Biomarkers for Monitoring of Changes in Disease Activity in Ulcerative Colitis.
LRG (leucine-rich alpha-2-glycoprotein)
anti-TNF antibody therapy
biomarkers
fecal calprotectin
ulcerative colitis
Journal
Journal of clinical medicine
ISSN: 2077-0383
Titre abrégé: J Clin Med
Pays: Switzerland
ID NLM: 101606588
Informations de publication
Date de publication:
18 Nov 2023
18 Nov 2023
Historique:
received:
29
09
2023
revised:
01
11
2023
accepted:
07
11
2023
medline:
25
11
2023
pubmed:
25
11
2023
entrez:
25
11
2023
Statut:
epublish
Résumé
In recent years, various biomarkers of ulcerative colitis (UC) have emerged; however, few studies have simultaneously examined the utility of multiple biomarkers for monitoring disease activity. Additionally, serum leucine-rich alpha-2 glycoprotein (LRG), a new biomarker, may show a blunt response to anti-TNF antibody therapy. This prospective study explored effective biomarkers that could monitor disease activity changes in patients with UC. In addition, we examined the effect of anti-TNF antibody therapy on changes in LRG. Blood and stool samples were collected twice from patients with UC: at baseline and at least 8 weeks later. Changes in serum LRG, interleukin (IL)-6, prealbumin (pre-Alb), high-sensitivity C-reactive protein (hs-CRP), CRP, and fecal calprotectin (FC) were measured and correlated with changes in disease activity. The relationship between anti-TNF antibody therapy and LRG levels was also examined in patients with the same disease activity. Forty-eight patients with UC (96 samples) were analyzed. ΔLRG and ΔIL-6 correlated strongly with the change in the partial Mayo (pMayo) score between the two time points (ΔpMayo) (r = 0.686, 0.635, respectively). In contrast, FC and IL-6 were particularly accurate predictors of clinical remission, and their area under the curves (AUCs) were significantly higher than that of CRP (AUC: 0.81, 0.76 vs. 0.50; Correlations were found between changes in UC disease activity and LRG, IL-6, pre-Alb, hs-CRP, CRP, and FC. LRG reflects disease activity during anti-TNF antibody therapy.
Sections du résumé
BACKGROUND
BACKGROUND
In recent years, various biomarkers of ulcerative colitis (UC) have emerged; however, few studies have simultaneously examined the utility of multiple biomarkers for monitoring disease activity. Additionally, serum leucine-rich alpha-2 glycoprotein (LRG), a new biomarker, may show a blunt response to anti-TNF antibody therapy. This prospective study explored effective biomarkers that could monitor disease activity changes in patients with UC. In addition, we examined the effect of anti-TNF antibody therapy on changes in LRG.
METHODS
METHODS
Blood and stool samples were collected twice from patients with UC: at baseline and at least 8 weeks later. Changes in serum LRG, interleukin (IL)-6, prealbumin (pre-Alb), high-sensitivity C-reactive protein (hs-CRP), CRP, and fecal calprotectin (FC) were measured and correlated with changes in disease activity. The relationship between anti-TNF antibody therapy and LRG levels was also examined in patients with the same disease activity.
RESULTS
RESULTS
Forty-eight patients with UC (96 samples) were analyzed. ΔLRG and ΔIL-6 correlated strongly with the change in the partial Mayo (pMayo) score between the two time points (ΔpMayo) (r = 0.686, 0.635, respectively). In contrast, FC and IL-6 were particularly accurate predictors of clinical remission, and their area under the curves (AUCs) were significantly higher than that of CRP (AUC: 0.81, 0.76 vs. 0.50;
CONCLUSIONS
CONCLUSIONS
Correlations were found between changes in UC disease activity and LRG, IL-6, pre-Alb, hs-CRP, CRP, and FC. LRG reflects disease activity during anti-TNF antibody therapy.
Identifiants
pubmed: 38002777
pii: jcm12227165
doi: 10.3390/jcm12227165
pmc: PMC10672609
pii:
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : The Osaka Medical Research Foundation for Intractable Diseases
ID : 26-2-35
Références
Cell Biochem Biophys. 2022 Dec;80(4):595-608
pubmed: 35997934
Clin Gastroenterol Hepatol. 2016 Jun;14(6):818-824.e6
pubmed: 26844874
World J Gastroenterol. 2015 Oct 28;21(40):11246-59
pubmed: 26523100
J Cell Biol. 1986 Sep;103(3):787-93
pubmed: 3017995
Am J Gastroenterol. 2015 Jun;110(6):802-19; quiz 820
pubmed: 25964225
Inflamm Bowel Dis. 2012 Dec;18(12):2218-24
pubmed: 22344983
Gut. 1979 Jan;20(1):22-7
pubmed: 761832
PLoS One. 2020 May 29;15(5):e0233811
pubmed: 32470973
Clin Gastroenterol Hepatol. 2008 Nov;6(11):1218-24
pubmed: 18799360
J Gastroenterol. 2021 Jun;56(6):560-569
pubmed: 33942166
J Leukoc Biol. 2002 Sep;72(3):478-85
pubmed: 12223515
Postepy Hig Med Dosw (Online). 2016 Nov 7;70(0):1124-1130
pubmed: 27892896
Inflamm Bowel Dis. 2008 Dec;14(12):1660-6
pubmed: 18623174
Clin Gastroenterol Hepatol. 2010 Jul;8(7):591-9.e1; quiz e78-9
pubmed: 20139033
J Thorac Dis. 2022 May;14(5):1332-1341
pubmed: 35693615
World J Gastroenterol. 2012 Dec 14;18(46):6782-9
pubmed: 23239916
Semin Immunol. 2014 Feb;26(1):2-12
pubmed: 24325804
Scand J Gastroenterol. 1975;10(5):537-44
pubmed: 1153950
Biomolecules. 2021 Oct 05;11(10):
pubmed: 34680097
Inflamm Bowel Dis. 2012 Nov;18(11):2169-79
pubmed: 22374925
Scand J Gastroenterol. 2010 Mar;45(3):325-31
pubmed: 20034360
Inflamm Bowel Dis. 2008 May;14(5):669-73
pubmed: 18240279
Scand J Gastroenterol. 2006 Jun;41(6):720-5
pubmed: 16716972
Inflamm Bowel Dis. 2011 Jan;17(1):118-26
pubmed: 20848538
Proc Natl Acad Sci U S A. 1985 Apr;82(7):1906-10
pubmed: 3856868
Annu Rev Biophys. 2013;42:443-68
pubmed: 23495970
Digestion. 2006;73(4):205-9
pubmed: 16837810
Gastroenterology. 2022 Apr;162(5):1456-1475.e1
pubmed: 35101422
Gut. 2006 Mar;55(3):426-31
pubmed: 16474109
Biochem Biophys Res Commun. 2009 May 15;382(4):776-9
pubmed: 19324010