Evidence map›Paper›PMID 34357455›Full record

ArticleRheumatology international2022

Immunogenicity of subcutaneous TNF inhibitors and its clinical significance in real-life setting in patients with spondyloarthritis.

J Hiltunen, P Parmanne, T Sokka, T Lamberg, P Isomäki, O Kaipiainen-Seppänen, R Peltomaa, T Uutela, L Pirilä, K Taimen and 21 more

Open access · hybridAbstract read
In one paragraph

Article in Rheumatology international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Pharmacogenomics of TNF inhibitors.Frontiers in immunology · 2025
    Review
  3. Article
  4. Article
  5. Observational
  6. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

31 authors at 11 institutions in 1 country.

J HiltunenDepartment of Rheumatology, Helsinki University and Helsinki University Hospital, Haartmaninkatu 4, P. O. Box 372, 00029 HUS, Helsinki, Finland. johanna.hiltunen@hus.fi.ORCID 0000-0003-2280-3392
P ParmanneDepartment of Rheumatology, Helsinki University and Helsinki University Hospital, Haartmaninkatu 4, P. O. Box 372, 00029 HUS, Helsinki, Finland.
T SokkaDepartment of Rheumatology, Jyväskylä Central Hospital, Jyväskylä, Finland.
T LambergUnited Medix Laboratories, Helsinki, Finland.
P IsomäkiDepartment of Rheumatology, Tampere University Hospital, Tampere, Finland.
O Kaipiainen-SeppänenDepartment of Rheumatology, Kuopio University Hospital, Kuopio, Finland.
R PeltomaaDepartment of Rheumatology, Helsinki University and Helsinki University Hospital, Haartmaninkatu 4, P. O. Box 372, 00029 HUS, Helsinki, Finland.
T UutelaDepartment of Rheumatology, Central Hospital of Lapland, Rovaniemi, Finland.
L PiriläDepartment of Rheumatology, Turku University Hospital, Turku, Finland.
K TaimenDepartment of Rheumatology, Turku University Hospital, Turku, Finland.
M J KauppiDepartment of Rheumatology, Päijät-Häme Central Hospital, Lahti, Finland.
T Yli-KerttulaDepartment of Rheumatology, Satakunta Central Hospital, Rauma, Finland.
R TuompoDepartment of Rheumatology, Helsinki University and Helsinki University Hospital, Haartmaninkatu 4, P. O. Box 372, 00029 HUS, Helsinki, Finland.
H RelasDepartment of Rheumatology, Helsinki University and Helsinki University Hospital, Haartmaninkatu 4, P. O. Box 372, 00029 HUS, Helsinki, Finland.
S KortelainenDepartment of Rheumatology, Turku University Hospital, Turku, Finland.
K PaalanenDepartment of Rheumatology, Jyväskylä Central Hospital, Jyväskylä, Finland.
J AsikainenDepartment of Rheumatology, Jyväskylä Central Hospital, Jyväskylä, Finland.
P EkmanDepartment of Rheumatology, Satakunta Central Hospital, Rauma, Finland.
A SantistebanDepartment of Rheumatology, Mikkeli Central Hospital, Mikkeli, Finland.
K-L VidqvistDepartment of Rheumatology, Tampere University Hospital, Tampere, Finland.
K TadesseDepartment of Rheumatology, Helsinki University and Helsinki University Hospital, Haartmaninkatu 4, P. O. Box 372, 00029 HUS, Helsinki, Finland.
M RomuDepartment of Rheumatology, Helsinki University and Helsinki University Hospital, Haartmaninkatu 4, P. O. Box 372, 00029 HUS, Helsinki, Finland.
J BorodinaDepartment of Rheumatology, Jyväskylä Central Hospital, Jyväskylä, Finland.
P ElfvingDepartment of Rheumatology, Kuopio University Hospital, Kuopio, Finland.
H VallealaDepartment of Rheumatology, Helsinki University and Helsinki University Hospital, Haartmaninkatu 4, P. O. Box 372, 00029 HUS, Helsinki, Finland.
M Leirisalo-RepoDepartment of Rheumatology, Helsinki University and Helsinki University Hospital, Haartmaninkatu 4, P. O. Box 372, 00029 HUS, Helsinki, Finland.
V RantalaihoDepartment of Rheumatology, Tampere University Hospital, Tampere, Finland.
H KautiainenMedcare Foundation, Äänekoski, Finland.
T S JokirantaSYNLAB Finland, Helsinki, Finland.
K K EklundDepartment of Rheumatology, Helsinki University and Helsinki University Hospital, Haartmaninkatu 4, P. O. Box 372, 00029 HUS, Helsinki, Finland.
FinADASpA Study Group
Helsinki University Hospital · FIUniversity of Eastern Finland · FITampere University Hospital · FITurku University Hospital · FIKuopio University Hospital · FISatakunta Central Hospital · FILapland Central Hospital · FIMoisio Hospital · FITampere University · FIUniversity of Helsinki · FIVetcare (Finland) · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

key messagesConsiderable proportion of patients with SpA have been immunized to the subcutaneous anti-TNF drug they are using. Concomitant use of MTX protects from immunization, whereas SASP does not. Patients with SpA using subcutaneous anti-TNF drugs can benefit from monitoring of the drug trough levels. Immunization to biological drugs can lead to decreased efficacy and increased risk of adverse effects. The objective of this cross-sectional study was to assess the extent and significance of immunization to subcutaneous tumor necrosis factor (TNF) inhibitors in axial spondyloarthritis (axSpA) patients in real-life setting. A serum sample was taken 1-2 days before the next drug injection. Drug trough concentrations, anti-drug antibodies (ADAb) and TNF-blocking capacity were measured in 273 patients with axSpA using subcutaneous anti-TNF drugs. The clinical activity of SpA was assessed using the Bath AS Disease Activity Index (BASDAI) and the Maastricht AS Entheses Score (MASES). ADAb were found in 11% of the 273 patients: in 21/99 (21%) of patients who used adalimumab, in 0/83 (0%) of those who used etanercept, in 2/79 (3%) of those who used golimumab and in 6/12 (50%) of those who used certolizumab pegol. Use of methotrexate reduced the risk of formation of ADAb, whereas sulfasalazine did not. Presence of ADAb resulted in decreased drug concentration and reduced TNF-blocking capacity. However, low levels of ADAb had no effect on TNF-blocking capacity and did not correlate with disease activity. The drug trough levels were below the consensus target level in 36% of the patients. High BMI correlated with low drug trough concentration. Patients with low drug trough levels had higher disease activity. The presence of anti-drug antibodies was associated with reduced drug trough levels, and the patients with low drug trough levels had higher disease activity. The drug trough levels were below target level in significant proportion of patients and, thus, measuring the drug concentration and ADAb could help to optimize the treatment in SpA patients.

Indexed as

Antirheumatic AgentsSpondylarthritisSpondylitis, AnkylosingAntibodies, Monoclonal, HumanizedCross-Sectional StudiesHumansMethotrexateTumor Necrosis Factor-alphaTumor Necrosis Factor InhibitorsAntibodies, Monoclonal, HumanizedAntirheumatic AgentsMethotrexateTumor Necrosis Factor-alphaTumor Necrosis Factor InhibitorsAnkylosing spondylitisAnti-drug antibodiesBiological therapyDisease activitySpondyloarthritisTherapeutic drug monitoring

Identifiers

PMID34357455
PMCPMC9124652
OpenAlexW3188678012

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.