Current Evidence on the Use of Biomarkers for the Diagnosis of Acute Mesenteric Ischemia: A Narrative Review.

Acute mesenteric ischemia (AMI) is a life-threatening vascular emergency associated with high morbidity and mortality, largely because diagnosis is frequently delayed by non-specific clinical manifestations. Although computed tomography angiography (CTA) remains the diagnostic gold standard, considerable research has focused on identifying laboratory biomarkers that may facilitate earlier recognition and improve clinical decision-making. This narrative review summarizes the current evidence regarding routinely available and emerging laboratory biomarkers for the diagnosis of AMI. A comprehensive literature search was performed using PubMed/Medical Literature Analysis and Retrieval System Online (MEDLINE), Scopus, Web of Science, and the Cochrane Library, supplemented by manual review of reference lists. Routine laboratory markers, including leukocyte count, C-reactive protein (CRP), serum lactate, metabolic acidosis, D-dimer, amylase, phosphate, and procalcitonin (PCT), were evaluated alongside investigational biomarkers, such as intestinal fatty acid-binding protein (I-FABP), D-lactate, citrulline, ischemia-modified albumin (IMA), alpha-glutathione S-transferase (α-GST), interleukin-6 (IL-6), and cell-count-derived inflammatory indices. Current evidence demonstrates that no single laboratory biomarker possesses sufficient sensitivity and specificity to independently confirm or exclude AMI. Serum lactate and metabolic acidosis primarily reflect advanced intestinal injury and systemic hypoperfusion, rather than early ischemia, whereas D-dimer offers relatively high sensitivity but poor specificity. Enterocyte-specific biomarkers, particularly I-FABP, remain biologically attractive because they may detect early mucosal injury; however, inconsistent diagnostic performance, limited assay availability, and methodological heterogeneity have prevented routine clinical implementation. Emerging multimarker strategies integrating indicators of enterocyte injury, coagulation activation, inflammation, and tissue hypoperfusion may improve diagnostic accuracy but require prospective validation. At present, laboratory investigations should be regarded as complementary tools that increase clinical suspicion, assist with risk stratification, and reinforce the need for urgent CTA. They should never delay definitive imaging or revascularization when AMI is suspected. Further high-quality prospective studies are required to establish standardized biomarker panels capable of facilitating earlier diagnosis and improving patient outcomes.