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Does TNF-α blockade play any role in cardiovascular risk among rheumatoid arthritis (RA) patients?
Clinical Rheumatology, 06/18/09
Cuchacovich R et al. – Finding of elevated levels of sTNFRII and IFN-γ in patients with rheumatoid arthritis (RA) on anti-TNF suggests that this therapy does not completely suppress the inflammatory process and may promote atherogenesis.
Methods- Aim was to determine the association and potential mechanisms between TNF-antagonists and increased CV risk in RA pts
- 3 groups of RA pts were studied:
- 10 treated with TNF-antagonists
- 13 with methotrexate, and
- 14 were naïve to treatment
- Mean age: 47.2, 52.3, and 51.2 yrs; mean disease duration: 102, 72.9, and 71.3 mo; treatment duration: 24.2, 34.7, and 0 mo for each group
- Clinical data: systolic and diastolic BP and BMI were assessed
- Disease activity was determined by DAS-28 index
- An ELISA assay for IL-6, sIL-6 R, IFN-γ, TNF-α, sTNFRI, sTNFRII, IGF I, and adiponectin were performed
- Fasting glucose, insulin, lipid profile, CRP, and ESR were also done
- HOMA-IR and QUICKI indexes were calculated
- Statistically significant differences observed between the TNF group and the other 2 groups were:
- TNF-α levels (p, 0.0014)
- Soluble TNF RII (p, 0.0432)
- IFN-γ (p, 0.008), and
- DAS-28 <2.6 (p, 0.033)
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