Glucose Levels in Acute Pancreatitis and the Impact of Insulin Depletion and Bacterial Endotoxaemia

There are currently no early predictive biomarkers for severity of acute pancreatitis (AP) that would allow stratification of patients for potential early interventional therapies. Hyperglycaemia is frequently observed to accompany and contribute to severe AP. However, the underlying mechanism is multifactorial, including in the acute phase of injury, where elevated adrenaline, cortisol and glucagon and inflammatory cytokine-induced insulin resistance all contribute to hyperglycaemia. The investigators propose that the extent of collateral injury of pancreatic β-cells and consequent loss of insulin secretion during the course of acute pancreatitis (AP) underlies disease severity. The investigators will measure plasma C-peptide (as a reliable readout of endogenous insulin), with moment-to-moment glucose monitoring (using subcutaneous continuous glucose monitoring devices), and bacterial endotoxin (lipopolysaccharide (LPS) in a prospective cohort of 30 severe AP patient blood samples taken every 5 days for up to 5 weeks of hospitalization.

NCT Number	NCT06972238
Lead Sponsor	Manchester University NHS Foundation Trust
Conditions	Pancreatitis, Acute, Hyperglycaemia
Enrollment	30 participants
Start Date	2025-12-01
Primary Completion	2026-06-30 (estimated)
Study Completion	2026-08-30 (estimated)
Updated on ClinicalTrials.gov	2025-05-21