Abstract
Copeptin, an equimolar indicator of serum antidiuretic hormone levels, has been associated with higher mortality in critically ill patients and with the development of diabetes in the general population. The aim of the present study was to investigate the association of copeptin levels with glycemic parameters in critically ill patients and to compare the time-course of copeptin in survivors and non-survivors. Prospective cohort study. From June to October 2019, critically ill patients were prospectively enrolled and followed for 90 days. Plasma copeptin levels were determined at intensive care unit (ICU) admission (copeptin T1), 24 h (copeptin T2), and 48 h (copeptin T3) after study entry. Blood glucose and glycated hemoglobin levels were measured. ICU, in-hospital, and 90-day mortality, and length of stay in the ICU and hospital were evaluated. 104 patients were included. No significant correlation was detected between copeptin levels and blood glucose (r = -0.17, p = 0.09), HbA1c (r = 0.01, p = 0.9), glycemic gap (r = -0.16, p = 0.11), and stress hyperglycemia ratio (r = -0.14, p = 0.16). Copeptin T3 levels were significantly higher in survivors than in non-survivors at hospital discharge (561 [370-856] vs 300 [231-693] pg/mL, p = 0.015) and at 90 days (571 [380-884] vs 300 [232-698] pg/mL, p = 0.03). No significant correlations were found between copeptin levels and glycemic parameters, suggesting that copeptin is not a relevant factor in the induction of hyperglycemia during critical illness. Copeptin levels at ICU day 3 were higher in survivors than in non-survivors.
Highlights
Facing acute stress, the human body responds with a hypercatabolic state that reduces and redirects energy consumption, delays anabolism, and activates the immune response [1]
No significant correlation was detected between copeptin levels and blood glucose (r = -0.17, p = 0.09), HbA1c (r = 0.01, p = 0.9), glycemic gap (r = -0.16, p = 0.11), and stress hyperglycemia ratio (r = -0.14, p = 0.16)
No significant correlations were found between copeptin levels and glycemic parameters, suggesting that copeptin is not a relevant factor in the induction of hyperglycemia during critical illness
Summary
The human body responds with a hypercatabolic state that reduces and redirects energy consumption, delays anabolism, and activates the immune response [1]. The main metabolic response mechanism is the activation of the hypothalamic-pituitary-adrenal axis, and several studies have shown higher levels of stress hormones during an acute injury [2, 3]. Stress hormone hypersecretion is associated with worse outcomes in critically ill patients [4]. Arginine-vasopressin (AVP), known as antidiuretic hormone, is a hypothalamic hormone involved in stress response. It exerts a potentiating action on corticotropin-releasing hormone and, on adrenocorticotropic hormone (ACTH) release [5]. As a matter of fact, AVP is a marker for the endogenous stress levels of a patient and low levels of AVP have been correlated with longer hemodynamic dysfunction [7]
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