Percorrer por autor "Dias, S."
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- P0397 Soluble transferrin receptor as a reliable inflammation-independent marker of iron deficiency in crohn’s disease and ulcerative colitisPublication . Portela, F.; Santos, M. P. Ministro dos; Sousa, Helena Tavares; Roseira, Joana; Fernandes, S. R.; Crespo, R.; Domingues, B.; Santiago, M.; Miranda, R.; Dias, S.; Dias, C. C.; Magro, F.Background: Iron deficiency is a common complication in inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn’s disease (CD).1 However, standard iron markers are influenced by inflammation, complicating the diagnosis of true iron deficiency.1,2 Soluble transferrin receptor (sTfR) has been proposed as a more reliable, inflammation-independent marker of iron demand.3 This study aimed to assess the utility of sTfR in identifying iron deficiency without anaemia (IDWA). Methods: The ID_IBD study was a multicentre, cross-sectional study. Iron status was classified using two approaches: the ECCO consensus definition, focusing on ferritin thresholds adjusted for inflammatory markers (C-reactive protein [CRP] and faecal calprotectin [FCAL]), and a stricter definition that adds transferrin saturation to the ECCO criteria. sTfR levels were compared across groups, and ROC curve analysis was used to identify optimal diagnostic cut-offs. Results: This analysis included 411 IBD patients (130 UC, 281CD) and 178 controls. sTfR showed no correlation with CRP or FCAL. In UC, patients with IDWA had significantly higher sTfR levels (median 1.20mg/L, IQR 1.02-1.42) compared to non-IDWA patients (median 1.05mg/L, IQR 0.92-1.22; p=0.013). Anaemic UC patients also showed elevated sTfR levels (median 1.27mg/L, IQR 1.14-1.59) compared to non-IDWA individuals (patients but was significantly higher in anaemic patients (p=0.003). Conclusion: sTfR appears to be an inflammation-independent marker of iron status in IBD. It showed potential for identifying IDWA in UC, while in CD it mainly reflected increased iron demand in anaemia. Further longitudinal studies are warranted to validate its role and assess its clinical utility in IBD.
- P0463 Distinct hepcidin dynamics in crohn’s disease and ulcerative colitis: links to iron homeostasis and inflammatory activityPublication . Magro, F.; Santos, M. P. Ministro dos; Sousa, Helena Tavares; Roseira, Joana; Fernandes, S. R.; Crespo, R.; Dias, S.; Beatriz, D.; Dias, C. C.; Miranda, R.; Santiago, M.; Portela, F.Background: Hepcidin, the master regulator of systemic iron metabolism, is influenced by iron availability and inflammation.1 In inflammatory bowel disease (IBD), iron deficiency and anaemia are common, yet how hepcidin is regulated in relation to disease phenotype, iron status and inflammatory burden remains incompletely understood.2 We aimed to characterise hepcidin regulation in ulcerative colitis (UC) and Crohn’s disease (CD) according to iron status and inflammatory markers. Methods: In this cross-sectional multicentre study, 589 individuals were enrolled (178 healthy controls, 130 UC, 281CD). Patients were stratified by iron status and activity. Serum hepcidin, iron parameters, and inflammatory and clinical data were collected. Iron deficiency was defined using the ECCO criteria2 , which focuses on ferritin, and a combined ferritin and transferrin saturation definition. Group comparisons, correlations, and multivariable linear regressions were performed. Results: Hepcidin correlated positively with C-reactive protein (CRP) in CD (r=0.125; p=0.038) and negatively with faecal calprotectin (FCAL) in UC (r=-0.311; p.
- Serum neutrophil biomarkers to predict crohn's disease progression and infliximab treatment outcomesPublication . Magalhaes, D.; Santiago, M.; Patita, M.; Arroja, B.; Lago, P.; Rosa, I.; Sousa, Helena Tavares; Ministro, P.; Mocanu, I.; Vieira, A.; Castela, J.; Moleiro, J.; Roseira, J.; Eugenia, C.; Sousa, P.; Portela, F.; Correia, L.; Dias, S.; Afonso, J.; Danese, S.; Peyrin‐Biroulet, L.; Dias, C. C.; Magro, F.Background and aims: Predicting the treatment outcomes of biological therapies is an unmet need in Crohn's Disease. In this study, we explored the potential of serum neutrophil-related biomarkers to predict infliximab therapeutic results and disease progression in Crohn's Disease patients, over a 2-year period, in a real-world setting. Methods: The study included 100 asymptomatic Crohn's Disease patients in the IFX maintenance phase from the prospective, observational, multicenter DIRECT study. Patients were categorized according to a composite outcome reflecting progression that included surgery, hospitalizations, new fistulae, abscess or stricture, and drug treatment escalation. Serum neutrophil elastase, lipocalin-2, lactoferrin, and resistin (non-neutrophil control) were analyzed via multiplex magnetic bead assays at multiple touchpoints. Fecal calprotectin was assessed by ELISA. Results: Over up to 2 years of follow-up, serum biomarkers did not differentiate between the composite outcome groups, whereas fecal calprotectin was significantly higher in patients with worse outcomes. During the infliximab maintenance phase, there was a significant, sustained reduction of neutrophil elastase (p < 0.001), lipocalin-2 (p < 0.001), and lactoferrin (p < 0.001), but not of resistin, despite stable neutrophil levels. Correlations between NE and NGAL levels were strong (Pearson correlations 0.75-0.85); all other correlations were of small magnitude. Conclusion: Our real-world data do not support using serum neutrophil elastase, lipocalin-2, or lactoferrin concentrations as predictors of treatment outcomes or disease evolution in infliximab -treated Crohn's Disease patients. On the other hand, the sustained decrease in biomarkers over time suggests that neutrophil stabilization might be an additional infliximab mechanism of action.