Stress Hyperglycemia Is Independently Associated with Persistent Organ Failure in Acute Pancreatitis

Abstract

Background/Aims Stress hyperglycemia is common in critical illness but it has not been clearly studied in patients with acute pancreatitis (AP). This study aimed to investigate the specific blood glucose (BG) level that defines stress hyperglycemia and to determine the impact of stress hyperglycemia on clinical outcomes in AP patients. Methods AP patients admitted ≤ 48 h after abdominal pain onset were retrospectively analyzed. Patients were stratified by pre-existing diabetes and stress hyperglycemia was defined using stratified BG levels for non-diabetes and diabetes with clinical outcomes compared. Results There were 967 non-diabetic and 114 diabetic (10.5%) patients met the inclusion criteria and the clinical outcomes between these two groups were not significantly different. In non-diabetes, the cut-off BG level of ≥ 180 mg/dl was selected to define stress hyperglycemia with an 8.8-fold higher odds ratio for persistent organ failure (POF) (95% CI 5.4-14.3; P < 0.001). For diabetes, ≥ 300 mg/dl was selected with a 7.5-fold higher odds ratio for POF (95% CI 1.7-34.3; P = 0.009). In multivariable logistic regression, stress hyperglycemia was independently associated with POF, acute necrotic collection, major infection and mortality. The combination of BG and systemic inflammatory response syndrome (SIRS) score in predicting POF was better than SIRS or Glasgow score alone. Conclusions This study identifies a cut-off BG level of ≥ 180 mg/dl and ≥ 300 mg/dl was optimal to define stress hyperglycemia for non-diabetic and diabetic AP patients, respectively. There was a significant relationship between stress hyperglycemia and adverse clinical outcomes.

Ketogenesis acts as an endogenous protective programme to restrain inflammatory macrophage activation during acute pancreatitis

“…Of note, our proof-of-concept therapeutic potential for βOHB would not apply to AP patients who have pre-existing diabetes. 67 Moreover, when considering a boosting ketogenesis strategy for AP, we need to rule out the possibility of using a ketone diet (high fat and low carbohydrates) for patients who have existing metabolic syndrome at baseline.…”

Acute Pancreatitis: Diagnosis and Treatment

“…Initial investigations for suspected acute pancreatitis include serum amylase and/or lipase, triglycerides and lipid panel, full blood count, renal and liver function tests, glucose, HbA1c, calcium and TUS (Fig. 3) [157]. Chest x-ray or ultrasound should be done to identify pleural effusion, an indicator of more severe disease; this is also important in the assessment of patients with an acute abdomen.…”

Inhibition of Notch activity suppresses hyperglycemia-augmented polarization of macrophages to the M1 phenotype and alleviates acute pancreatitis

“…Although studies have assessed the impact of diabetes on the progression of AP, the role of hyperglycemia in AP patients remains poorly understood. In clinical practice, hyperglycemia is observed in most patients with AP, potentially resulting from an acute stress response that activates the neuroendocrine system and causes the release of glucagon [ 30 , 31 ]. In addition, AP-induced β-cell injury reduces insulin secretion [ 32 ], and the complex interplay between multiple hormones and cytokines causes insulin resistance, which further aggravates hyperglycemia [ 31 ].…”