Factors Associated with Response to Systemic Corticosteroids in Active Ulcerative Colitis: Results from a Prospective, Multicenter Trial.
inflammatory bowel disease
systemic corticosteroids
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:
24 Jul 2023
24 Jul 2023
Historique:
received:
16
06
2023
revised:
19
07
2023
accepted:
20
07
2023
medline:
29
7
2023
pubmed:
29
7
2023
entrez:
29
7
2023
Statut:
epublish
Résumé
Among patients with ulcerative colitis, 30-50% receive corticosteroids within the first five years after diagnosis. We aimed to reconsider their effectiveness in the context of the biologic era. In this prospective, multicenter study, patients with active ulcerative colitis (Lichtiger score ≥ 4) were eligible if initiating systemic corticosteroids. The primary endpoint was clinical response (decrease in the Lichtiger score of ≥50%) at week 4. Secondary endpoints included combined response defined as clinical response and any reduction in elevated biomarkers (CRP and/or calprotectin). Steroid dependence was assessed after three months. A total of 103 patients were included. Clinical response was achieved by 73% of patients, and combined response by 68%. A total of 15% of patients were steroid-dependent. Activity of colitis did not influence short-term response to treatment but increased the risk for steroid dependence. Biologic-naïve patients responded better than biologic-experienced patients. Past smoking history (OR 5.38 [1.71, 20.1], Disease activity was not associated with short-term response to systemic corticosteroids but was associated with steroid dependence in patients with active ulcerative colitis. Exposure to biologics negatively affects response rates.
Sections du résumé
BACKGROUND
BACKGROUND
Among patients with ulcerative colitis, 30-50% receive corticosteroids within the first five years after diagnosis. We aimed to reconsider their effectiveness in the context of the biologic era.
METHODS
METHODS
In this prospective, multicenter study, patients with active ulcerative colitis (Lichtiger score ≥ 4) were eligible if initiating systemic corticosteroids. The primary endpoint was clinical response (decrease in the Lichtiger score of ≥50%) at week 4. Secondary endpoints included combined response defined as clinical response and any reduction in elevated biomarkers (CRP and/or calprotectin). Steroid dependence was assessed after three months.
RESULTS
RESULTS
A total of 103 patients were included. Clinical response was achieved by 73% of patients, and combined response by 68%. A total of 15% of patients were steroid-dependent. Activity of colitis did not influence short-term response to treatment but increased the risk for steroid dependence. Biologic-naïve patients responded better than biologic-experienced patients. Past smoking history (OR 5.38 [1.71, 20.1],
CONCLUSION
CONCLUSIONS
Disease activity was not associated with short-term response to systemic corticosteroids but was associated with steroid dependence in patients with active ulcerative colitis. Exposure to biologics negatively affects response rates.
Identifiants
pubmed: 37510968
pii: jcm12144853
doi: 10.3390/jcm12144853
pmc: PMC10382050
pii:
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : Nationalbank Österreich
ID : 17936
Organisme : ÖGGH
ID : Science Award
Références
Clin Transl Gastroenterol. 2020 May;11(5):e00174
pubmed: 32677804
Am J Gastroenterol. 2018 Mar;113(3):384-395
pubmed: 29317770
Clin Gastroenterol Hepatol. 2007 Jan;5(1):103-10
pubmed: 17142106
Front Pediatr. 2021 Feb 17;9:634739
pubmed: 33681110
Inflamm Bowel Dis. 2023 Jul 18;:
pubmed: 37463118
Clin Gastroenterol Hepatol. 2022 Dec;20(12):2868-2875.e1
pubmed: 35272029
Aliment Pharmacol Ther. 2020 May;51(9):880-888
pubmed: 32237087
Inflamm Bowel Dis. 2014 Apr;20(4):622-30
pubmed: 24583478
Dig Liver Dis. 2014 Nov;46(11):974-9
pubmed: 25096964
Gut. 1960 Sep;1:217-22
pubmed: 13760840
Gastroenterology. 2020 Apr;158(5):1450-1461
pubmed: 31945371
N Engl J Med. 2021 Sep 30;385(14):1280-1291
pubmed: 34587385
Aliment Pharmacol Ther. 2020 Jun;51(11):1039-1046
pubmed: 32291786
Lancet. 2017 Apr 29;389(10080):1756-1770
pubmed: 27914657
Lancet. 2021 Jun 19;397(10292):2372-2384
pubmed: 34090625
Scand J Gastroenterol. 2021 Nov;56(11):1304-1311
pubmed: 34415803
J Clin Med. 2022 Mar 18;11(6):
pubmed: 35330005
Clin Gastroenterol Hepatol. 2011 Jun;9(6):483-489.e3
pubmed: 21195796
Br Med J. 1962 Dec 29;2(5321):1708-11
pubmed: 13994348
Lancet. 2012 Dec 1;380(9857):1909-15
pubmed: 23063316
J Clin Med. 2020 Jul 10;9(7):
pubmed: 32664204
Clin Gastroenterol Hepatol. 2017 Feb;15(2):229-239.e5
pubmed: 27639327
J Crohns Colitis. 2021 Jul 5;15(7):1120-1129
pubmed: 33438008
Gut. 2010 Sep;59(9):1207-12
pubmed: 20801771
Gastroenterology. 2007 Feb;132(2):763-86
pubmed: 17258735
J Crohns Colitis. 2008 Mar;2(1):1-23
pubmed: 21172194
Lancet. 1990 Jul 7;336(8706):16-9
pubmed: 1973211
J Crohns Colitis. 2017 Oct 27;11(11):1309-1316
pubmed: 29088461
J Crohns Colitis. 2022 Jan 28;16(1):2-17
pubmed: 34635919
Inflamm Bowel Dis. 2022 Dec 1;28(12):1833-1837
pubmed: 35134899
Dig Liver Dis. 2017 Jan;49(1):11-16
pubmed: 27693318
Inflamm Bowel Dis. 2008 Dec;14(12):1660-6
pubmed: 18623174
Aliment Pharmacol Ther. 2020 Jul;52(2):292-302
pubmed: 32506695