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Anti-tumour necrosis factor α therapy modulates ghrelin in patients with severe rheumatoid arthritis
  1. M A Gonzalez-Gay1,
  2. M T Garcia-Unzueta4,
  3. A Berja4,
  4. T R Vazquez-Rodriguez1,
  5. C Gonzalez-Juanatey2,
  6. J M de Matias3,
  7. J Martin5,
  8. P H Dessein6,
  9. J Llorca7
  1. 1
    Division of Rheumatology, Hospital Xeral Calde, Lugo, Spain
  2. 2
    Division of Cardiology, Hospital Xeral Calde, Lugo, Spain
  3. 3
    Division of Endocrinology, Hospital Xeral Calde, Lugo, Spain
  4. 4
    Endocrinology Research Unit, Hospital Universitario Valdecilla, Santander, Spain
  5. 5
    Consejo Superior de Investigaciones Cientificas, Granada, Spain
  6. 6
    The Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand and Rheumatology Unit, Milpark Hospital, Johannesburg, South Africa
  7. 7
    Division of Epidemiology and Computational Biology, School of Medicine, University of Cantabria, Santander and CIBER Epidemiología y Salud Pública (CIBERESP), Spain
  1. Miguel A Gonzalez-Gay, Rheumatology Division, Hospital Xeral-Calde, c) Dr Ochoa s/n, 27004, Lugo, Spain; miguelaggay{at}hotmail.com

https://doi.org/10.1136/ard.2008.088773

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    The mechanisms involved in inflammation related accelerated atherosclerosis and cardiovascular disease in rheumatoid arthritis (RA) require further study.1

    Ghrelin, the endogenous ligand for the growth hormone secretagogue receptor, a gastric peptide playing a role in the appetite regulation, possesses anti-inflammatory properties.2 Otero et al showed reduced ghrelin plasma concentrations in patients with RA compared to controls.3

    Improvement of insulin resistance in patients with severe disease who started anti-tumour necrosis factor (TNF)α therapy has been described previously.4 Additionally, we have reported a rapid improvement in endothelial dysfunction5 and insulin sensitivity6 following the infusion of the chimeric anti-TNFα/monoclonal antibody/infliximab in patients with RA with severe disease on periodical treatment with this drug. Moreover, inhibition of basal …

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    Footnotes

    • MAGG and JL share senior authorship

    • Funding: This study was supported by a grant from Fondo de Investigaciones Sanitarias PI06-0024 (Spain).

    • Competing interests: Subsequent to this study, MAGG has accepted a role on the advisory board of Centocor. This study was not supported by any pharmaceatical company.

    • Ethics approval: Local institutional committee approval and patients’ informed consent was obtained.