Association between route of nutrition and serum I-FABP and MMP-9 levels in critically ill patients with acute ischemic stroke: a prospective cohort study.

BACKGROUND

Gut barrier dysfunction and neuroinflammation are increasingly recognised as linked pathophysiological processes in acute ischaemic stroke (AIS). However, the influence of nutritional routes on these processes remains poorly characterised.

OBJECTIVE

To compare the longitudinal effects of enteral nutrition (EN) versus parenteral nutrition (PN) on serum intestinal fatty acid-binding protein (I-FABP), a marker of intestinal epithelial integrity, and matrix metalloproteinase-9 (MMP-9), a marker of neuroinflammatory activity, in critically ill AIS patients.

DESIGN

Prospective observational cohort study.

SETTING

A tertiary neurology intensive care unit (ICU) in Türkiye.

PATIENTS AND

METHODS

Consecutive adults (≥18 years) admitted to the neurology ICU within 24 hours of a confirmed AIS diagnosis were enrolled between October 2024 and January 2026. Nutritional route was assigned by the treating clinician according to ESPEN guidelines. Serum I-FABP and MMP-9 concentrations were measured using commercial enzyme-linked immunosorbent assay (ELISA) kits at baseline and on day 7.

MAIN OUTCOME MEASURES: Longitudinal changes in serum I-FABP and MMP-9 concentrations between baseline and day 7, and their correlations with neurological severity (NIHSS).

SAMPLE SIZE: 73 patients (40 EN, 33 PN).

RESULTS

Median age was 73 years (interquartile range, 64-80) and 37 (51%) were female. At baseline, I-FABP and MMP-9 levels were comparable between groups (all P>.05). Over the 7-day observation period, I-FABP trajectories diverged between groups (EN: 7.22 (2.68) to 6.69 (2.78) ng/mL; PN: 6.74 (3.09) to 7.82 (2.97) ng/mL), as did MMP-9 trajectories (EN: 11.5 (1.45) to 10.9 (2.31) ng/mL; PN: 11.3 (2.41) to 11.8 (1.87) ng/mL). At day 7, both biomarkers correlated significantly with NIHSS score (ρ=0.385 and ρ=0.440, respectively; both P<.001). Repeated measures analysis of covariance, adjusted for baseline NIHSS score, confirmed significant time × nutritional route interactions for both biomarkers (I-FABP: F[1,70]=4.22, P=0.044, P_FDR=.044, η2p=.057; MMP-9: F[1,70]= 4.76, P=.033, P_FDR=.044, η2p=0.064).

CONCLUSION

In critically ill AIS patients, EN was associated with more favourable 7-day trajectories of gut barrier integrity and neuroinflammatory activity compared with PN, after adjustment for baseline stroke severity.

LIMITATIONS: Single-center design, biomarker sampling restricted to two time points, reliance on delivered rather than utilised nutritional measures, and non-randomised nutritional route assignment with residual potential for confounding by indication.