questions related to clinical practice remain to be answered. More clinical trials and studies are needed in the future to provide a sufficient basis for clinical practice.