# Hemorheology in Inflammatory Bowel Disease: A Case–Control Study

## TL;DR

This study finds that inflammatory bowel disease patients have increased red blood cell aggregation, which may explain their higher risk of blood clots.

## Contribution

The study identifies erythrocyte aggregation as a prothrombotic alteration in IBD, primarily driven by fibrinogen rather than disease activity.

## Key findings

- IBD patients showed significantly higher erythrocyte aggregation index and threshold shear rate compared to controls.
- Fibrinogen was the strongest predictor of erythrocyte aggregation outcomes, not IBD activity markers.
- After adjusting for covariates, IBD no longer predicted erythrocyte aggregation differences.

## Abstract

Background: Venous thromboembolism is more prevalent among patients with inflammatory bowel disease (IBD). This study aimed to identify prothrombotic hemorheological alterations in IBD. Methods: We conducted a case–control study with patients with ulcerative colitis, Crohn’s disease, and non-IBD control subjects. We measured hemorheological indicators including plasma viscosity (PV), whole blood viscosity (WBV), erythrocyte aggregation (EA), and erythrocyte deformability (ED). Uni- and multivariate tests were employed for analysis. Results: A total of 53 IBD patients and 77 control subjects were recruited. IBD patients showed significantly higher aggregation index (68.8% (35.3–83.5%) vs. 66.9% (35.2–83.5%), p = 0.003) and threshold shear rate (120 1/s (55–325 1/s) vs. 110 1/s (55–325 1/s), p < 0.001), with lower aggregation half-time (1.6 s (0.6–7.1 s) vs. 1.8 s (0.6–7.1 s), p = 0.004), indicating enhanced EA. However, after adjusting for covariates, including inflammatory markers, IBD no longer predicted EA. There were no significant differences in EA. PV, WBV, and ED between the groups. Fibrinogen, rather than the Crohn’s Disease Activity Index, was the strongest predictor of the outcomes. Conclusions: Our study demonstrates that IBD patients exhibit enhanced EA, predicted mainly by fibrinogen. These results confirm that inflammation plays the cardinal role in the increased tendency for venous thromboembolism in IBD.