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

NCT06972238 · Status: NOT_YET_RECRUITING · Type: OBSERVATIONAL · Enrollment: 30

Last updated 2025-05-21

No results posted yet for this study

Summary

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.

Conditions

  • Pancreatitis, Acute
  • Hyperglycaemia

Sponsors & Collaborators

  • Manchester University NHS Foundation Trust

    lead OTHER_GOV

Principal Investigators

  • Hood M Thabit · Manchester Royal Infirmary

Eligibility

Min Age
18 Years
Sex
ALL
Healthy Volunteers
No

Timeline & Regulatory

Start
2025-12-01
Primary Completion
2026-06-30
Completion
2026-08-30

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Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT06972238 on ClinicalTrials.gov