Key points are not available for this paper at this time.
Background: Inflammatory bowel disease (IBD), encompassing ulcerative colitis (UC) and Crohn’s disease (CD), is characterized by chronic intestinal inflammation with fluctuating clinical severity. Although fecal calprotectin (FC) and fecal occult blood (FOBT) are established noninvasive biomarkers of intestinal inflammation, their interplay with nutritional status and disease activity has not been fully elucidated. This study aimed to explore the relationship between FC, FOBT, and disease activity in IBD, and to assess the potential mediating role of nutritional status as measured by the prognostic nutritional index (PNI). Methods: This retrospective study includes 128 adult patients with confirmed IBD (50 UC and 78 CD) examined at a tertiary care center between December 2023 and August 2025. Disease activity was assessed using the Mayo score for UC and the Harvey–Bradshaw Index for CD. FC levels were quantitatively measured using an enzyme-linked immunosorbent assay (ELISA), and fecal occult blood testing was performed with an automated latex agglutination-based system. Multivariable linear regression models were conducted to identify independent predictors of disease activity. Results: UC patients had significantly higher FC levels (278.0 vs. 133.5 µg/g, p < 0.001), FOBT positivity rates (76.7% vs. 43.6%, p = 0.002), and lower PNI (49.2 ± 4.2 vs. 51.5 ± 4.6, p = 0.048) compared to CD patients. In both UC and CD, disease activity scores were positively correlated with FC, FOBT positivity, CRP, and duration of illness, and negatively correlated with PNI (p < 0.05). In multivariable regression, PNI lost predictive value when FC and FOBT were included; FC and FOBT remained strong independent predictors of disease activity. Conclusions: FC and fecal occult blood are independently associated with higher disease activity in IBD, and may mediate the observed relationship between poor nutritional status and inflammation severity. The loss of significance of PNI in adjusted models suggests that intestinal inflammation and bleeding may act as intermediaries linking malnutrition to disease activity.
Bilgen et al. (Tue,) studied this question.