Subjective loss of clinical response to TNFi in axSpA relates to recurrence of MRI bone marrow oedema particularly with long-acting agents.


Journal

Rheumatology (Oxford, England)
ISSN: 1462-0332
Titre abrégé: Rheumatology (Oxford)
Pays: England
ID NLM: 100883501

Informations de publication

Date de publication:
18 04 2022
Historique:
received: 11 04 2021
revised: 05 07 2021
pubmed: 18 7 2021
medline: 21 4 2022
entrez: 17 7 2021
Statut: ppublish

Résumé

Subjective loss of response immediately prior to routine TNFi therapy can occur in axial spondyloarthritis (axSpA). We investigated clinical outcomes in patients taking the first three licenced TNFis and correlated this with recurrence of MRI bone marrow oedema (MRI-BMO). Proof-of-concept study including axSpA patients established on etanercept (ETA), adalimumab (ADA) or infliximab (IFX) reporting symptom deterioration prior to next dose. MRI/clinical data were collected prior to scheduled dose (v1), 4 days post-dose (v2) and at the time of patient-reported symptom return (v3). MRI spine/sacroiliac joints utilizing 3 T were scored using the semi-quantitative Leeds MRI scoring system. A total of 113 clinical assessments and MRIs were performed in 38 participants (ADA = 16, ETA = 12, IFX = 10), mean age 42.1 years ± 24.4(2SD, n = 38), 71.1% male (n = 27/38), 69.7% HLA-B27 positive (n = 23/33). At v1, all patients had high disease activity [ASDAS-CRP = 3 (2.7-3.7)] and 57.9% had MRI-BMO (number of MRI-BMO: ETA = 26, ADA = 59, IFX = 28). Improved clinical responses were seen at v2 [ASDAS-CRP -0.41(-0.81 - 0.30), P =0.018; BASDAI -0.58(-2.2 - 0.52), P =0.024]. Despite just a 4-day interval between v1 and v2, a numerical reduction in MRI-BMO lesions between v1/v2 was observed (ETA = -6, ADA = -10, IFX = -3). By v3, comparatively fewer new BMO lesions were detected in the ETA and ADA groups compared with IFX (ETA = -1, ADA = +3, IFX = +8), although the numbers were too small to enable testing for statistical significance. Short-lived fluctuations in MRI-BMO were commoner with longer-acting agents and corresponded with subjective loss of clinical response before next scheduled TNFi dose. Larger studies are needed to confirm the possible pathogenic implications of this phenomenon.

Identifiants

pubmed: 34273162
pii: 6323373
doi: 10.1093/rheumatology/keab571
doi:

Substances chimiques

Tumor Necrosis Factor-alpha 0
Infliximab B72HH48FLU
Adalimumab FYS6T7F842
Etanercept OP401G7OJC

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

SI86-SI91

Informations de copyright

© The Author(s) 2021. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For permissions, please email: journals.permissions@oup.com.

Auteurs

Stephanie R Harrison (SR)

NIHR Leeds Biomedical Research Centre, Leeds Teaching Hospitals Trust.
Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds.

Rebecca Ansell (R)

NIHR Leeds Biomedical Research Centre, Leeds Teaching Hospitals Trust.
Department of Rheumatology, Bradford Teaching Hospitals, St Luke's Hospital, Bradford, UK.

Hannah R Mathieson (HR)

NIHR Leeds Biomedical Research Centre, Leeds Teaching Hospitals Trust.
Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds.
Department of Rheumatology, Bradford Teaching Hospitals, St Luke's Hospital, Bradford, UK.

Mira Merashli (M)

Department of Internal Medicine, Division of Rheumatology, American University Hospital, Beirut, Lebanon.

Noemi Busquets-Pérez (N)

Department of Rheumatology, Hospital General de Granollers, Granollers, Spain.

Dennis McGonagle (D)

NIHR Leeds Biomedical Research Centre, Leeds Teaching Hospitals Trust.
Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds.

Helena Marzo-Ortega (H)

NIHR Leeds Biomedical Research Centre, Leeds Teaching Hospitals Trust.
Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds.

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Classifications MeSH