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Updated: Jun 11, 2026
Murine Model of Intestinal Ischemia-reperfusion Injury
Published on: May 11, 2016
Serum markers and intestinal mucosal injury in chronic gastrointestinal ischemia
Désirée van Noord1, Peter B F Mensink, Robert J de Knegt
1Department of Gastroenterology and Hepatology, Erasmus MC-University Medical Center, Rotterdam, The Netherlands. d.vannoord@erasmusmc.nl
Insights
Diagnosing chronic gastrointestinal ischemia (CGI) is difficult. Postprandial increases in L-lactate and D-dimer serum levels show promise as non-invasive indicators for CGI diagnosis.
Area of Science:
- Gastroenterology
- Vascular Medicine
- Diagnostic Biomarkers
Background:
- Chronic gastrointestinal ischemia (CGI) diagnosis presents clinical challenges.
- Non-invasive serum markers are needed for accurate CGI detection.
Purpose of the Study:
- Investigate serum markers for diagnosing well-defined ischemia.
- Evaluate intestinal mucosal injury in CGI patients.
Main Methods:
- Prospective enrollment of patients suspected of CGI.
- Diagnostic work-up included tonometry, CT/MR angiography.
- Serum analysis for I-FABP, D-dimer, LDH, CRP, L-lactate, glutamine, citrulline, arginine pre- and post-meal.
- Intestinal mucosal injury assessed via amino acid levels and sugar absorption test (SAT).
Main Results:
- 32 of 40 patients diagnosed with ischemia.
- No significant differences in I-FABP, LDH, CRP, or leucocyte counts between ischemic and non-ischemic groups.
- Elevated L-lactate levels observed in ischemia patients.
- Postprandial D-dimer elevation noted in ischemia patients, without evidence of mucosal injury.
Conclusions:
- I-FABP, LDH, CRP, and leucocyte counts are not reliable diagnostic markers for CGI.
- Postprandial elevations in L-lactate and D-dimer show potential as non-invasive indicators for CGI.
Background:
Diagnosing chronic gastrointestinal ischemia (CGI) is a challenging problem in clinical practice. Serum markers for CGI would be of great diagnostic value as a non-invasive test method.
Aims:
This study investigated serum markers in patients with well-defined ischemia. Furthermore, intestinal mucosal injury was also evaluated in CGI patients.
Methods:
Consecutive patients suspected of CGI were prospectively enrolled and underwent a diagnostic work-up consisting of gastrointestinal tonometry and either CT or MR angiography. Blood samples for analysis of intestinal fatty acid-binding protein (I-FABP), D-dimer, lactate dehydrogenase (LDH), leucocyte counts, C-reactive protein (CRP), and L-lactate were drawn before and after a standard meal. Intestinal mucosal injury was assessed with glutamine, citrulline and arginine in blood samples and compared to a sugar absorption test (SAT). Test reproducibility was validated in healthy subjects.
Results:
Forty patients and nine healthy subjects were included. Ischemia was diagnosed in 32 patients (80%). I-FABP, leucocyte counts, LDH, CRP, glutamine, citrulline, arginine and SAT levels did not differ between patients with and without ischemia. L-lactate concentration showed a significant elevation in ischemia patients as compared to non-ischemia patients. In ischemia patients, D-dimer levels showed a significant elevation postprandially as compared to D-dimer levels at baseline. However, these ischemia patients did not show intestinal mucosal injury.
Conclusions:
I-FABP, leucocyte counts, LDH and CRP levels are not clinically useful for the diagnosis of CGI. However, postprandial rises in L-lactate and D-dimer serum levels can serve as non-invasive indicators of CGI.
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