Abstract |
Patients with active rheumatoid arthritis (RA) frequently show an atherogenic lipid profile, which has been linked with the inflammatory reaction. Inflammatory cytokines, and particularly tumor necrosis factor-alpha (TNF-α), are implicated in the pathogenesis of both atherosclerosis and RA, and also involved in the development of the impaired lipid profile detected in active RA. Although anti-TNF-α agents have been proven effective in controlling joint damage and systemic inflammation, controversy remains about the effect of these drugs on the lipid profile; therefore, the aim of our study was to investigate the effect of anti-TNF-α treatment, in combination with disease-modifying anti-rheumatic drugs (DMARDs) and corticosteroid therapy, on the lipid profile of patients with active RA. Our data suggest that the combination anti-TNF-α/DMARDs/ steroids do not significantly interfere with the lipid profile of RA patients. However, analysis of clinical response data showed that patients achieving low disease activity or remission seem to have a protective lipid profile, suggesting that better control of inflammation and disease activity can affect lipid metabolism. The available evidence indicates that high inflammation interferes with lipid metabolism, whereas good control of the chronic inflammatory state may positively influence the lipid profile and cardiovascular risk. Low cholesterol levels at baseline could predict a favorable outcome with anti-TNF-α treatment, but these data need to be confirmed by large prospective studies with long-term follow-up.
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Authors | Fabio Cacciapaglia, Maria Grazia Anelli, Angela Rinaldi, Lucia Serafino, Michele Covelli, Crescenzio Scioscia, Florenzo Iannone, Giovanni Lapadula |
Journal | Drug development research
(Drug Dev Res)
Vol. 75 Suppl 1
Pg. S77-80
(Nov 2014)
ISSN: 1098-2299 [Electronic] United States |
PMID | 25381986
(Publication Type: Clinical Trial, Journal Article)
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Copyright | © 2014 Wiley Periodicals, Inc. |
Chemical References |
- Adrenal Cortex Hormones
- Antibodies, Monoclonal
- Antibodies, Monoclonal, Humanized
- Antirheumatic Agents
- Immunoglobulin Fab Fragments
- Immunoglobulin G
- Receptors, Tumor Necrosis Factor
- Triglycerides
- Tumor Necrosis Factor-alpha
- Polyethylene Glycols
- Sulfasalazine
- Hydroxychloroquine
- Cyclosporine
- golimumab
- Cholesterol
- Infliximab
- Adalimumab
- Etanercept
- Aspirin
- Certolizumab Pegol
- Methotrexate
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Topics |
- Adalimumab
- Adrenal Cortex Hormones
(pharmacology, therapeutic use)
- Adult
- Aged
- Antibodies, Monoclonal
(pharmacology, therapeutic use)
- Antibodies, Monoclonal, Humanized
(pharmacology, therapeutic use)
- Antirheumatic Agents
(pharmacology, therapeutic use)
- Arthritis, Rheumatoid
(blood, drug therapy)
- Aspirin
(pharmacology, therapeutic use)
- Certolizumab Pegol
- Cholesterol
(blood)
- Cyclosporine
(pharmacology, therapeutic use)
- Drug Therapy, Combination
- Etanercept
- Female
- Humans
- Hydroxychloroquine
(pharmacology, therapeutic use)
- Immunoglobulin Fab Fragments
(pharmacology, therapeutic use)
- Immunoglobulin G
(pharmacology, therapeutic use)
- Infliximab
- Lipid Metabolism
(drug effects)
- Male
- Methotrexate
(pharmacology, therapeutic use)
- Middle Aged
- Polyethylene Glycols
(pharmacology, therapeutic use)
- Receptors, Tumor Necrosis Factor
(therapeutic use)
- Severity of Illness Index
- Sulfasalazine
(pharmacology, therapeutic use)
- Treatment Outcome
- Triglycerides
(blood)
- Tumor Necrosis Factor-alpha
(antagonists & inhibitors)
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