Background: Acute infectious gastroenteritis (GE) and inflammatory bowel disease (IBD) may have similar clinical characteristics at onset, and discrimination between these two diagnoses can initially be challenging. Aim: To explore faecal biomarkers reflecting neutrophil, eosinophil, and epithelial activity to distinguish between acute GE and IBD onset. Methods: Faecal samples were collected from patients presenting with acute GE (n = 28), treatment-naïve patients with newly diagnosed IBD (n = 40), and healthy controls, HC (n = 40). Faecal biomarkers, including faecal calprotectin (FC), myeloperoxidase (MPO), human neutrophil lipocalin (HNL), eosinophil cationic protein (ECP), and eosinophil-derived neurotoxin (EDN), were assessed by ELISA. The Kruskal–Wallis test was used for biomarker comparisons. To evaluate the discriminative capability of biomarkers, receiver operating characteristic (ROC) curves were established. Result: Patients with acute GE displayed elevated levels of all the tested biomarkers compared with HC (p < 0.001). Higher levels of faecal HNL (p < 0.001), EDN (p < 0.01), and MPO (p < 0.05) were seen in acute GE patients than in patients with newly diagnosed IBD. HNL yielded the highest discriminative capability between acute GE and IBD with AUC 0.74, 95%CI: 0.62–0.84. Conclusions: This exploratory study suggests that faecal biomarkers may provide complementary information in the differentiation of patients with suspected acute GE and new-onset IBD. Our findings indicate that faecal HNL may have the ability to distinguish between these conditions. However, given the exploratory design and limited sample size, findings should be interpreted with caution, and the discriminative value of HNL and the other biomarkers requires further validation in larger, well-characterised acute GE cohorts.
M. Lundström, Christer G. B. Peterson, David Amcoff et al.· Biomedicines· 0 citations
BACKGROUND
/Aims: Few studies have explored how family history of colorectal cancer (CRC) affects CRC incidence in inflammatory bowel disease (IBD). We estimated CRC incidence rates (IRs) and IR differences, by family history of CRC, and the interaction between IBD and family history.
METHODS
Nationwide, register-based cohort study 1996-2023, including patients with IBD and matched (age, sex, parish, year) comparators from the general population. The exposure was family history, defined as the number of first-degree relatives (parent, sibling, or child) and their age at CRC diagnosis (<50 or ≥50 years).
RESULTS
During a median follow-up of 11 years, 1,882 CRC events occurred in 124,387 patients with IBD (IR 1.17[95%CI:1.12-1.23]/1,000 person-years) and 14,177 CRC events in 1,213,641 comparators (IR 0.88[95%CI:0.86-0.89]/1,000 person-years). In IBD, the greatest CRC risk increase was seen in those with ≥2 affected relatives: 2.69(95%CI:0.60-4.78) additional cases per 1,000 person-years versus no family history, while risk increase with early-onset CRC heredity was modest: 0.42(95%CI: -0.47-1.31)/1,000 person-years. The IRs were comparable between patients and matched comparators with the same family history, except among those without family history of CRC, where the CRC incidence was higher in IBD. The relative effect of family history was weaker in IBD, where the baseline CRC risk was already elevated.
CONCLUSION
On the absolute scale, family history of CRC increased CRC incidence similarly in IBD and matched comparators, with the greatest increase in individuals with multiple affected relatives. Guidelines advise special attention to patients with family history of early-onset CRC; our findings raise the question if surveillance strategies should instead prioritize patients with multiple affected relatives.
Å. H. Everhov, Kári Kristjánsson, J. Ludvigsson et al.· Gastroenterology· 0 citations
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