Pretreatment Vitamin D Concentrations Do Not Predict Therapeutic Outcome to Anti-TNF Therapies in Biologic-Naïve Patients With Active Luminal Crohn's Disease.
Crohn’s disease
IBD
PANTS
vitamin D
Journal
Crohn's & colitis 360
ISSN: 2631-827X
Titre abrégé: Crohns Colitis 360
Pays: England
ID NLM: 101752188
Informations de publication
Date de publication:
Jul 2023
Jul 2023
Historique:
received:
23
03
2023
medline:
2
6
2023
pubmed:
2
6
2023
entrez:
2
6
2023
Statut:
epublish
Résumé
Vitamin D has a regulatory role in innate and adaptive immune processes. Previous studies have reported that low pretreatment vitamin D concentrations are associated with primary non-response (PNR) and non-remission to anti-TNF therapy. This study aimed to assess whether pretreatment 25-hydroxyvitamin D concentrations predicted PNR and non-remission to infliximab and adalimumab in patients with active luminal Crohn's disease. 25-Hydroxyvitamin D concentrations were measured in stored baseline samples from 659 infliximab- and 448 adalimumab-treated patients in the Personalised Anti-TNF Therapy in Crohn's disease (PANTS) study. Cut-offs for vitamin D were deficiency <25 nmol/L, insufficiency 25-50 nmol/L, and adequacy/sufficiency >50 nmol/L. About 17.1% (189/1107; 95% CI, 15.0-19.4) and 47.7% (528/1107; 95% CI, 44.8-50.6) of patients had vitamin D deficiency and insufficiency, respectively. 22.2% (246/1107) of patients were receiving vitamin D supplementation. Multivariable analysis confirmed that sampling during non-summer months, South Asian ethnicity, lower serum albumin concentrations, and non-treatment with vitamin D supplementation were independently associated with lower vitamin D concentrations. Pretreatment vitamin D status did not predict response or remission to anti-TNF therapy at week 14 (infliximab Vitamin D deficiency is common in patients with active Crohn's disease. Unlike previous studies, pretreatment vitamin D concentration did not predict PNR to anti-TNF treatment at week 14 or nonremission at week 54.
Sections du résumé
Background and Aims
UNASSIGNED
Vitamin D has a regulatory role in innate and adaptive immune processes. Previous studies have reported that low pretreatment vitamin D concentrations are associated with primary non-response (PNR) and non-remission to anti-TNF therapy. This study aimed to assess whether pretreatment 25-hydroxyvitamin D concentrations predicted PNR and non-remission to infliximab and adalimumab in patients with active luminal Crohn's disease.
Methods
UNASSIGNED
25-Hydroxyvitamin D concentrations were measured in stored baseline samples from 659 infliximab- and 448 adalimumab-treated patients in the Personalised Anti-TNF Therapy in Crohn's disease (PANTS) study. Cut-offs for vitamin D were deficiency <25 nmol/L, insufficiency 25-50 nmol/L, and adequacy/sufficiency >50 nmol/L.
Results
UNASSIGNED
About 17.1% (189/1107; 95% CI, 15.0-19.4) and 47.7% (528/1107; 95% CI, 44.8-50.6) of patients had vitamin D deficiency and insufficiency, respectively. 22.2% (246/1107) of patients were receiving vitamin D supplementation. Multivariable analysis confirmed that sampling during non-summer months, South Asian ethnicity, lower serum albumin concentrations, and non-treatment with vitamin D supplementation were independently associated with lower vitamin D concentrations. Pretreatment vitamin D status did not predict response or remission to anti-TNF therapy at week 14 (infliximab
Conclusions
UNASSIGNED
Vitamin D deficiency is common in patients with active Crohn's disease. Unlike previous studies, pretreatment vitamin D concentration did not predict PNR to anti-TNF treatment at week 14 or nonremission at week 54.
Identifiants
pubmed: 37265586
doi: 10.1093/crocol/otad026
pii: otad026
pmc: PMC10231451
doi:
Types de publication
Journal Article
Langues
eng
Pagination
otad026Informations de copyright
© The Author(s) 2023. Published by Oxford University Press on behalf of Crohn's & Colitis Foundation.
Déclaration de conflit d'intérêts
S.L. reports nonfinancial support from Pfizer outside the submitted work. N.A.K. reports grants from F. Hoffmann-La Roche AG, grants from Biogen Inc, grants from Celltrion Healthcare, grants from Galapagos NV, nonfinancial support from Immundiagnostik, grants and nonfinancial support from AbbVie, grants and personal fees from Celltrion, personal fees and nonfinancial support from Janssen, personal fees from Takeda, personal fees and nonfinancial support from Dr Falk, outside the submitted work. T.A. reports grants and nonfinancial support from F. Hoffmann-La Roche AG, grants from Biogen Inc, grants from Celltrion Healthcare, grants from Galapagos NV, nonfinancial support from Immundiagnostik, personal fees from Biogen inc, grants and personal fees from Celltrion Healthcare, personal fees and nonfinancial support from Immundiagnostik, personal fees from Takeda, personal fees from ARENA, personal fees from Gilead, personal fees from Adcock Ingram Healthcare, personal fees from Pfizer, personal fees from Genentech, nonfinancial support from Tillotts, outside the submitted work. J.R.G. reports grants from F. Hoffmann-La Roche AG, grants from Biogen Inc, grants from Celltrion Healthcare, grants from Galapagos NV, nonfinancial support from Immundiagnostik, outside the submitted work. The following authors have nothing to declare: N.C., R.S., C.R., R.N., T.J.M., C.B., B.H., and M.B.
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