Intestinal fatty acid binding protein is a disease biomarker in paediatric coeliac disease and Crohn’s disease

BMC Gastroenterology

Umer Zeeshan Ijaz¹  Paraic McGrogan²  Richard Hansen²  Mwansa Jere²  Richard K. Russell³  Clare Martha Clark⁴  Konstantinos Gerasimidis⁴  Michael Logan⁴  Aikaterini Kountouri⁴  Mary MacKinder⁴ 

[1] Civil Engineering, School of Engineering, University of Glasgow;Department of Paediatric Gastroenterology, Royal Hospital for Children;Department of Paediatric Gastroenterology, Royal Hospital for Sick Children;Human Nutrition, School of Medicine, Dentistry and Nursing, College of Medical, Veterinary and Life Sciences, University of Glasgow;

关键词: Crohn’s disease;    Ulcerative colitis;    Inflammatory bowel disease;    Coeliac disease;    Biomarkers;    Paediatric;   

DOI  :  10.1186/s12876-022-02334-6

来源: DOAJ

【 摘 要 】

Abstract Background There is a clinical need to develop biomarkers of small bowel damage in coeliac disease and Crohn’s disease. This study evaluated intestinal fatty acid binding protein (iFABP), a potential biomarker of small bowel damage, in children with coeliac disease and Crohn’s disease. Methods The concentration iFABP was measured in plasma and urine of children with ulcerative colitis, coeliac disease, and Crohn’s disease at diagnosis and from the latter two groups after treatment with gluten free diet (GFD) or exclusive enteral nutrition (EEN), respectively. Healthy children (Controls) were also recruited. Results 138 children were recruited. Plasma but not urinary iFABP was higher in patients with newly diagnosed coeliac disease than Controls (median [Q1, Q3] coeliac disease: 2104 pg/mL 1493, 2457] vs Controls: 938 pg/mL [616, 1140], p = 0.001). Plasma or urinary iFABP did not differ between patients with coeliac on GFD and Controls. Baseline iFABP in plasma decreased by 6 months on GFD (6mo GFD: 1238 pg/mL [952, 1618], p = 0.045). By 12 months this effect was lost, at which point 25% of patients with coeliac disease had detectable gluten in faeces, whilst tissue transglutaminase IgA antibodies (TGA) continued to decrease. At diagnosis, patients with Crohn’s disease had higher plasma iFABP levels than Controls (EEN Start: 1339 pg/mL [895, 1969] vs Controls: 938 pg/mL [616, 1140], p = 0.008). iFABP did not differ according to Crohn’s disease phenotype. Induction treatment with EEN tended to decrease (p = 0.072) iFABP in plasma which was no longer different to Controls (EEN End: 1114 pg/mL [689, 1400] vs Controls: 938 pg/mL [616, 1140], p = 0.164). Plasma or urinary iFABP did not differ in patients with ulcerative colitis from Controls (plasma iFABP, ulcerative colitis: 1309 pg/mL [1005, 1458] vs Controls: 938 pg/mL [616, 1140], p = 0.301; urinary iFABP ulcerative colitis: 38 pg/mg [29, 81] vs Controls: 53 pg/mg [27, 109], p = 0.605). Conclusions Plasma, but not urinary iFABP is a candidate biomarker with better fidelity in monitoring compliance during GFD than TGA. The role of plasma iFABP in Crohn’s disease is promising but warrants further investigation. Trial registration: Clinical Trials.gov, NCT02341248. Registered on 19/01/2015.

【 授权许可】

Unknown