Evidence map›Paper›PMID 16079165›Full record

Trial reportAnnals of the rheumatic diseases2006

Anti-TNF antibody treatment improves glucocorticoid induced insulin-like growth factor 1 (IGF1) resistance without influencing myoglobin and IGF1 binding proteins 1 and 3.

P Sarzi-Puttini, F Atzeni, J Schölmerich, M Cutolo, R H Straub

Open access · greenAbstract readClinical Trial
In one paragraph

Trial report in Annals of the rheumatic diseases, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 39 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Review
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  8. Review
  9. Article
  10. Brain-immune interactions and the neural basis of disease-avoidant ingestive behaviour.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2011
    Review
  11. Bone, inflammation, and inflammatory bowel disease.Current osteoporosis reports · 2011
    Review
  12. Article
  13. Article
  14. Article
  15. The Anti-Inflammatory Actions of Exercise Training.American journal of lifestyle medicine · 2007
    Article
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

5 authors at 4 institutions in 2 countries.

P Sarzi-PuttiniLaboratory of Experimental Rheumatology and Neuroendocrino-immunology, Department of Internal Medicine I, University Hospital, 93042 Regensburg, Germany.
F Atzeni
J Schölmerich
M Cutolo
R H Straub
University Hospital Regensburg · DEIstituti di Ricovero e Cura a Carattere Scientifico · ITUniversity of Genoa · ITUniversity of Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInsulin-like growth factor 1 (IGF1) is an important determinant of muscle mass because it promotes growth and suppresses protein degradation. IGF1 is decreased in rheumatoid arthritis and juvenile idiopathic arthritis because its synthesis is inhibited by inflammation. In parallel, glucocorticoids induce IGF1 resistance and add to muscle degradation.

objectiveTo investigate the influence of anti-tumour necrosis factor antibody treatment (anti-TNF) with adalimumab on levels of myoglobin (degradation marker) and IGF1 in patients with rheumatoid arthritis with and without prednisolone treatment.

methodsSubcutaneous adalimumab was given to 32 patients with longstanding rheumatoid arthritis (16 with and 16 without prednisolone) in a longitudinal study. IGF1, IGF1 binding protein 1 (IGFBP-1), IGFBP-3, and myoglobin were measured by enzyme linked immunosorbent assay.

resultsRheumatoid patients had normal serum myoglobin. Patients on prednisolone had higher myoglobin than patients not receiving prednisolone, indicating increased muscle degradation. On treatment with anti-TNF, myoglobin levels did not change in either patient group. Serum IGF1 was increased in patients with v without prednisolone, indicating IGF1 resistance (mean (SEM): 221 (23) v 122 (14) microg/l, p<0.001). Adalimumab treatment decreased the raised IGF1 levels in patients with prednisolone, so that after 12 weeks of treatment they reached the level of patients without prednisolone. Serum IGFBP-1 and IGFBP-3 did not differ in the two groups, and anti-TNF did not change these concentrations.

conclusionsAnti-TNF antibody treatment over 12 weeks improved glucocorticoid induced IGF1 resistance without influencing myoglobin and IGF1 binding proteins. Thus, in rheumatoid patients on glucocorticoids with generally decreased muscle mass anti-TNF treatment with adalimumab has favourable effects.

Indexed as

AdalimumabAgedAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntirheumatic AgentsArthritis, RheumatoidDrug ResistanceDrug Therapy, CombinationFemaleGlucocorticoidsHumansInsulin-Like Growth Factor Binding Protein 1Insulin-Like Growth Factor Binding Protein 3Insulin-Like Growth Factor IInterleukin-6Longitudinal StudiesAdalimumabAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntirheumatic AgentsGlucocorticoidsInsulin-Like Growth Factor Binding Protein 1Insulin-Like Growth Factor Binding Protein 3Insulin-Like Growth Factor IInterleukin-6MyoglobinPrednisoloneTumor Necrosis Factor-alpha

Identifiers

PMID16079165
PMCPMC1798065
OpenAlexW2132511355

What OpenQuestion holds

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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.